Academic literature on the topic 'Cerebral neurodegenerative disease'
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Journal articles on the topic "Cerebral neurodegenerative disease"
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Bass, Nancy. "Cerebral palsy and neurodegenerative disease." Current Opinion in Pediatrics 11, no. 6 (December 1999): 504–7. http://dx.doi.org/10.1097/00008480-199912000-00005.
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Maruyama, Hirofumi. "Cerebral blood flow of neurodegenerative disease." Cerebral Blood Flow and Metabolism (Japanese journal of cerebral blood flow and metabolism) 28, no. 2 (2017): 337–39. http://dx.doi.org/10.16977/cbfm.28.2_337.
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Dusek, Petr, Tim Hofer, Jan Alexander, Per M. Roos, and Jan O. Aaseth. "Cerebral Iron Deposition in Neurodegeneration." Biomolecules 12, no. 5 (May 17, 2022): 714. http://dx.doi.org/10.3390/biom12050714.
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Disruption of cerebral iron regulation appears to have a role in aging and in the pathogenesis of various neurodegenerative disorders. Possible unfavorable impacts of iron accumulation include reactive oxygen species generation, induction of ferroptosis, and acceleration of inflammatory changes. Whole-brain iron-sensitive magnetic resonance imaging (MRI) techniques allow the examination of macroscopic patterns of brain iron deposits in vivo, while modern analytical methods ex vivo enable the determination of metal-specific content inside individual cell-types, sometimes also within specific cellular compartments. The present review summarizes the whole brain, cellular, and subcellular patterns of iron accumulation in neurodegenerative diseases of genetic and sporadic origin. We also provide an update on mechanisms, biomarkers, and effects of brain iron accumulation in these disorders, focusing on recent publications. In Parkinson’s disease, Friedreich’s disease, and several disorders within the neurodegeneration with brain iron accumulation group, there is a focal siderosis, typically in regions with the most pronounced neuropathological changes. The second group of disorders including multiple sclerosis, Alzheimer’s disease, and amyotrophic lateral sclerosis shows iron accumulation in the globus pallidus, caudate, and putamen, and in specific cortical regions. Yet, other disorders such as aceruloplasminemia, neuroferritinopathy, or Wilson disease manifest with diffuse iron accumulation in the deep gray matter in a pattern comparable to or even more extensive than that observed during normal aging. On the microscopic level, brain iron deposits are present mostly in dystrophic microglia variably accompanied by iron-laden macrophages and in astrocytes, implicating a role of inflammatory changes and blood–brain barrier disturbance in iron accumulation. Options and potential benefits of iron reducing strategies in neurodegeneration are discussed. Future research investigating whether genetic predispositions play a role in brain Fe accumulation is necessary. If confirmed, the prevention of further brain Fe uptake in individuals at risk may be key for preventing neurodegenerative disorders.
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Trujillo-Estrada, Laura, Angela Gomez-Arboledas, Stefânia Forner, Alessandra Cadete Martini, Antonia Gutierrez, David Baglietto-Vargas, and Frank M. LaFerla. "Astrocytes: From the Physiology to the Disease." Current Alzheimer Research 16, no. 8 (October 11, 2019): 675–98. http://dx.doi.org/10.2174/1567205016666190830110152.
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Astrocytes are key cells for adequate brain formation and regulation of cerebral blood flow as well as for the maintenance of neuronal metabolism, neurotransmitter synthesis and exocytosis, and synaptic transmission. Many of these functions are intrinsically related to neurodegeneration, allowing refocusing on the role of astrocytes in physiological and neurodegenerative states. Indeed, emerging evidence in the field indicates that abnormalities in the astrocytic function are involved in the pathogenesis of multiple neurodegenerative diseases, including Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’s Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). In the present review, we highlight the physiological role of astrocytes in the CNS, including their communication with other cells in the brain. Furthermore, we discuss exciting findings and novel experimental approaches that elucidate the role of astrocytes in multiple neurological disorders.
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Turturici, Giuseppina, Gabriella Sconzo, and Fabiana Geraci. "Hsp70 and Its Molecular Role in Nervous System Diseases." Biochemistry Research International 2011 (2011): 1–18. http://dx.doi.org/10.1155/2011/618127.
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Heat shock proteins (HSPs) are induced in response to many injuries including stroke, neurodegenerative disease, epilepsy, and trauma. The overexpression of one HSP in particular, Hsp70, serves a protective role in several different models of nervous system injury, but has also been linked to a deleterious role in some diseases. Hsp70 functions as a chaperone and protects neurons from protein aggregation and toxicity (Parkinson disease, Alzheimer disease, polyglutamine diseases, and amyotrophic lateral sclerosis), protects cells from apoptosis (Parkinson disease), is a stress marker (temporal lobe epilepsy), protects cells from inflammation (cerebral ischemic injury), has an adjuvant role in antigen presentation and is involved in the immune response in autoimmune disease (multiple sclerosis). The worldwide incidence of neurodegenerative diseases is high. As neurodegenerative diseases disproportionately affect older individuals, disease-related morbidity has increased along with the general increase in longevity. An understanding of the underlying mechanisms that lead to neurodegeneration is key to identifying methods of prevention and treatment. Investigators have observed protective effects of HSPs induced by preconditioning, overexpression, or drugs in a variety of models of brain disease. Experimental data suggest that manipulation of the cellular stress response may offer strategies to protect the brain during progression of neurodegenerative disease.
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Salvadori, Claudia, Laura Lossi, Mario Arispici, and Carlo Cantile. "Spongiform neurodegenerative disease in a Persian kitten." Journal of Feline Medicine and Surgery 9, no. 3 (June 2007): 242–45. http://dx.doi.org/10.1016/j.jfms.2006.12.001.
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A congenital encephalopathy with spongiform degeneration and prominent neuronal apoptosis was observed in a 4-month-old Persian male cat with a history of depressed mental status and ataxia. On clinical examination, signs included right head tilt, ventroflexion of the head and neck, and tetraparesis. Histological examination of the central nervous system revealed multifocal, bilateral and symmetrical vacuolar degeneration of the neuropil, mainly involving the cerebellar and vestibular nuclei area, the caudal colliculi, the mesencephalic nuclei, the tegmental area and the deeper layer of the cerebral cortex. Accumulation of phosphorylated neurofilaments was detected in neuronal perikarya of the deep cortical layers, hippocampus and thalamus. Numerous pyknotic and apoptotic neurons were also observed in the cerebral cortex. These neuropathological changes differ from those observed in previous reports of spongiform degeneration of the grey matter in cats and were suggestive of a congenital neurodegenerative disease.
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Beaman, Charles, Krystyna Kozii, Saima Hilal, Minghua Liu, Anthony J. Spagnolo-Allende, Guillermo Polanco-Serra, Christopher Chen, et al. "Cerebral Microbleeds, Cerebral Amyloid Angiopathy, and Their Relationships to Quantitative Markers of Neurodegeneration." Neurology 98, no. 16 (February 28, 2022): e1605-e1616. http://dx.doi.org/10.1212/wnl.0000000000200142.
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Background and ObjectivesAge-related cognitive impairment is driven by the complex interplay of neurovascular and neurodegenerative disease. There is a strong relationship between cerebral microbleeds (CMBs), cerebral amyloid angiopathy (CAA), and the cognitive decline observed in conditions such as Alzheimer disease. However, in the early, preclinical phase of cognitive impairment, the extent to which CMBs and underlying CAA affect volumetric changes in the brain related to neurodegenerative disease remains unclear.MethodsWe performed cross-sectional analyses from 3 large cohorts: The Northern Manhattan Study (NOMAS), Alzheimer's Disease Neuroimaging Initiative (ADNI), and the Epidemiology of Dementia in Singapore study (EDIS). We conducted a confirmatory analysis of 82 autopsied cases from the Brain Arterial Remodeling Study (BARS). We implemented multivariate regression analyses to study the association between 2 related markers of cerebrovascular disease—MRI-based CMBs and autopsy-based CAA—as independent variables and volumetric markers of neurodegeneration as dependent variables. NOMAS included mostly dementia-free participants age 55 years or older from northern Manhattan. ADNI included participants living in the United States age 55–90 years with a range of cognitive status. EDIS included community-based participants living in Singapore age 60 years and older with a range of cognitive status. BARS included postmortem pathologic samples.ResultsWe included 2,657 participants with available MRI data and 82 autopsy cases from BARS. In a meta-analysis of NOMAS, ADNI, and EDIS, superficial CMBs were associated with larger gray matter (β = 4.49 ± 1.13, p = 0.04) and white matter (β = 4.72 ± 2.1, p = 0.03) volumes. The association between superficial CMBs and larger white matter volume was more evident in participants with 1 CMB (β = 5.17 ± 2.47, p = 0.04) than in those with ≥2 CMBs (β = 1.97 ± 3.41, p = 0.56). In BARS, CAA was associated with increased cortical thickness (β = 6.5 ± 2.3, p = 0.016) but not with increased brain weight (β = 1.54 ± 1.29, p = 0.26).DiscussionSuperficial CMBs are associated with larger morphometric brain measures, specifically white matter volume. This association is strongest in brains with fewer CMBs, suggesting that the CMB/CAA contribution to neurodegeneration may not relate to tissue loss, at least in early stages of disease.
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Yadav, Dharmendra Kumar. "Potential Therapeutic Strategies of Phytochemicals in Neurodegenerative Disorders." Current Topics in Medicinal Chemistry 21, no. 31 (December 23, 2021): 2814–38. http://dx.doi.org/10.2174/1568026621666211201150217.
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Neurodegeneration is a syndrome that occurs through the loss of the neuronal system's structure and function. In the 21st century, major health issues are related to cognitive impairment and neurological disorders such as autism, learning disabilities, Huntington’s, cerebral palsy, schizophrenia, Alzheimer's, neuromuscular, lateral sclerosis, and Parkinson’s disease may be life-threatening. Various experimental and epidemiological studies reveal the risk factors associated with the disease, like oxidative stress, hypertension, antioxidant enzyme abnormalities, metabolic toxicity, advanced age, cytoskeletal abnormalities, genetic defects, autoimmunity, mineral deficiencies, and other vascular disorders. Various compounds have been screened for the treatment of neurodegenerative diseases (NDs), but, due to their side effects, they have solitary symptomatic benefits. Phytochemicals play a crucial role in maintaining the chemical balance of the brain by affecting the receptor function of specific inhibitory neurotransmitters. This review highlights the importance of phytochemicals for neurodegenerative diseases, in particular the possible mechanism of action of these natural compounds used for the treatment.
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Ribe, Elena M., Esther Serrano-Saiz, Nsikan Akpan, and Carol M. Troy. "Mechanisms of neuronal death in disease: defining the models and the players." Biochemical Journal 415, no. 2 (September 25, 2008): 165–82. http://dx.doi.org/10.1042/bj20081118.
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Dysregulation of life and death at the cellular level leads to a variety of diseases. In the nervous system, aberrant neuronal death is an outstanding feature of neurodegenerative diseases. Since the discovery of the caspase family of proteases, much effort has been made to determine how caspases function in disease, including neurodegenerative diseases. Although many papers have been published examining caspases in neuronal death and disease, the pathways have not been fully clarified. In the present review, we examine the potential players in the death pathways, the current tools for examining these players and the models for studying neurological disease. Alzheimer's disease, the most common neurodegenerative disorder, and cerebral ischaemia, the most common cause of neurological death, are used to illustrate our current understanding of death signalling in neurodegenerative diseases. A better understanding of the neuronal death pathways would provide targets for the development of therapeutic interventions for these diseases.
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Accogli, Andrea, Kether Guerrero, Maria Daniela D’Agostino, Luan Tran, Cécile Cieuta-Walti, Isabelle Thiffault, Sébastien Chénier, Jeremy Schwartzentruber, Jacek Majewski, and Geneviève Bernard. "Biallelic Loss-of-Function Variants in AIMP1 Cause a Rare Neurodegenerative Disease." Journal of Child Neurology 34, no. 2 (November 28, 2018): 74–80. http://dx.doi.org/10.1177/0883073818811223.
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AIMP1/p43, is a noncatalytic component of the mammalian multi-tRNA synthetase complex that catalyzes the ligation of amino acids to their cognate tRNAs. AIMP1 is largely expressed in the central nervous system, where it is part of the regulatory machine of the neurofilament assembly, playing a crucial role in neuronal development and function. To date, nonsense mutations in AIMP1 have been associated with a primary neurodegenerative disorder consisting of cerebral atrophy, hypomyelination, microcephaly and epilepsy, whereas missense mutations have recently been linked to intellectual disability without neurodegeneration. Here, we report the first French-Canadian patient with a novel frameshift AIMP1 homozygous mutation (c.191_192delAA, p.Gln64Argfs*25), resulting in a severe neurodegenerative phenotype. We review and discuss the phenotypic spectrum associated with AIMP1 pathogenic variants.
Dissertations / Theses on the topic "Cerebral neurodegenerative disease"
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Augé, Marí Elisabet. "Categorització dels cossos de poliglucosà cerebrals basada en la presència de neoepítops reconeguts per IgMs naturals." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/586351.
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El terme cossos de poliglucosà (PGBs) fa referència a agregats complexos formats per polímers de glucosa que arriben a fer diàmetres de desenes de micròmetres. Aquestes estructures s’han observat en el sistema nerviós central, però també en altres òrgans i teixits, com ara al cor, al múscul esquelètic i al fetge. Els PGBs han estat descrits en humans i altres espècies, però sobretot s’han estudiat més àmpliament en els mamífers. Diferents formes de PGBs estan relacionades amb determinades situacions o malalties. Durant el procés d'envelliment, el cervell humà acumula un tipus de PGBs anomenat cossos amilacis o corpora amylacea (CA). Encara que els CA han estat estudiats durant diversos anys, el seu origen i la seva funció encara romanen incerts. Els PGBs també es troben associats a la malaltia de Lafora, un trastorn neurodegeneratiu que es caracteritza per la presència d'estructures de tipus de poliglucosà denominades cossos de Lafora (LBs). D'altra banda, l'envelliment cerebral en ratolins condueix a l’aparició i l’expansió progressiva d’uns PGBs granulars degeneratius anomenats grànuls periodic acid Schiff (PAS). Aquests grànuls, que es troben principalment a l'hipocamp, s'originen en processos astrocítics i solen agrupar-se formant clústers. Cada clúster correspon al conjunt de grànuls d'un astròcit determinat. Recentment, el nostre grup de recerca ha descrit la presència d’uns neo-epítops en aquestes estructures que són reconeguts per IgMs. Aquestes IgMs, que es troben com a contaminants en alguns anticossos comercials, són les responsables de produir falsos marcatges positius d’aquests cossos quan s'utilitzen procediments immunohistoquímics.
Aquesta tesi pretén estudiar l'origen, la composició i la funció dels PGBs que apareixen amb l'edat i en condicions neurodegeneratives, com la malaltia d'Alzheimer i la malaltia de Lafora.
Els resultats obtinguts mostren que els CA són estructures similars als grànuls PAS de ratolí i que els CA també contenen neo-epítops. En ambdós casos, els neo-epítops poden ser reconeguts per IgMs naturals, fet que suggereix una nova relació entre els PGBs i el sistema immunitari innat. A més a més, els falsos marcatges positius que es produeixen degut a les IgMs naturals que es troben com a contaminants en alguns anticossos comercials aclareixen alguns resultats controvertits en quant a la presència d'alguns components descrits prèviament als CA. També s’ha determinat que els CA acumulen productes no degradables generats durant el procés d'envelliment i augmentats en malalties neurodegeneratives, com per exemple la malaltia d'Alzheimer. Tenint en compte aquests resultats, es planteja la hipòtesi que els CA són uns elements encarregats de l’eliminació de productes perjudicials o residuals a través de l'acció del sistema immunitari innat. D'altra banda, s’ha observat que els ratolins deficients de malina, un model de la malaltia de Lafora, presenten un elevat nombre de dos tipus diferents de PGBs: els grànuls PAS o CA-like, originats en astròcits i que contenen neo-epítops i els neuronal LBs, que són exclusius de la malaltia de Lafora i no contenen neo-epítops. Així doncs, l'absència de malina provoca la formació de PGBs a les neurones, però també augmenta el seu desenvolupament en astròcits. Postulem, en contra el que s’havia descrit prèviament, que els astròcits podrien intervenir en l'etiopatogènesi de la malaltia de Lafora.
En global, els resultats obtinguts mostren que, fins ara, els diferents PGBs han estat estudiats amb una perspectiva específica i limitada. Una imatge global o principal és necessària per obtenir el coneixement de la seva importància fisiopatològica.The term polyglucosan bodies (PGBs) refers to complex aggregates composed of relatively large glucose polymers reaching diameters of tens of micrometres. PGBs have been reported in the central nervous system, but also in other organs and tissues. During the ageing process, human brain accumulates one type of PGBs called corpora amylacea (CA). Although CA have been studied for several years, their origin and function remain unclear. PGBs are also associated with Lafora disease, a neurodegenerative condition that is characterized by the presence of PGBs structures called Lafora bodies (LBs). On the other hand, brain ageing in mice leads to the progressive appearance and expansion of degenerative granular PGBs frequently referred to as Periodic Acid Schiff (PAS) granules. These granules, which are present mainly in the hippocampus, originate in astrocytes processes and tend to appear in clusters. Recently, our research group have reported the presence of neo-epitopes on these structures, responsible of numerous false positive staining on these bodies when immunohistochemical procedures are used. This thesis aimed to study the origin, composition and function of PGBs that appear with age and in neurodegenerative conditions such as Alzheimer’s disease and Lafora disease, focusing on the possible presence of neo-epitopes on these structures. The results obtained in this thesis show, firstly, that CA are structures similar to PAS granules from mice brain and that CA also contain neo-epitopes. In both cases, the neo-epitopes can be recognized by natural IgM antibodies, suggesting a new relation between PGBs and the natural immune system. This fact explains the controversial results previously described about the presence of some components in CA. In this work, some of these components have been discarded. Secondly, malin deficient mice, a mouse model of Lafora disease, present distinct types of PGBs: PAS granules or CA-like granules, originated in astrocytes, and neuronal LBs. This last type of PGBs is specific of this condition and does not contain neo-epitopes. Overall results suggest that CA are PGBs related to the aggregation of non-degradable products produced during ageing process and increased in neurodegenerative conditions, whereas LBs are pathogenic structures responsible of the neurodegeneration observed in Lafora disease.
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Simões, Ana Carolina Viana. "Avaliação do efeito neuroprotetor do canabidiol em mitocôndrias isolados de córtex cerebral de rato." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-29062011-202616/.
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As doenças neurodegenerativas (DN) estão entre as principais causas de mortalidade e morbidade nos países ocidentais. Não há ainda um tratamento definitivo para estas neuropatias, mas os estudos têm indicado mecanismos comuns de toxicidade que incluem disfunção mitocondrial, estresse oxidativo e apoptose. Assim, as mitocôndrias constituem alvos importantes para futuras estratégias de neuroproteção a fim de tratar, prevenir ou até mesmo retardar a neurodegeneração. Neste contexto, o canabidiol (CBD), um constituinte não psicoativo da Cannabis sativa e cuja propriedade neuroprotetora tem sido sugerida por diferentes estudos, surge como uma alternativa bastante promissora. Diferentes mecanismos moleculares podem estar envolvidos na neuroproteção exercida pelo CBD. Embora o potencial efeito benéfico do canabidiol com relação às doenças neurodegenerativas já tenha sido sugerido, não há ainda estudos que abordem precisamente os mecanismos de proteção contra a toxicidade mitocondrial cerebral, evento chave no processo neurodegenerativo. O presente estudo teve como objetivo investigar os efeitos do CBD em mitocôndrias cerebrais de rato, bem como possíveis mecanismos de neuroproteção. Foram avaliados os seguintes parâmetros: função mitocondrial, estresse oxidativo mitocondrial e transição de permeabilidade de membrana mitocondrial (TPMM). Os resultados obtidos sugerem que o canabidiol é capaz de proteger as mitocôndrias cerebrais contra o intumescimento osmótico induzido por cálcio/fosfato, contra a produção de H2O2 induzida por terc-butil hidroperóxido e contra a peroxidação lipídica induzida por Fe2+ e citrato. A captação mitocondrial de cálcio e a capacidade fosforilativa não foram afetadas.Neurodegenerative diseases (ND) are among the leading causes of mortality and morbidity in Western countries. There is not a definitive treatment for these neuropathies, but studies have indicated mechanisms of toxicity which include mitochondrial dysfunction, oxidative stress and apoptosis. Therefore, mitochondria are important targets for future neuroprotective strategies to treat, prevent or even slow the neurodegeneration. In this context, cannabidiol (CBD), a constituent of non-psychoactive Cannabis sativa and whose neuroprotective property has been suggested by different studies, emerges as a promising alternative. Different molecular mechanisms may be involved in the neuroprotection exerted by CBD. Although the potential beneficial effects of cannabidiol in relation to neurodegenerative diseases has already been suggested, there are no studies addressing specifically the mechanisms of protection against mitochondrial toxicity brain, a key event in the neurodegenerative process. This study aimed to investigate the effects of CBD on rat brain mitochondria, as well as the mechanisms of neuroprotection. The following parameters were evaluated: mitochondrial function, mitochondrial oxidative stress and permeability transition of the mitochondrial membrane (MPT). The results suggest that cannabidiol can protect brain mitochondria against: the osmotic swelling induced by calcium/phosphate, the production of H2O2 induced by tert-butyl hydroperoxide and the lipid peroxidation induced by Fe2+ and citrate. The mitochondrial calcium uptake and phosphorylative capacity were not affected.
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Melton, Lisa M. "Neuropathological studies of glial activation in experimental head injury and a novel model of chronic cerebral inflammation." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339406.
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Salvadores, Bersezio Natalia. "Amyloid-β and chronic cerebral hypoperfusion in the early pathogenesis of Alzheimer's disease." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23388.
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Alzheimer’s disease (AD) is a severe age-related neurodegenerative disorder and is the most common form of dementia. Although the pathogenesis of AD remains unknown, the deterioration of the cerebrovascular system constitutes a risk factor associated with the development of the disease. Notably, brain hypoperfusion, a feature of healthy ageing brain and AD, occurs prior to the onset of cognitive decline in AD and correlates with the severity of dementia. Although there is a clear link between hypoperfusion and cognitive alterations in AD, a causal relationship remains to be established. It was hypothesised that chronic cerebral hypoperfusion leads to the accumulation of parenchymal and vascular amyloid-β (Aβ), triggering the development of vascular lesion (microinfarcts (MIs) and haemorrhages) and altering the neurovascular unit (NVU) integrity. Second to this, it was hypothesised that reductions in Aβ levels by immunotherapy targeted to amyloid in young mice, reduce amyloid levels, and prevent vascular lesions improving cognitive performance. Three studies were conducted to test these hypotheses. In the first study, the aim was to characterise age-dependent changes in amyloidrelated pathology in a transgenic mouse model (Tg-SwDI). The temporal amyloid precursor protein (APP) expression, accumulation of parenchymal and cerebrovascular Aβ and Aβ-related microglial and astrocytic activation in the cortex, hippocampus and thalamus of the Tg-SwDI mice at 3, 6 and 9 months of age was compared to wild-type controls. Significantly higher APP expression (p < 0.05), as well as Aβ aggregation (p < 0.001) as the animals aged was found in the Tg-SwDI mice in all the brain regions analysed, which was accompanied by extensive and progressive activation of microglial (p < 0.001) and astrocytic (p < 0.01) cells. These data provided a basis to design the next studies, as it was planned to induce hypoperfusion in these mice before significant Aβ deposition occurs. In the second study, the aim was to investigate the effect of hypoperfusion on Aβ dynamics and subsequently, to study the contribution of hypoperfusion and Aβ pathology to the development of MIs and haemorrhages, and to the potential alteration of astrocyte and tight junction (TJ) integrity. To address this, mild chronic cerebral hypoperfusion was induced in Tg-SwDI and wild-type mice by bilateral common carotid stenosis for 1 and 3 months. A significant increase in soluble Aβ40/42 levels was initially found after 1 month of hypoperfusion in the parenchyma (Aβ40, p = 0.0239; Aβ42 p = 0.0198) in parallel with elevated APP levels and APP proteolytic cleavage products (p < 0.05). Thereafter, following 3 months, a significant increase in insoluble Aβ40/42 levels was determined in the parenchyma (Aβ40, p = 0.0024; Aβ42 p = 0.008) and vasculature (Aβ40, p = 0.0046; Aβ42 p = 0.0118) of Tg-SwDI mice. There was no change in the levels of Aβ co-localised to vessels following 1 month of hypoperfusion; however Aβ levels were significantly increased in cerebral vessels after 3 months (p = 0.0483). The proportion of Aβ containing vessels was significantly higher in the small vessels of the hypoperfused animals compared to sham mice (p < 0.05). MIs associated with microglial proliferation were present in the Tg-SwDI mice and the burden was exacerbated by hypoperfusion at 1 and 3 months (p < 0.05). Significantly higher levels of NADPH Oxidase-2 (NOX2) were found in the transgenic mice compared to the wild-type controls at both time-points analysed (p < 0.05), and this was exacerbated after 1 month of hypoperfusion in the Tg-SwDI mice (p < 0.05). There was a positive correlation between NOX2 and soluble parenchymal Aβ levels (r = 0.6643, p = 0.0019). A minimal effect on the development of haemorrhages at these time-points was observed. In parallel to this, astrocyte activation was significantly higher in the Tg-SwDI mice compared to the wild-type controls at both time-points studied (p < 0.05); however, no effect of hypoperfusion was observed. Also, significantly higher levels of aquaporin-4 (AQP4) in the Tg-SwDI mice compared to the wild-type controls following 1 month of hypoperfusion were found (p < 0.001). There was a positive correlation between AQP4 and soluble parenchymal Aβ levels (r = 0.4735, p = 0.0095). Claudin-5 levels were significantly higher in the Tg-SwDI mice compared to the wild-type controls at both time-points analysed (p < 0.0001), and this was exacerbated following 1 month of hypoperfusion in the transgenic model (p < 0.05). A positive correlation between claudin-5 and vascular Aβ levels was observed (r = 0.6113, p = 0.0004). Together, these data suggest a synergistic contribution of amyloid and hypoperfusion pathologies to the tissue damage and implicate a role of oxidative stress and inflammation. In the third study, the aim was to determine the effects of passive amyloid immunisation on Aβ levels, development of MIs and haemorrhages and behavioural performance in the Tg-SwDI mice. To address this, the mice underwent weekly intraperitoneal injections with either 3D6 or 10D5 antibodies during 3 months. Although there were no significant changes between control and 10D5/3D6 treated mice in amyloid levels, appearance of MIs and cognitive performance, it was noted that there was a trend towards a reduction in amyloid levels and MI area in the 10D5/3D6 treated mice compared to the control animals. Furthermore, there was no evidence of microhaemorrhages in response to the immunisation. These results demonstrate that Aβ immunotherapy with the antibodies 3D6 and 10D5 may potentially decrease parenchymal and vascular amyloid accumulation, reducing the appearance of MIs and notably without triggering the development of microhaemorrhages. Collectively, the findings presented in the current thesis demonstrate that chronic cerebral hypoperfusion increases parenchymal and vascular Aβ levels and point towards a mechanism in which the cascade of events including inflammation and oxidative stress, triggered synergistically by hypoperfusion and Aβ, resulted in the widespread development of MIs and NVU changes which may further induce the alteration of cognition networks. A mixed therapy, aimed at improving cerebrovascular health and targeting the accumulation of Aβ, represents a promising strategy to prevent neurodegenerative processes and further cognitive decline in AD.
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Bufill, Soler Enric. "Cambios heterocrónicos en la evolución cerebral humana y su implicación en la enfermedad de alzheimer y otras enfermedades neurodegenerativas." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/399143.
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La malatia d'Alzheimer és freqüent en els éssers humans i extremadament infreqüent en altres mamífers. Per tant, alguns dels canvis que van tenir lloc durant l'evolució cerebral humana podrien tenir relació amb aquesta malaltia.
Durant l'evolució cerebral humana s'han produït canvis heterocrònics, consistents en la retenció de caràctes juvenils en l'edat adulta, com una elevada plasticitat sinàptica, en algunes árees cerebrals (neotènia neuronal).
Les lesions pròpies de la malaltia d'Alzheimer coincideixen amb les àrees en que s'ha produït una neotènia neuronal. Aquestes àrees es caracteritzen per un elevat turn-over sinàptic.
Les proteïnes que formen part de la via de senyalització de la reelina intervenen en la plasticitat sinàptica. Hem trobat tres gens que participen en aquesta via que presenten polimorfismes de nucleòtid únic que poden augmentar o disminuir significativament el risc de presentar Alzheimer o deteriorament cognitiu lleu.
Aquests genotips són RELN (rs 528528 i rs 2299356), PLK2 (rs 15009 i rs 702723) i CAMK2A (rs 3756577 i rs 3822606).
Tres dels genotips trobats són a la regió promotora del gen. Això suggereix que en la malaltia d'Alzheimer podrien intervenir canvis epigenètics que alterin l'expressió de determinats gens relacionats amb la plasticitat sinàptica.La enfermedad de Alzheimer es frecuente en los seres humanos y extremadamente infrecuente en otros mamíferos. Por lo tanto, algunos de los cambios ocurridos durante la evolución cerebral humana podrían tener relación con esta enfermedad. Durante la evolución cerebral humana se han producido cambios heterocrónicos, consistentes en la retención de caracteres juveniles en la edad adulta, como una elevada plasticidad sináptica, en algunas áreas cerebrales (neotenia neuronal). Las lesiones propias de la enfermedad de Alzheimer coinciden con las áreas en que se ha producido una neotenia neuronal. Dichas áreas se caracterizan por un elevado turn-over sináptico. Las proteínas que forman parte de la vía de señalización de la reelina intervienen en la plasticidad sináptica. Hemos encontrado tres genes que participan en dicha vía que presentan polimorfismos de nucleótido único que pueden aumentar o disminuir significativamente el riesgo de presentar Alzheimer o deterioro cognitivo leve. Dichos genotipos son RELN (rs 528528 y rs 2299356), PLK2 (rs 15009 y rs 702723) y CAMK2A (rs 3756577 y rs 3822606). Tres de los genotipos encontrados están en la región promotora del gen, lo que sugiere que en la enfermedad de Alzheimer podrían intervenir cambios epigenéticos que alteren la expresión de determinados genes relacionados con la plasticidad sináptica.
Alzheimer's disease is very common in the humans and extremely rare in other mammals. Therefore, some of the changes that have occurred during human brain evolution may be related with this disease. During the human brain evolution heterocronic changes have occurred, consisting in the retention of juvenile characters in adulthood, as a high synaptic plasticity in some brain areas (neuronal neoteniy). The characteristic lesions of Alzheimer's disease coincide with the areas in which there has been a neuronal neoteny. These areas are characterized by a high synaptic turn-over . The proteins that form part of the reelin signaling pathway are involved in the synaptic plasticity.We found three genes that participate in the reelin signaling pathway that present single nucleotide polymorphisms that may increase or decrease significantly the risk of presenting Alzheimer or mild cognitive impairment. These genotypes are RELN (*rs 528528 and *rs 2299356), PLK2 (*rs 15009 and *rs 702723) and CAMK2To (*rs 3756577 and *rs 3822606). Three of the genotypes are found in the promoter region of the gene, which suggests that in Alzheimer's disease could intervene epigenetic changes that alter the expression of certain genes related with the synaptic plasticity.
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Coutinho, Artur Martins Novaes. "Análise de alterações volumétricas e metabólicas cerebrais nos diferentes subtipos de comprometimento cognitivo leve." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5151/tde-12012016-084122/.
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Introducão: o comprometimento cognitivo leve (CCL) é reconhecido como um estágio transicional sintomático entre o envelhecimento normal e a demência, particularmente a doença de Alzheimer (DA). Apresenta como subtipos principais o amnéstico (CCLa), com comprometimento de memória, e o não amnéstico (CCLna), que apresenta perda de outras funções, principalmente executivas, de atenção, de linguagem e visuoespaciais. Aparentemente o CCLna tem menor taxa de conversão para demências ao longo do tempo que o subtipo amnéstico, particularmente para a DA. Dessa forma, o CCLna poderia apresentar um perfil de biomarcadores diferente do CCLa no momento do diagnóstico. Estudos na literatura investigando o padrão de biomarcadores no CCLna como grupo independente são raros, alguns destes indicando perfil menos relacionado à DA no CCLna que o visto no CCLa. Segundo nosso conhecimento, não há estudos investigando concomitantemente volume e metabolismo cerebrais, além de biomarcadores no LCR de uma mesma amostra de CCLna, em comparação com CCLa e um grupo de idosos cognitivamente normais. Objetivo: investigar as alterações de volume e metabolismo cerebral em grupos de indivíduos com os subtipos amnéstico e não amnésico de CCL, comparativamente a voluntários idosos sem comprometimento cognitivo, com o intuito de avaliar se há concordância entre estas alterações. Avaliou-se ainda possíveis associações entre os perfis dos estudos de imagem com padrões classicamente descritos na para CCL em risco de evolução para DA, investigando ainda a existência de correlações entre destes achados com o dos diferentes biomarcadores no LCR e com dados clínicos. Métodos: cento e quatorze voluntários foram incluídos em três diferentes grupos: gCCLna (N = 38), gCCLa (N = 46) e GC (N = 30). Após entrevista clínica, exame neurológico e classificação por uma bateria de testes neuropsicológicos, estes foram submetidos a exames de RM cerebral (para excluir outras causas de comprometimento cognitivo e para análise de morfometria baseada em voxels - VBM) e de PET-18FDG cerebral. Analisou-se ainda os valores de biomarcadores no LCR (A?, tau e p-tau) de uma subamostra de pacientes (CCLna = 33, CCLa = 38). Resultados: os três grupos não apresentaram diferenças em relação às variáveis idade, escolaridade, sexo, fatores de risco cardiovascular (exceto por maior prevalência de dislipidemia no gCCLa) e hiperintensidades de substância branca na RM. Menores valores de mini-exame do estado mental foram observado nos grupos CCLa e CCLna em relação ao GC. O subgrupo amnéstico apresentou redução de volume em porções mediais e polares de ambos os lobos temporais em comparação com GC e gCCLna, além de áreas de redução do metabolismo no giro do cíngulo posterior e pré-cúneo direitos e giro temporal médio esquerdo em relação ao GC. Esse padrão de redução volumétrica e metabólica não foi visto no gCCLna, que demonstrou discreta redução volumétrica nos giros temporal inferior esquerdo e frontal médio direito em comparação com o GC. Nenhuma alteração metabólica persistiu no subgrupo não amnéstico após correção para efeito de volume parcial em comparação com o GC, havendo redução metabólica bilateral no giro frontal médio em comparação com o gCCLa. Não houve diferenças significativas nos biomarcadores de LCR entre os grupos CCLa e CCLna. Houve, porém, tendência de menores valores de peptídeo A? no gCCLa. Observou-se correlação positiva entre metabolismo no giro temporal médio esquerdo e rendimento em testes de memória; correlação negativa também foi observada entre os valores de A? e os de tau e p-tau no LCR. Conclusão: os grupos CCLa e CCLna apresentaram alterações de volume e metabolismo diferentes em comparação com o grupo controle, e estas alterações não apresentaram concordância entre si. Também não foram encontradas correlações entre os diferentes biomarcadores de imagem e no LCR, notando-se apenas correlação positiva entre metabolismo temporal e desempenho em testes de memória. O gCCLa apresentou padrões de metabolismo e volume cerebrais classicamente relacionados a risco de evolução para DA. Por outro lado, o grupo CCLna apresentou um padrão diferente de alterações metabólicas e volumétricas, com áreas menores de redução de volume e padrão mais heterogêneo de alterações metabólicas em relação ao grupo controle. O conjunto de achados de biomarcadores no gCCLna não é indicativo de nenhum perfil específico de evolução para demênciasIntroduction: Mild cognitive impairment (MCI) is presumably a transitional stage between normal aging and dementia, particularly Alzheimer\'s disease (AD). Non-amnestic subtypes (naMCI) present with executive, attention, visuospatial and language dysfunctions. They have a lower conversion rate to dementia compared to amnestic subtypes (aMCI). Investigations regarding biomarker profiles of naMCI as an independent group are scarce. To our knowledge there is no study investigating the brain volumetric and metabolic features, as well as the profile of cerebrospinal fluid (CSF) biomarkers of naMCI patients as a single group in comparison to aMCI and cognitively normal elderly patients (control group - CG). Objective: to investigate the brain volumetric and metabolic changes in individuals presenting amnestic and non-amnestic MCI subtypes in comparison to elderly volunteers without cognitive impairment, aiming to verify if there are agreements between these changes. Possible associations between the imaging profile of these groups and classical patterns of high risk for developing AD were also evaluated, as well as possible correlations between imaging biomarkers, CSF biomarkers and clinical data. Methods: a hundred and fourteen (114) patients were included in three different groups: naMCIg (N = 38), aMCIg (N = 46) and CG (N = 30). Patients underwent brain MRI (in order to exclude other causes of the cognitive impairment but also for VBM analysis) and [18F]FDG-PET. A subsample (naMCIg = 33, aMCIg = 38) also underwent a lumbar puncture in order to assess the profile of amyloid-ß peptide, tau and phosphorylated tau protein levels in the CSF. Results: There was no difference in CSF biomarkers, education years, age, gender and cardiovascular risk factors between the naMCI and aMCI groups, except for a higher prevalence of dyslipidemia in aMCI. The amnestic MCI group had lower rBGM in relation to control group in the precuneus, posterior cingulate and left medium temporal gyrus. Compared to aMCIg, naMCIg presented with bilateral prefrontal cortex hypometabolism, but without metabolic changes in relation to CG after correction for partial volume effect. Amnestic MCI group had bilateral temporal lobe volume reduction in comparison to naMCI and CG, particularly in the polar and mesial parts of the temporal lobe. Non-amnestic MCI presented with discrete volumetric reductions in comparison to CG, Conclusion: Volumetric and metabolic alterations were different and essentially discordant between aMCI and naMCI groups in comparison to CG. Amnestic MCI showed metabolic and volumetric profiles classically related to MCI due to AD, while naMCI group presented with less-significant areas of volumetric and metabolic reductions in relation to control group. Our non-amnestic MCI group probably represents a heterogeneous group with a different pattern of neurodegeneration than the classical MCI due to AD
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Martínez, Moreno Margot. "Efecte de l'activació del canal K(ATP) al perfil d'expressió microglial durant la neurodegeneració a l'hipocamp de la rata." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/121511.
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En aquesta tesi s'ha estudiat l'efecte de l'activació del canal de potassi dependent de ATP (KATP) amb un fàrmac activador, la diazoxida, sobre el perfil fenotípic de la microglia en dos models diferenciats: un de in vitro amb una línia cel•lular i un de in vivo en un model de lesió excitotòxica a l'hipocamp de la rata. També s'ha estudiat com aquesta modulació afecta a la progressió de la lesió excitotòxica i la neurogènesis que porta associada. Finalment, s'ha descrit la presència del canal de calci dependent de voltatge (VGCC) a microglia i com la seva inhibició també regula la activitat microglial in vivo i in vitro.In this thesis we have studied the effect of the activation of the potassium channetl ATP-dependent (KATP channel) with the drug diazoxida, a KCO (potassium channel opener), over the phenotypic expression profile of microglial cells. We did it with two different approaches: an in vitro model with the murine cell line BV2; and an in vivo model of excitotòxic lesion in rat hippocampus. We have also studied how this modulation affects the progression of the damage of the excitotòxic lesion and the hipocampal neurogènesis associated. Finally, we have described the presence of voltage-gated calcium channels (VGCC) in microglia and how its regulation also affects to the activity of microglia in vivo and in vitro.
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Chou, Chia-Mei, and 周嘉玫. "Molecular pathogenesis of experimental cerebral toxocariasis progress into neurodegenerative diseases." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/dt7fd8.
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博士臺北醫學大學
醫學科學研究所
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Toxocariasis is a worldwide parasitic zoonosis and mainly caused by Toxocara canis. Long-term residence of T. canis larvae in a paratenic host’s brain can cause cerebral toxocariasis (CT). In human CT and mouse model of CT, T. canis larval brain invasion can cause cerebral damage and neuroinflammation, further contributing to several neurological symptoms and neurodegenerative disorders. Hippocampus is characterized for synaptic plasticity and spatial learning and memory; however parasitic invasion of hippocampus may trigger neuroinflammatory and neurodegenerative disorders. Astrocytes are the most abundant glia cells manipulating the host’s defense in the brain; moreover, they are proposed to pathologically involve in neurodegenerative disorders, including Alzheimer’s disease. The present study intended to assess pathological changes, expressions of neurodegeneration-associated factors (NDAFs) and ubiquitin-proteasome system (UPS) function in hippocampus and associated cognitive behavior in ICR mice orally inoculated with a high, medium or low-dose of T. canis embryonated ova during a 20-week investigation. Secondly, the cytotoxic effects of T. canis larval excretory-secretory antigens (TcES Ag) on astrocytes were assessed by apoptosis and autophagy expressions in vitro. Our results indicated there were insignificant differences in learning and memory function between the experimental and uninfected control mice, possibly because the site where T. canis larvae invaded was the surrounding area but not the hippocampus per se. Nevertheless, enhanced expressions of NDAF, persistent UPS impairment and excess amyloid β (Aβ) accumulation concomitantly emerged in the experimental mice hippocampus at 8, 16 and 20 weeks post-infection. In addition, TcES Ag treatment reduced cell viability and caused morphological changes. Expressions of autophagy associated proteins including Beclin 1, phosphor-mTOR and LC3-Ⅱ were not significantly changed; however, p62 as well as the cell survival protein, mTOR, was concomitantly decreased in TcES Ag treatment. Significantly accelerated cleaved caspase-3 and cytochrome c expression as well as enhanced caspase-9 and caspase-8 activation were found in astrocytes with TcES Ag treatment. Caspase-3 activity and apoptotic cells numbers were also increased as detected by fluorescence microscopy, implying that TcES Ag may trigger astrocytes apoptosis predominantly through intrinsic and extrinsic pathways rather autophagy to further contribute to the disease progression of CT. This study provides a comprehensive role in the pathogenesis of CT progress into neurodegenerative diseases.
Books on the topic "Cerebral neurodegenerative disease"
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Cerebral plasticity: New perspectives. Cambridge, Mass: MIT Press, 2011.
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Attems, Johannes, and Kurt A. Jellinger. Neuropathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0006.
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This chapter describes the main neuropathological features of the most common age associated neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies as well as other less frequent ones such as multiple system atrophy, Pick's disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology and Huntington's disease. Likewise cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia and prion diseases are described. A main aim of this chapter is to assist the reader in interpreting neuropathological reports, hence criteria for the neuropathological classifications of the major diseases are provided. One section covers general considerations on neurodegeneration and basic pathophysiological mechanisms of tau, amyloid-β, α-synuclein, TDP-43 and prions are briefly described in the sections on the respective diseases. Finally, one section is dedicated to cerebral multimorbidity and we give a view on currently emerging neuropathological methods.
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Forsyth, Rob, and Richard Newton. Specific conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784449.003.0004.
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This chapter adopts a systematic approach to common diagnoses in paediatric neurology, aetiologies, management to include investigation and treatment, and outcome. For each condition current knowledge on cause and underlying biology is summarized. A rational approach to investigation and treatment is summarized for each topic. These include: acquired brain injury; autoimmune and autoinflammatory disease of the CNS; cerebral palsy and neurodisability which covers feeding, communication, special senses, and respiratory disease; demyelinating disease; epilepsy including its impact on daily life; non-epileptic paroxysmal phenomena; functional illness, illness behaviour; headache; hydrocephalus; spina bifida and related disorders; idiopathic intracranial hypertension; infection of the CNS; congenital infection; mitochondrial disease; movement disorders; neuromuscular disease which covers neuropathy, anterior horn cell disease, and myasthenic syndromes; neurocutaneous syndromes; neurodegenerative conditions; late presentations of metabolic disease; neurotransmitter disorders; sleep disorders; stroke and intracerebral haemorrhage; tumours of the CNS; and vitamin-responsive disorders.
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Chalupa, Leo M., Nicoletta Berardi, Nicoletta Berardi, and Matteo Caleo. Cerebral Plasticity: New Perspectives. MIT Press, 2011.
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Chalupa, Leo M., Nicoletta Berardi, and Matteo Caleo. Cerebral Plasticity: New Perspectives. MIT Press, 2011.
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Hodges, John R. Localized Cognitive Functions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749189.003.0003.
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This chapter discusses localized cognitive functions. The functions ascribed to the dominant, usually left, cerebral hemisphere show much more clear-cut laterality than those associated with the so-called minor hemisphere. This applies particularly to spoken language. This chapter discusses aspects of normal and abnormal language function in the framework of contemporary cognitive neuroscience with descriptions of the classic post-stroke variants of aphasia (Broca’s, Wernicke’s, conduction, etc.) although these are rarely seen in the context of neurodegenerative diseases. There is also a description of disorders of written language (the dyslexias and dysgraphias), of calculation (acalculia), and of higher-order motor control (apraxia). This is followed by descriptions of the syndromes associated with disturbed right hemisphere functions: neglect phenomena, dressing and constructional apraxia, and complex visuoperceptual disorders (agnosias). Each cognitive syndrome is placed in the context of its neural basis, disorders which affect the ability and methods of assessment at the bedside and using neuropsychological tasks.
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Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.
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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.
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(Editor), Bruce Trembly, and William Slikker (Editor), eds. Neuroprotective Agents: Fourth International Conference (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1999.
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M.D.) International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (4th : 1998 : Annapolis. Neuroprotective Agents: Fourth International Conference (Annals of the New York Academy of Sciences, V. 890). New York Academy of Sciences, 1999.
Find full textBook chapters on the topic "Cerebral neurodegenerative disease"
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Sahni, Jasjeet Kaur, Sihem Doggui, Lé Dao, and Charles Ramassamy. "Nanotechnology for Cerebral Delivery of Nutraceuticals for the Treatment of Neurodegenerative Diseases." In Functional Foods, Nutraceuticals, and Degenerative Disease Prevention, 263–83. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9780470960844.ch10.
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Vogt, Brent A., Alex Martin, Kent E. Vrana, John R. Absher, Leslie J. Vogt, and Patrick R. Hof. "Multifocal Cortical Neurodegeneration in Alzheimer’s Disease." In Cerebral Cortex, 553–601. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4885-0_16.
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Fiskum, Gary, and Robert E. Rosenthal. "Metabolic Failure, Oxidative Stress, and Neurodegeneration Following Cerebral Ischemia and Reperfusion." In Neurodegenerative Diseases, 203–9. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0209-2_26.
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Farrer, Lindsay A. "Locating Genetic Modifiers for Inherited Neurodegenerative Diseases." In Cerebral Cortex, 433–59. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4885-0_12.
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Khan, Shagufta, Aarti Belgamwar, and Pramod Yeole. "Nanopharmaceuticals for the Improved Treatment of Cerebral Stroke." In Nanobiotechnology in Neurodegenerative Diseases, 369–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-30930-5_15.
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Mehler, Mark E. "Regional Forebrain Patterning and Neural Subtype Specification: Implications for Cerebral Cortical Functional Connectivity and the Pathogenesis of Neurodegenerative Diseases." In Results and Problems in Cell Differentiation, 157–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-540-46006-0_8.
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V., Hugh Perry. "Environmental Influences on Neurodegenerative Disease: The Impact of Systemic Inflammation." In Cerebral Plasticity, 315–24. The MIT Press, 2011. http://dx.doi.org/10.7551/mitpress/9780262015233.003.0025.
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Tam, J. H. K., and S. H. Pasternak. "Alzheimer’s Disease." In The Cerebral Cortex in Neurodegenerative and Neuropsychiatric Disorders, 83–118. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-801942-9.00004-5.
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Kim, E. H., N. Mehrabi, L. J. Tippett, H. J. Waldvogel, and R. L. M. Faull. "Huntington Disease." In The Cerebral Cortex in Neurodegenerative and Neuropsychiatric Disorders, 195–221. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-801942-9.00008-2.
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Attems, Johannes, and Kurt A. Jellinger. "Neuropathology." In Oxford Textbook of Old Age Psychiatry, 77–98. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198807292.003.0005.
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This chapter describes the main neuropathological features of the most common age-associated neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and dementia with Lewy bodies, as well as other less frequent ones such as multiple system atrophy, Pick’s disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle-dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology, and Huntington’s disease. Likewise, cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia, and prion diseases are described. A main aim of this chapter is to assist the reader in interpreting neuropathological reports; hence criteria for the neuropathological classifications of the major diseases are provided. One section covers general considerations on neurodegeneration, and basic pathophysiological mechanisms of tau, amyloid-β, α-synuclein, TDP-43, and prions are briefly described in the sections on the respective diseases. Finally, one section is dedicated to cerebral multimorbidity, and a view on currently emerging neuropathological methods is given.
Conference papers on the topic "Cerebral neurodegenerative disease"
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Elkan, Eva-Maria, Ana-Maria Papuc, Roxana Elena Bogdan Goroftei, Elena Ariela Banu, Monica Laura Zlati, Adriana Gabriela Albeanu, and Alina Pleșea Condratovici. "DREAMING AND PARASOMNIAS FROM A CEREBRAL STRUCTURAL VIEW." In The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.6.
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Introduction: Parasomnias are disorders that may appear during sleep with and/or without dreams. To describe them we must take in account a subjective description by the patient and his relatives. Objective measurement of this phenomenology is made with Polysomnography, Electromyography and Holter EKG. Material and Methods: We searched the recent data about parasomnia in the Medline, Pubmed, Google academic databases as also in classic books and reviews. Results: The clinical picture is various from motor and neurological signs to autonomic signs as also sleep related hallucinations. There are more rare presentations with associated disorders due to excretion and involuntary urinary emission during sleep disorders. Parasomnias are often preceded by a traumatic event for the patient and his family members which can be a head trauma or an infection or an intoxication which can be accompanied by psycho vulnerable events. On the other part parasomnias can be themselves a preamble announcing neurodegenerative diseases like Parkinson disease, Lewy Body Dementia or some synucleopathies. Conclusions: The fluctuations of neurotransmitters (Dopamine, Serotonine or Acetylcholine) due to specific neurologic pathology can lead to particular parasomnias, their evolution corresponding to each impairment. The knowledge of accompanying parasomnias of neurologic disorders like those from Parkinson disease helps manage diseases of neurological patients already known with Parkinson's disease or other neurological diseases, leading to increased quality of life for these patients as a result of specialized intervention.
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Collar, Giovanna Carello, Marco Antônio De Bastiani, and Eduardo R. Zimmer. "HUNTINGTON’S DISEASE AND EARLYONSET ALZHEIMER’S DISEASE SHARE A TRANSCRIPTOMIC SIGNATURE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda082.
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Background: Neurodegenerative diseases share progressive loss of neurons and protein misfolding, which ultimately culminates in dementia; many diseases have been identified as causes of early-onset dementia (< 65 years of age) such as Huntington’s disease (HD) and early-onset Alzheimer’s disease (EOAD). Importantly, disease-specific genetic mutations have already been identified for HD and EOAD. Thus, one could suggest that the molecular link between these diseases may arise from alterations at the transcriptomic level, which is yet to be determined. Objective: We aimed at identifying transcriptome similarities between HD and EOAD. Methods: We collected data of the postmortem cerebral cortex from 1 HD and 6 AD microarray studies in the Gene Expression Omnibus. Of note, only subjects with age at death under 65 were selected (HD: n = 158, controls: n = 158; EOAD: n = 65, controls: n = 266). Differential expression and functional enrichment analyses were performed. Results: We identified 1,260 differentially expressed genes and 675 enriched gene ontology terms between HD and EOAD. Conclusion: Our results demonstrate a transcriptomic signature shared by HD and EOAD. Unveiling the similarities between these diseases at the transcriptomic level could advance our knowledge about pathogenesis and may help to develop therapeutic strategies targeting early-onset dementias.
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Grah, Vitor Matias, Guilherme Sampaio Silva, Karla Viana Rezende, Ayrton Senna do Brasil Amaral Alves, Maria Inês Vaz de Oliveira, Maria Paula Banhara Rodrigues, and Juliana Carollyne Amorim. "The relationship between apolipoprotein e4 and bloodbrain barrier dysfunction in Alzheimer Disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.091.
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Background: Alzheimer disease(AD) is a progressive neurodegenerative dysfunction with a cognitive deficit and amyloid-β(Aβ) accumulation. That said, the apolipoprotein E (ApoE) has 4 variants, with E4 being linked to decreased cerebral blood flow and fragile blood-brain barrier (BBB). In this way, the BBB has an important role in removing substances that are toxic to the brain such as βA protein. Objective: Demonstrate the relationship of ApoE4 and BBB dysfunction in the pathophysiology of AD. Methods: Bibliographic review using the CAPES journals portal, in the last 5 years. Results: After analyzing the studies, it is inferred that in cases of homozygosity for ApoE4 in relation to ApoE3 there is a 15 fold increased chance of developing AD and 3 fold heterozygosity. It is concluded that the mechanism that probably explain is related to the secretion of ApoE by the pericytes that lining brain vessels in the BBB, whilst the subtype E4 exacerbates cyclophilinA, which promotes the activation of metalloproteinase-9, causing junctions rupture between adjacent endothelial cells, promoting the loss of βA homeostasis. Conclusion: It can be inferred, that ApoE has great importance in the regulation of the integrity of BBB’s integrity, is undeniable that such protein has a significant contribution in the pathophysiology of AD, hereupon, it’s urgent that these studies need to be continued to develop new therapies in individuals who express ApoE4.
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Barbosa, Mateus Gonçalves de Sena, Ghaspar Gomes de Oliveira Alves Francisco, Rafaela Luiza Vilela de Souza, João Marcos Alcântara de Souza, and Nicollas Nunes Rabelo. "Chronic traumatic encephalopathy in military and sportsists: a factual problem?: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.324.
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Background: Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease linked to tau protein associated with recurrent brain trauma, clinically marked by mood, personality, cognitive and behavioral changes. Objectives: The objective of the study was to demonstrate whether athletes and military personnel can really be victims of CTE and to elucidate this same pathology. Design and setting: This is a systematic review, based on the PRISMA guidelines and a literature review with a summary of the evidence found. Methods: Articles were selected, published from 1934 to 2020, in PubMed and Scielo using the descriptors: “chronic traumatic encephalopathy”, “cerebral concussion”, “players”, “boxers”, “athletes” and “military”. Inclusion criteria were: studies available in English, Spanish and Portuguese published, with randomized clinical trial, cohort study or meta-analysis. Results: In 52 articles, 14 were selected for qualitative synthesis in the results table that addresses chronic traumatic encephalopathy in football, soccer and rugby players, boxers and the military. Neuropathologically, CTE is characterized by cerebral atrophy, a pelvic septum cavity with fenestrations, dense diffuse immunoreactive inclusions and a TDP-43 proteinopathy. Microscopically, there are extensive neurofibrillary tangles and spindle-shaped and filiform neurites throughout the brain. Conclusions: American football players, boxers and military men are more likely to trigger CTE, due to the constant mechanical shocks from their heads. The most frequent clinical manifestations were: headache, aggression, dementia, executive dysfunction and suicide. CTE is definitely diagnosed only at autopsy.
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Saito, Monalisa Moura, Dhyego Ferreira Moreira de Lacerda, Ana Claudia Marque Gouveia de Melo, Lucas Monteiro Barros Nunes, Luana Cristina Rodrigues de Oliveira Costa, and Eduarda Silvestre Ribeiro da Costa Gomes. "Neurodegeneration with cerebral iron accumulation: a case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.145.
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Introduction: NBIA is a rare disease, with a prevalence of 1/1,000,000.It is characterized by abnormal iron accumulation. Clinical findings may include progressive extrapyramidal disorders, involvement of the pyramidal, peripheral, autonomic nervous systems, superior cortical, visual and cerebellar functions. The diagnosis is made through the association of clinical findings and complementary exams. Currently, the treatment is only symptomatic, with no specific therapy. Case report: 5-year-old female, reporting involuntary movements and difficulty walking a day ago. Presented agitation and delayed neuropsychomotor development, seen since 1 year of age. On examination, dysarthria, dystonia and parkinsonian stiffness were observed. MRI of the brain showed the radiological signal “tiger’s eye” and the ophthalmological evaluation showed retinal dystrophy. Positive acanthocyte screening. NBIA’s NGS panel confirmed the diagnosis. Triexfenid was started and there was an improvement in movement disorders. In outpatient follow-up, the symptoms worsened. Levodopa was associated with the return of walking without support and ability to pick up objects. Discussion: In this case, Triexafenid 2mg/day was initially prescribed, with a slight improvement in movement disorders. Levodopa was started with the aim of improving symptoms of parkinsonian stiffness. The excellent response to the association of the drug in low doses stands out, enabling ambulation and functionality for daily activities. Conclusion: NBIA is a rare disease, with rapid onset and progression. Studies show limited benefits of levodopa in the case of PKAN. We emphasize significant clinical improvement, with a return to walking after administration of the drug.
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Clemotte, Alejandro, Harbil Arregui, Miguel Ángel Velasco, Luis Unzueta, Jon Goenetxea, Unai Elordi, Eduardo Rocon, et al. "Trajectory clustering for the classification of eye-tracking users with motor disorders." In Actas de las XXXVII Jornadas de Automática 7, 8 y 9 de septiembre de 2016, Madrid. Universidade da Coruña, Servizo de Publicacións, 2022. http://dx.doi.org/10.17979/spudc.9788497498081.0150.
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This paper presents a pilot study completed in the framework of the INTERAAC project. The aim of the project is to develop a new human-computer interaction (HCI) solution based on eye-gaze estimation from webcam images for people with motor disorders such as cerebral palsy, neurodegenerative diseases, and spinal cord injury that are otherwise unable to use a keyboard or mouse. In this study, we analyzed cursor trajectories recorded during the experiment and validated that users with different diseases can be automatically classified in groups based on trajectory metrics. For the clustering, Ward's method was used. The metrics are based on speed and acceleration statistics from full filtered tracks. The results show that the participants can be grouped into two main clusters. The main contribution of this work is the evaluation of the clustering techniques applied to eye-gaze trajectories for the automatic classification of users diseases based on a real experiment carried with the help of three clinical partners in Spain.
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Marques, Daiane Silva, Roseane Oliveira Veras, Maria Dhescyca Ingrid Silva Arruda, João Felipe Tinto Silva, and Francisco Lucas de Lima Fontes. "REPERCUSSÕES CLÍNICAS E FISIOPATOLÓGICAS DA DOENÇA DE HUNTINGTON: REVISÃO INTEGRATIVA DA LITERATURA." In II CONGRESSO ON-LINE NACIONAL DE CIÊNCIAS & SAÚDE (II CONCS). Literacia Cientifica Editora & Cursos, 2022. http://dx.doi.org/10.53524/lit.edt.978-65-84528-09-3/72.
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INTRODUÇÃO: A Doença de Huntington (DH) é considerada uma patologia neurodegenerativa, crônica, letal, com herança autossômica dominante que codifica a proteína huntingtina e caracteriza-se por diversas repercussões clínicas como: coreia progressiva, diminuição da cognição, depressão, dentre outras. Habitualmente, a DH manifesta-se entre 30 a 50 anos, no entanto, tem possibilidade de ocorrer o fenômeno de antecipação (Huntington juvenil), atingindo jovens e crianças. Ainda não possui cura para a DH, contudo, apresenta tratamento. OBJETIVO: Apresentar os aspectos clínicos e fisiopatológicos da DH. MÉTODOS: Trata-se de uma abordagem qualitativa de revisão integrativa da literatura, efetuada em fevereiro de 2022, em que a pergunta norteadora foi fundamentada no acrônimo PICo (População, Interesse e Contexto), definida como: Quais são as repercussões clínicas e fisiopatológicas da DH? A pesquisa foi executada nas bases de dados: Literatura Latino-americana e do Caribe em Ciências da Saúde (LILACS), Medical Literature Analysis and Retrieval System Online (MEDLINE) via Biblioteca Virtual em Saúde (BVS) e Science Direct. Utilizaram-se os seguintes Descritores em Ciências da Saúde (DeCS) e Medical Subject Headings (MeSH): “Doença de Huntington”, “Huntington Disease” “Proteína Huntingtina”, “Huntingtin Protein”, “Glutamina” e “Glutamine”. As estratégias de busca foram formuladas baseadas nos descritores mencionados, aplicando o operador booleano “AND”. Os critérios de inclusão compreenderam: estudos disponíveis na íntegra, estudos observacionais, revisões sistemáticas e capítulos de livros no idioma português e inglês, no período de 2013 a 2018, com a finalidade de encontrar evidências atuais acerca da temática. Excluíram-se, monografias, teses, artigos incompletos, indisponíveis e aqueles que não tinham correlação ao objetivo. Desse modo, foram identificados 891 estudos, dos quais, após a utilização dos critérios de elegibilidade e exclusão, restaram 235 estudos. Posteriormente a realização da leitura dos títulos e resumos, somente 10 responderam a finalidade da revisão. RESULTADOS: Diante das evidências científicas analisadas, clinicamente, a DH caracteriza-se por coreia progressiva (movimentos involuntários), declínio cognitivo e implicações psiquiátricas. Nos estágios iniciais, observa-se irritabilidade, depressão e alterações motoras, estas associadas à perda de coordenação dos movimentos voluntários. Já os movimentos involuntários tornam-se mais severos, implicando na piora da mobilidade e cognição. Em indivíduos jovens, a repercussão clínica é distinta, sendo representada por bradicinesia, tremores, rigidez e distonia. Durante a evolução da DH, a disfunção intracelular provocada pela huntingtina mutante implica na degeneração de relevantes vias neuronais e aniquilamento celular no corpo estriado, córtex cerebral e demais áreas do cérebro. A DH não é baseada, necessariamente, no impacto direto da proteína mutante, possui também mecanismos de excitotoxicidade, toxicidade dopaminérgica, desregulação do metabolismo, disfunção mitocondrial, estresse oxidativo, apoptose e autofagia, fatores estes que compõem a fisiopatologia da DH. Alguns destes mecanismos, além do desenvolvimento gradativo, acentuamse tardiamente na doença, podendo até levar à morte neuronal. CONCLUSÃO: Percebe-se que a DH possui evolução crônica e progressiva. Até o momento, não apresenta possibilidade de cura, entretanto, existe tratamento multiprofissional. Assim, além da avaliação, é necessário compreender os aspectos clínicos e fisiopatológicos, para que o tratamento proporcione uma qualidade de vida eficaz nestes pacientes.
Reports on the topic "Cerebral neurodegenerative disease"
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Zhu, Qiaochu, Jin Zhou, Hai Huang, Jie Han, Biwei Cao, Dandan Xu, Yan Zhao, and Gang Chen. Risk factors associated with amyotrophic lateral sclerosis: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0118.
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Review question / Objective: To identify and list the risk factors associated with the onset and progression of ALS. Condition being studied: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting the upper and lower motor neurons in the spinal bulb, cerebral cortex, and spinal cord. The clinical processing symptoms accompany muscle atrophy, fasciculation, and fatigue of limbs, which can lead to general paralysis and death from respiratory failure within 3-5 years after the onset of this disease. Though the pathogenesis of ALS is still unclear, exploring the associations between risk factors and ALS can provide reliable evidence to find the pathogenesis in the future. This meta-analysis aims to synthesize all related risk factors on ALS, comprehensively understand this disease, and provide clues to mechanism research and clinicians.