Готові списки джерел за темами / Alzheimers’s disease

Добірка наукової літератури з теми "Alzheimers’s disease"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Alzheimers’s disease"

1

Zhou, Can-Can, Zhen-Yan Gao, Ju Wang, Mei-Qin Wu, Shuang Hu, Fei Chen, Jun-Xia Liu, Hui Pan, and Chong-Huai Yan. "Lead exposure induces Alzheimers’s disease (AD)-like pathology and disturbes cholesterol metabolism in the young rat brain." Toxicology Letters 296 (October 2018): 173–83. http://dx.doi.org/10.1016/j.toxlet.2018.06.1065.

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2

Sun, Binggang, Kay Chow, Amy Zhao, Jason Lehmann, Weiping Jiang, and Shaoquan Ji. "Novel Flow-Based Multiplex Assay Panel for Quantifying Human Neuroinflammation Biomarkers." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 130.25. http://dx.doi.org/10.4049/jimmunol.202.supp.130.25.

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Abstract The inflammation of neuronal tissues is triggered by various stimuli such as traumatic brain injury, stroke, protein aggregation and pathogens. Neuroinflammation cues such as brain injury lead to protein release and microglia activation, which in turn activate glial cells. Activated glial cells produce both pro- and anti-inflammatory factors to regulate cell migration, growth, tissue repair or cell death. Neuroinflammation is involved in acute brain injury, stroke, and many neurodegenerative diseases, such as Alzheimers’s and Parkinson’s diseases, as well as disruption and permeability of the blood-brain barrier. Measurement of the cytokines, chemokines, growth factors and other neuronal disease biomarkers is essential in understanding the mechanisms of neuronal disease progression, but this is limited by the small sample size of CSF. It is therefore desirable to be able to measure a panel of important neuroinflammation biomarkers simultaneously. We have developed an assay panel targeting neuroinflammation biomarkers using fluorescence-encoded beads that are suitable for use on common lab flow cytometers. It allows for simultaneous quantification of the 13 key targets involved in neuroinflammation including VILIP-1, BDNF, free active TGF-β1, VEGF, IL-6, sTREM-1, β-NGF, IL-18, TNF-α, soluble RAGE, and CX3CL1 (Fractialkine). This panel has been developed with superior assay performance and specificity and has been validated by detecting expected values in biological samples including CSF samples from healthy and disease individuals. This high quality, low cost and easy to use panel will be a useful tool to the neuroinflammation research community.
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Zarrouk, Amira, Meryam Debbabi, Maryem Bezine, El Mostafa Karym, Asmaa Badreddine, Olivier Rouaud, Thibault Moreau, et al. "Lipid Biomarkers in Alzheimer's Disease." Current Alzheimer Research 15, no. 4 (February 22, 2018): 303–12. http://dx.doi.org/10.2174/1567205014666170505101426.

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Background: There are now significant evidences that lipid metabolism is affected in numerous neurodegenerative diseases including Alzheimer’s disease. These dysfunctions lead to abnormal levels of certain lipids in the brain, cerebrospinal fluid and plasma. It is consequently of interest to establish lipid profiles in neurodegenerative diseases. This approach, which can contribute to identify lipid biomarkers of Alzheimers' disease, can also permit to identify new therapeutic targets. It was therefore of interest to focus on central and peripheral biomarkers in Alzheimer's disease. Methods: A review of the literature on 148 papers was conducted. Based on this literature, the involvement of lipids (cholesterol and oxysterols, fatty acids, phospholipids) in Alzheimer's disease has been proposed. Results: Of the 148 references cited for lipid biomarkers for Alzheimer's disease, 65 refer to cholesterol and oxysterols, 35 to fatty acids and 40 to phospholipids. Among these lipids, some of them such as 24S-hydroxyckolesterol, open up new therapeutic perspectives in gene therapy, in particular. The results on the very long-chain fatty acids suggest the potential of peroxisomal dysfunctions in Alzheimer's disease. As for the phospholipids, they could constitute interesting biomarkers for detecting the disease at the prodromal stage. Conclusion: There are now several lines of evidence that lipids play fundamental roles in the pathogenesis of AD and that some of them have a prognostic and diagnosis value. This may pave the way for the identification of new therapeutic targets, new effective drugs and / or new treatments.
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Nesteruk, Marta, Tomasz Nesteruk, Maria Styczyńska, and Maria Barcikowska. "Wpływ obciążenia chorobami naczyniowymi na progresję łagodnych zaburzeń poznawczych do choroby Alzheimera." Aktualności Neurologiczne 15, no. 1 (April 30, 2015): 18–21. http://dx.doi.org/10.15557/an.2015.0003.

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5

Hemangkorn, Nicha, Pamonphon Phummai, and Patranan Punyacharoen. "Effects of Essential Oils and Aromatic Plants on Alzheimer’s Disease and Dementia." International Journal of Science and Healthcare Research 6, no. 3 (September 3, 2021): 350–58. http://dx.doi.org/10.52403/ijshr.20210760.

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The primary objective of this research was to investigate how beneficial essential oils and aromatic plants are at curing Alzheimer’s disease and dementia. Alzheimer’s Disease (AD) is known to be one of the most incurable prevalent diseases in the elderly. Agitation, cognitive impairments, communication difficulty, irritability, and confusion may advance in AD patients. Even though the behavioral causes contributing to the disease have not yet been discovered, aggregation of tau and amyloid proteins is found in the brain of patients with Alzheimer’s. With numerous experiments conducted on these proteins, scientists have surmised that this accumulation is a causative factor of Alzheimer’s disease. Multiple scientists and experts have carried out several studies regarding the enlargement of amyloid plaques on Alzheimer’s. In addition, the effects of aromatherapy, including divergent results of alternative essential oils, have been analyzed. This paper examines the distinctions between Alzheimer's disease and dementia. The review elaborates on the causes and the symptoms before describing the effects of essential oils and aromatic plants. Subsequently, this provides rudiments regarding the benefits and hazards of applying essential oils and aromatic plants to treat either Alzheimer's disease or dementia. This study focuses on utilizing essential oils and aromatic plants in the medical profession as an alternative treatment for Alzheimer's disease and dementia. Likewise, a couple of case studies are shown in the paper with the analysis of amyloid plaques in mice and the effectiveness of lavender, rosemary, and orange essential oils on participants. Keywords: Alzheimer’s disease Dementia Essential oils Aromatic plants Aromatherapy Amyloid and Tau
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6

Kyselova, A. A., E. S. Kravtsova, D. O. Mishchenko, and E. R. Chernishova. "The Modern View on Alzheimer’s Disease." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 3, no. 4 (May 18, 2018): 169–73. http://dx.doi.org/10.26693/jmbs03.04.169.

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7

Monisha, M., K. M. Harshitha, N. H. Dhanalakshmi, Kokatam Sai Prakash Reddy, C. R. Nagarathna, and M. Kusuma. "Early detection of Alzheimer’s: Modalities and Methods." March 2022 4, no. 1 (May 4, 2022): 69–79. http://dx.doi.org/10.36548/jaicn.2022.1.005.

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Alzheimer’s disease belongs to the group of neurodegenerative diseases and is considered as one of the most destructive and severe diseases of the human nervous system. There is presently no quick and cost-effective method for routinely screening individuals of age 65 and older for Alzheimer's disease, the most prevalent type of neurodegenerative dementia. Over 5.2 million Americans already suffer from this condition, with the number anticipated to rise to 7.7 million by 2030. This paper discusses how the use of Machine learning concepts has upgraded the detection of Alzheimer's disease in the early stage.
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8

Bombón-Albán, Paulina E., and Pablo E. Fierro-Altamirano. "Criterios de diagnóstico de la enfermedad de Alzheimer: Aplicaciones prácticas." Revista Ecuatoriana de Neurologia 31, no. 1 (May 10, 2022): 12–14. http://dx.doi.org/10.46997/revecuatneurol31100012.

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Los avances en el campo de la Enfermedad de Alzheimer (EA) han llevado a una reconceptualización de la enfermedad, trasladando nuestro conocimiento más allá de la presentación clínica centrada en la demencia, a un constructo que incluye cambios fisiopatológicos tempranos en individuos asintomáticos. El concepto de etapa preclínica de una enfermedad no debe ser nuevo para los médicos en ejercicio, ni tampoco el concepto de diagnosticar una enfermedad en ausencia de síntomas.
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9

Shahzadi, Maria, Bareera Saeed, Muhammad Azzam Khan, Amna Rashid, Muhammad Bilal, Roma Imtiaz, and Tallat Anwar Faridi. "A Review on the Techniques for Early Diagnosis of Alzheimer’s Disease." Lahore Garrison University Journal of Life Sciences 6, no. 03 (September 15, 2022): 268–81. http://dx.doi.org/10.54692/lgujls.2022.0603228.

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Alzheimer’s disease is a neurological condition in which there is rapid deterioration of the brain and it affects around 50 million people globally. The most obvious sign of Alzheimer’s is dementia which is primarily an affliction of old age. Majority of the people presenting with dementia in old age are Alzheimer’s patients. The symptoms of Alzheimer’s disease are debilitating and have the ability to utterly disrupt a person's normal life. It is only discovered after this terrible disease has destroyed all neurons, thus there is little chance to cure it or reverse the adverse effects. There are two types of techniques for detecting Alzheimer's disease: invasive and non-invasive techniques. Invasive method obtains data from the patient bydrawing a small amount of blood or performing a lumbar puncture, whereas noninvasive method collects data using imaging techniques like MRI and CT scan. Invasive technique, on the other hand, is thought to be a more accurate indicator of Alzheimer's disease than non-invasive technique since it provides strong biomarkers. Once Alzheimer's disease has progressed to its final stage, it is incurable. Treatment is only viable when the disease is in its initial stages. Future treatments for Alzheimer's disease will focus on the causative maladies of neurofibrillary tangles (ptau) and senile plaques (A). The pathological traits connected to debilitating disease, special protein, b proteins, are critical for future therapeutics
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10

Fiore, Vincenzo, Antonia De Rosa, Paolo Falasca, Massimo Marci, Edoardo Guastamacchia, Brunella Licchelli, Vito Angelo Giagulli, Giovanni De Pergola, Antonella Poggi, and Vincenzo Triggiani. "Focus on the Correlations between Alzheimer’s Disease and Type 2 Diabetes." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 5 (June 3, 2019): 571–79. http://dx.doi.org/10.2174/1871530319666190311141855.

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Background: In the last decades, both diabetes mellitus and Alzheimer's disease are constantly increasing. Affected individuals, therefore, represent an enormous problem for the society, governments and global organizations. These diseases are usually considered as independent conditions, but increasing evidence shows that there are links between these two disorders. Methods: In this review, we analyzed common features present in Alzheimer’s disease and diabetes mellitus, showing how these two diseases are strictly correlated to each other. Results: Some pathogenetic factors are shared by Type 2 Diabetes and Alzheimer’s Disease: chronic inflammation, oxidative stress, mitochondrial dysfunction, adiponectin deficiency, different expression of plasma cholinesterase activity and vascular damage could represent a possible explanation for the coexistence of these two conditions in many patients. Conclusion: A better understanding of this issue and an appropriate management of diabetes by means of physical activity, low fat diet, and drugs to achieve a good glycemic control, avoiding both hyperglycemia and hypoglycemia, can represent a way to prevent cognitive decline and Alzheimer’s disease.
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Дисертації з теми "Alzheimers’s disease"

1

Holt, Jim. "Alzheimer’s Disease." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/6482.

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梁欣珮 and Yan-pui Irene Leung. "Potential impact of alzheimer's disease on retina." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42905059.

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Holt, Jim, J. Guduru, and S. Pathi. "Alzheimer’s Disease, 2nd Revision." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/6478.

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4

Holt, Jim, J. Guduru, M. Medipally, and S. Pathi. "Alzheimer’s Disease, 1st Revision." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/6480.

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5

Rickle, Annika. "PTEN and Akt signalling in Alzheimer's disease /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-514-3/.

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Holt, Jim, Christopher T. Bridges, and Christian B. Potter. "Dementia (Alzheimer’s Disease), 3rd Revision." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6472.

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7

Domingues, Catarina de Barros Pinto Salvador. "Chemokines impact in Alzheimer’s disease." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/16081.

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Mestrado em Biomedicina Molecular
Alzheimer’s Disease (AD) is a neurodegenerative disorder neuropathologically characterized by the presence of extracellular senile plaques, intracellular neurofibrillary tangles and synaptic loss. Neuroinflammation has been associated with some neurodegenerative diseases, such as AD. In AD, increased Aβ production and aggregation, have a fundamental role in the activation of the inflammatory process. In turn, this could be fundamental in the early stages of this pathology, regarding the Aβ clearance and brain protection. However, chronic inflammation leads to an increase of the inflammatory mediators, such as cytokines, released by activated microglia, astrocytes, and neurons. The excessive production of these inflammatory components promotes alterations in both amyloid precursor protein (APP) expression and processing, stimulating the increase of Aβ accumulation and abnormal tau phosphorylation. This results in neurotoxic effects, irreversible damage and neuronal loss. Chronic inflammation is a feature of AD however, little is known about the effects of some chemokines on its pathogenesis. Thus, the main aim of this thesis was to study the impact of the interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) on apoptosis, APP and tau. The both studied chemokines resulted in small alterations regarding the cytotoxicity on SH-SY5Y differentiated cells, being a significant increase in apoptosis observed only for the MCP-1 at the highest concentration. For the APP processing no significant differences were obtained, although a tendency to increase at different concentrations and periods was registered for both IL-8 and MCP-1. With respect to tau and other cytoskeleton-associated proteins, it was possible to observe a tendency to increase in the phosphorylated residue (Ser396) at the higher concentrations, as well as alterations on actin and tubulin with an increase on acetylated-α tubulin. This effect can be translated by neuronal architectural and survival alterations. Therefore additional studies could contribute to a better understanding of the way that these chemokines act on AD pathogenesis.
A Doença de Alzheimer (DA) é uma doença neurodegenerativa, caracterizada pela presença de placas senis extracelulares, tranças neurofibrilares intracelulares e perda sináptica. A neuroinflamação tem sido associada com algumas doenças neurodegenerativas, tal como a DA. Na DA, a produção e agregação aumentada do péptido Aβ, tem um papel fundamental na activação do processo inflamatório, que pode ser importante nas fases iniciais da doença, devido à remoção de Aβ e à proteção do cérebro. No entanto, uma inflamação crónica leva a um aumento de mediadores inflamatórios como são as citocinas, libertadas por microglia activada, astrócitos e neurónios. A produção excessiva de componentes inflamatórios promove alterações tanto na expressão como no processamento da proteína percursora amilóide (APP), levando a uma maior acumulação de Aβ e fosforilação anormal da proteína tau. Isto resulta em efeitos neurotóxicos, dano irreversível e perda neuronal. A inflamação crónica é uma característica da DA, no entanto pouco se sabe sobre os efeitos de algumas quimiocinas na sua patogénese. Assim, o principal objectivo desta tese foi o estudo do impacto da IL-8 e da MCP-1 na apoptose, APP e tau. Ambas as quimiocinas em estudo resultaram em pequenas alterações ao nível da citotoxicidade de células SH-SY5Y diferenciadas, tendo sido apenas observado um aumento significativo da apoptose para MCP-1 à concentração mais elevada. Relativamente ao processamento de APP, não foram observadas alterações significativas, no entanto alguma tendência para aumentar a diferentes concentrações e períodos foi obtida tanto para a IL-8 como para a MCP-1. Ao nível da tau e outras proteínas associadas ao citoesqueleto, foi possível observar uma tendência de aumento do resíduo fosforilado Ser396 às concentrações mais elevadas assim como alterações na actina e tubulina, com um aumento da αtubulina acetilada. Este efeito pode ser traduzido em alterações na arquitetura e sobrevivência neuronal. Assim sendo, estudos adicionais podem contribuir para uma melhor compreensão do modo de ação destas quimiocinas na patogénese da DA.
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Barra, Cátia Isabel de Almeida. "Inflammatory biomarkers in Alzheimer’s disease." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/13277.

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Mestrado em Biomedicina Molecular
Alzheimer’s disease (AD) is the most common form of dementia. Histopathologically it is characterized by the presence of two major hallmarks, the intracellular neurofibrillary tangles (NFT) and the extracellular senile plaques (SP), which are surrounded by activated astrocytes and microglia. Neuroinflammation has been associated with some neurodegenerative diseases. In AD the inflammatory process, prompted by increased Aβ production and aggregation, was reported to have a fundamental role in disease pathogenesis. In early stages the inflammation could have a beneficial role in the pathology, since it has been proposed that the microglia and astrocytes activated could be involved in (amyloid β) Aβ clearance. Nevertheless, the chronic activation of the microglia leads to excessive production of the inflammatory components, including cytokines. It promotes alterations in amyloid precursor protein (APP) expression and processing, stimulating the increase of Aβ accumulation, abnormal Tau phosphorylation and, consequently, neurotoxic effects, irreversible damage and loss of neurons. Since chronic neuroinflammation is a feature of AD, inflammatory proteins may constitute potential biomarkers candidates to assist clinical diagnosis of this dementia. Thus, the main aim of this study was to identify putative inflammatory biomarkers for AD by flow citometry analysis. For plasma samples of individuals examined by clinical dementia rating (CDR) and mini mental (MM) diagnostic tests were used. Subjects were subdivided in 3 distinct groups, a control group (CDR-/MM-) and two patient groups, CDR+/MM- and CRD+/MM+, the former may include mild cognitive impairment (MCI) patients and the latest group included 5 patients clinical diagnosed as AD. Data analysis revealed differences in the inflammatory proteins levels of both patients groups (CDR+/MM- and CDR+/MM+) in comparison to healthy individuals (CDR-/MM-). Interleukin-8 (IL-8) plasma levels were statistically different (P<0,05) from control group. Significant correlation between IL-8 concentrations and the CDR stages was also identified. Additionally, correlations of monocyte chemoattractant protein-1 (MCP-1) with both IL-8 and IL-6 were observed. Taken together these findings suggested that IL-8 could be a potential biomarker not only for AD but also for diagnosis of initial stages of dementia.
A doença de Alzheimer (DA) é o tipo de demência mais comum. Histopatologicamente é caracterizada pela presença de tranças neurofibrilares intracelulares (TNF) e de placas senis extracelulares (PS), as quais estão rodeadas pela microglia e por astrócitos. A neuroinflamação tem sido associada com várias doenças neurodegenerativas. Na DA o processo inflamatório, desencadeado pelo aumento da produção e agregação do péptido Aβ, desempenha um papel fundamental na patogénese da doença. Nas fases inicias, a inflamação possui um papel benéfico na patologia, uma vez que tem sido proposto que a microglia e os astrócitos quando ativados estão envolvidos na remoção de β-amilóide (Aβ). No entanto, a ativação crónica da microglia conduz à produção excessiva de componentes inflamatórios, incluindo citocinas. Isto provoca alterações na expressão e processamento da proteína percursora de amilóide (PPA), estimulando o aumento da produção e acumulação de Aβ, fosforilação anormal da proteína Tau e, consequentemente, efeitos neurotóxicos e perda de neurónios. Uma vez que a neuroinflamação crónica é uma característica da DA, proteínas inflamatórias poderão constituir potenciais candidatos a biomarcadores que auxiliem no diagnóstico clínico desta doença. Desta forma, o principal objectivo deste trabalho foi identificar biomarcadores inflamatórios para a DA através da técnica de citometria de fluxo. Para tal, foram analisadas amostras de plasma de doentes que foram, previamente, examinados por testes de avaliação cognitiva, clinical dementia rating (CDR) e mini mental (MM). Os sujeitos foram divididos em três grupos distintos, o grupo controlo (CDR-/MM-) e dois grupos de pacientes, CDR+/MM- e CDR+/MM+. O primeiro grupo de pacientes pode conter indivíduos com ligeiras alterações cognitivas (MCI) e o segundo inclui 5 pacientes clinicamente diagnosticados para DA. A análise dos dados revelou diferenças nos níveis de proteínas inflamatórias de ambos os grupos de doentes (CDR+/MM- e CDR+/MM+) em comparação com os indivíduos saudáveis (CDR-/MM-). Os níveis plasmáticos de interleucina-8 (IL-8) foram estatisticamente deferentes (p<0,05) do grupo controlo. Correlação significativa entre as concentrações de IL-8 e os estados de CDR foi identificada. Adicionalmente, foram observadas correlações entre MCP-1 e IL-8 e a IL-6. Em conjunto, estes resultados sugerem que a IL-8 poderá ser um potencial biomarcador não só para a DA mas também para o diagnóstico precoce de demência.
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9

Navaratnam, Dasakumar Selveraj. "Cholinesterases in Alzheimer's disease." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306734.

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10

Newman, Tracey Anne. "Ageing and Alzheimer's disease." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246220.

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Книги з теми "Alzheimers’s disease"

1

Altman, Harvey J., ed. Alzheimer’s Disease. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-6414-0.

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2

Jha, Arun, and Kaushik Mukhopadhaya. Alzheimer’s Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-56739-2.

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3

Sisodia, Sangram S., and Rudolph E. Tanzi, eds. Alzheimer’s Disease. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-35135-3.

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4

Harris, J. Robin, and Falk Fahrenholz, eds. Alzheimer’s Disease. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/b100942.

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5

Turner, J. D., K. Beyreuther, and F. Theuring, eds. Alzheimer’s Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-03248-0.

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6

Chun, Jerold, ed. Alzheimer’s Disease. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2655-9.

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7

Parks, Peggy J. Alzheimer's disease. San Diego: ReferencePoint Press, 2009.

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8

Sammons, Vivian O. Alzheimer's disease. Washington, D.C: Science Reference Section, Science and Technology Division, Library of Congress, 1987.

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9

Dempsey, Denise P. Alzheimer's disease. Washington, D.C: Science Reference Section, Science and Technology Division, Library of Congress, 1997.

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10

Parliament, Canada Library of. Alzheimer's Disease. Ottawa: Libray of Parliament, 1993.

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Частини книг з теми "Alzheimers’s disease"

1

Denham, Nathan C., James A. R. Nicoll, and Delphine Boche. "Synapses and Alzheimers’s Disease: Effect of Immunotherapy?" In Folding for the Synapse, 269–87. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7061-9_14.

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2

Gregori, Maria, and Francesca Re. "Neurodegenerative Diseases - Alzheimer's Disease." In Pharmaceutical Nanotechnology: Innovation and Production, 649–60. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527800681.ch27.

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Fuller, Stephanie J., Hamid R. Sohrabi, Kathryn G. Goozee, Anoop Sankaranarayanan, and Ralph N. Martins. "Alzheimer's Disease and Other Neurodegenerative Diseases." In Neurodegeneration and Alzheimer's Disease, 9–42. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119356752.ch2.

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Wakabayashi, Tomoko, Takeshi Iwatsubo, and Bart De Strooper. "The Biology of the Presenilin Complexes." In Alzheimer’s Disease, 35–58. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-35135-3_3.

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Jha, Arun, and Kaushik Mukhopadhaya. "Memory, Cognitive Impairment and Dementia." In Alzheimer’s Disease, 1–20. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_1.

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Jha, Arun, and Kaushik Mukhopadhaya. "Dementia Due to Alzheimer’s Disease (AD)." In Alzheimer’s Disease, 21–30. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_2.

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Jha, Arun, and Kaushik Mukhopadhaya. "Dementia Assessment." In Alzheimer’s Disease, 31–47. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_3.

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Jha, Arun, and Kaushik Mukhopadhaya. "RUDAS Cognitive Scale." In Alzheimer’s Disease, 49–56. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_4.

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Jha, Arun, and Kaushik Mukhopadhaya. "Diagnosis." In Alzheimer’s Disease, 57–64. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_5.

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Jha, Arun, and Kaushik Mukhopadhaya. "Supporting Diagnosis and Treatment." In Alzheimer’s Disease, 65–85. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56739-2_6.

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Тези доповідей конференцій з теми "Alzheimers’s disease"

1

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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Antonijević, Marko, Žiko Milanović, Edina Avdović, Dušica Simijonović, and Zoran Marković. "ANOTHER LOOK AT THE BIOLOGICAL ROLES OF A PLANT ALKALOID-BERBERINE." In XXVII savetovanje o biotehnologiji. University of Kragujevac, Faculty of Agronomy, 2022. http://dx.doi.org/10.46793/sbt27.455a.

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For millennia, berberine extracts or berberine itself has been the effective traditional drug with wide application due to its broad spectrum of antibiotic activity. A significant aspect of the berberine’s physiological activity that is often overlooked is the ability to go through the blood-brain barrier and has an impact on different processes and irregularities in the brain such as dementia and Alzheimer’s disease. Potential inhibitory activity towards enzymes for which is believed to be involved in these diseases, in this paper is confirmed by molecular docking simulations. Binding energies suggest that berberine exhibits good potential inhibitory activity and confirms that one of the aspects of suppression of Alzheimer’s disease and dementia is the inhibition of cholinesterase enzymes.
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Xavier, Lais de Paiva, Gabriella de Andrade Moreira, Luana Maria Amaral Cherain, Lucas Ferreira Flávio Souza, Tânia Maria da Silva Novaretti, and Valdeci de Oliveira Santos Rigolin. "Preliminary study on the number of deaths from neurodegenerative diseases in former Brazilian soccer players." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.212.

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Background: Neurodegenerative diseases have been reported in contact sports athletes. However, soccer has not been well characterized. Concerns were raised about the risk of neurodegenerative diseases being related to professional players in this sport. Objectives: To compare mortality from neurodegenerative diseases among Brazilian soccer players with the general population of the country. Methods: We conducted a retrospective cohort study. Causes of death were obtained from Brazilian teams’ databases and online content/public domain. Results: Among 1331 soccer players, 400 died. Acute Myocardial Infarction and Neoplasms were the highest causes of death, 58 and 53, respectively. We obtained a total of 35 deaths caused by neurodegenerative diseases. Alzheimer’s disease (18 deaths) and Stroke (14 deaths) were the most prevalent causes. These results are similar to the causes most found in the general population of Brazil: ischemic heart disease, cerebrovascular disease, airway infections and Alzheimer’s, in that order. This research had the following aspects as a limitation: the sources used were laymen, so the causes of death were not presented in a technical way in some moments; furthermore, the sampling space, still reduced, presented itself as another limitation. Conclusion: Preliminary results showed no correlation between soccer in Brazil and the higher occurrence of neurodegenerative diseases. The data sources and the sample space that were used may have contributed to such conclusions. These observations need to be confirmed on a larger scale with the prolongation of the study.
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Oliveira, Leonardo Santana Ramos, Lucca Ribeiro Alves, and Rodrigo Bartolomeu Sobral Neves. "Mortality of chronic-degenerative and infectious neurological disorders from 2009 to 2019: follow-up of epidemiological transition." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.527.

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Background: The epidemiological transition states that degenerative diseases are the main responsible for morbidity and mortality, assuming infectious diseases place. This trend can be explained by interaction between socio- environmental and demographic factors. Understand where Brazil is it’s important in the planning of cost-effective health policies and in reduction of morbidity and mortality. Objectives: Describe the number of deaths from infectious and degenerative neurological diseases between 2009 and 2019 in Brazil. Design and setting: This is an descriptive study considering brazilian deaths for neurological disorders. Methods: Using Ministry of Health database (DATASUS) from 2009 to 2019, mortality of following diseases were analyzed: Meningitis and Encephalitis, as infectous disorders; and Parkinson’s, Alzheimer’s and Epilepsy as degenerative disorders. Data from Human Development Index (HDI) were taken from the United Nations Development Program (UNDP). Proportions were calculated to simplify analysis and correlation between variables were verified using simple linear regression. Results: In the period, HDI increased by 6.4%, while mortality from infectious diseases decreased by 25% and from degenerative disordes grew 132%. Considering infectous disorders, Meningitis decreased by 33%, while Encephalitis increased 64%. In chronic-degenerative diseases, deaths due to Alzheimer’s disease increased by 158%, in Parkinson’s disease 90%, and 63% in Epilepsy. Correlation analysis using simple linear regression revealed a Pearson coefficient (r) of 0.924 and -0.967 for the relation between HDI and mortality from degenerative and infectious diseases, respectively. Conclusion: Brazil has followed the trend of epidemiological transition, with increase in mortality from chronic-degenerative diseases and reduction in infectious disorders.
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Chan, C., and S. Baek. "Model Based Surface Design to Incorporate the Effect of Soluble Cues." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53439.

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Many disease states such as obesity and Type 2 diabetes are polygenic and involve multiple organs with inter-related metabolic and vascular abnormalities, and furthermore are risk factors for other diseases such as nonalcoholic steatohepatitis (NASH), cardiovascular or Alzheimer’s diseases. Tissue engineering is attempting to address these diseases from the perspective of developing “spare” or “replacement” parts. Cell and tissue engineering integrates cellular and molecular biology with the principles and methods of chemical and mechanical engineering to develop biological substitutes that can restore, maintain, or control tissue function.
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Faria, Gustavo Hugo de Souza. "The impact of epigenetics on the development of neurodegenerative diseases." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.654.

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Introduction: Neurodegenerative diseases affect thousands of people in Brazil and have been increasing in frequency with the aging population. However, little is known about the molecular mechanisms and biomarkers of these diseases, which leads to a medical approach based on symptomatic and unresolving characteristics. Epigenetics, including DNA methylation, histone modifications, and changes in regulatory RNAs, emerges as a tool for prevention of neurodegenerative diseases. Objectives: To review studies that discuss the role of epigenetics in the development of neurodegenerative diseases. Methodology: This study involved an integrative review of papers published from 2016 to 2021 by searching PubMed and Scopus. Results: The studies showed that there is evidence that epigenetic mechanisms interfere with the development of major neurodegenerative diseases. Huntington’s disease presents an altered gene from birth, but transcriptional dysregulation is characteristic of the pathology that may be correlated to the age of disease onset in the cortex. In Parkinson’s disease dysregulation of expression of a specific protein is believed to play a central role in the disease and occurs through aberrant methylation that controls activation or suppression. In relation to Alzheimer’s disease, it has been found that deregulated DNA methylation and demethylation is linked to the onset and progression of the disease. In addition, these epigenetic factors are interfered with by diet, aging, and exercise. Conclusions: Investment in epigenetic studies is needed to understand possible markers of neurodegenerative diseases, for early diagnosis and the formation of epidrugs with the ability to treat.
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Rumao, Priti, and Mamta Padole. "Alzheimer's Disease." In DSMLAI '21': International Conference on Data Science, Machine Learning and Artificial Intelligence. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3484824.3484886.

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Rizzi, Liara, and Marcio Balthazar. "THE SUSPECTED NON-ALZHEIMER’S DISEASE PATHOPHYSIOLOGY." 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.rpda070.

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Background: Individuals that are negative for amyloid biomarkers and positive for p-Tau and/or neurodegeneration ones are known as with the suspected non-Alzheimer’s disease pathophysiology (SNAP). It is a biomarker-based concept that underlying etiology has not been completely understood. Objective: To report the main characteristics of the SNAP group. Methods: PubMed was searched to identify articles about the SNAP for inclusion. Results: The prevalence of SNAP varies from 18% to 35% among cognitively normal individuals, from 16,6% to 35% among mild cognitive impairment (MCI), and from 7% to 39% among clinical probable Alzheimer’s Disease (AD). SNAP subjects have a lower risk of clinical progression to MCI or AD dementia than those with positive amyloid biomarkers, but higher than those whose biomarkers for amyloid and neurodegeneration are negative. SNAP predominate in older men and have a lower incidence of the APOE ε4 allele than in individuals with AD. Cognitive decline in SNAP subjects is related to neuronal damage. They present greater hippocampal atrophy than AD, but a similar pattern of hypometabolism. Hippocampus-specific pathologies and cerebrovascular diseases may underlie neurodegeneration and cognitive impairments. Conclusion: The construct of SNAP has been challenging, therefore, a deeper understanding of the main pathways that underlie SNAP can allow substrates for disease prevention and/or remission in the future.
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"Hybrid CNN-SVM for Alzheimer's Disease Classification from Structural MRI and the Alzheimer’s Disease Neuroimaging Initiative (ADNI)." In 2018 International Conference on Biomedical Engineering, Machinery and Earth Science. Francis Academic Press, 2018. http://dx.doi.org/10.25236/bemes.2018.041.

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Elcin, Huseyn. "EARLY IDENTIFICATION OF THE NEUROLOGICAL COMPLICATIONS OF DIABETES MELLITUS." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/30032021/7474.

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Diabetes mellitus is still a very common disease in the world and affects the daily lives of patients negatively. Diabetes is also known to be associated with neurological diseases such as peripheral nerve diseases, stroke and dementia. Among these, the most common disease is a peripheral nerve disease, and it has been reported that poor diabetic control increases the risk of development and can be prevented by education of the patients. Vascular dementia is more common in patients with diabetes than Alzheimer's disease, and it is thought that cerebrovascular diseases may berelated to cognitive impairment in diabetes. Although the mechanisms by which diabetes affects the brain are not clearly revealed, it is thought that changes in vascular structure, insulin resistance, glucose toxicity, oxidative stress, accumulation of glycation end products, hypoglycemic episodes and amyloid metabolism are effective.The aim of this article is to describe the neurological complications of diabetes and to emphasize the importance of patient education, good diabetes control and early diagnosis in preventing these complications.
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Звіти організацій з теми "Alzheimers’s disease"

1

Lattaf, Sara, Lamiaa Abdallaoui, and Amal Bouziane. Effect of periodontal disease on Alzheimer’s disease: protocol of a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0033.

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Mehegan, Laura. Alzheimer's Disease and Dementia Awareness Poll 2018. AARP Research, June 2018. http://dx.doi.org/10.26419/res.00232.001.

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Chandra, Amitabh, Courtney Coile, and Corina Mommaerts. What Can Economics Say About Alzheimer's Disease? Cambridge, MA: National Bureau of Economic Research, August 2020. http://dx.doi.org/10.3386/w27760.

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Kamaruzzaman, Mohd Amir, Muhammad Hibatullah Romli, Razif Abas, Sharmili Vidyadaran, Mohamad Taufik Hidayat Baharuldin, Muhammad Luqman Nasaruddin, Vishnnumukkala Thirupathirao, et al. Impact of Endocannabinoid Mediated Glial Cells on Cognitive Function in Alzheimer’s Disease: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0094.

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Review question / Objective: This review aims to review systematically, and meta-analyse published pre-clinical research about the mechanism of endocannabinoid system modulation on glial cells and their effects on cognitive function in designated Alzheimer’s Disease (AD) in the animal model. Condition being studied: Its been acknowledged that the cure of Alzheimer's disease is still vague. Current medicine is working on symptoms only but never stop the disease progression due to neuronal loss. In recent years, researches have found that cannabinoid which is derived from cannabis sativa plant and its compounds exert neuroprotective effects in vitro and in vivo. In fact, cognitive improvement has been shown in some clinical studies. Therefore, the knowledge of cannabinoids and its interaction with living physiological environment like glial cells is crucial as immunomodulation to strategize the potential target of this substance. The original articles from related study relating endocannabinoid mediated glial cell were extracted to summarize and meta-analyze its impact and possible mechanism against cognitive decline in AD.
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Mintzer, Jacobo E., D. L. Bachman, M. Stuckey, M. Ebeling, M. T. Wagner, W. J. Evans, V. Hirth, A. Walker, R. Joglekar, and W. Faison. A State-Wide Research Network for Alzheimer's Disease. Office of Scientific and Technical Information (OSTI), March 2014. http://dx.doi.org/10.2172/1123171.

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Mehegan, Laura. Alzheimer's Disease and Dementia Awareness Poll 2018: Infographic. AARP Research, June 2018. http://dx.doi.org/10.26419/res.00232.002.

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Pericak-Vance, Margaret A. Whole Exome Analysis of Early Onset Alzheimer's Disease. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada602412.

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Pericak-Vance, Margaret A. Whole Exome Analysis of Early Onset Alzheimer's Disease. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada603027.

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Moran, Marcel Moran. Retrospective: Alzheimer’s Disease Research: An Overview of 1998-2015 Grantmaking. San Francisco, CA United States: S. D. Bechtel, Jr. Foundation, November 2017. http://dx.doi.org/10.15868/socialsector.37561.

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Han, Nana, Yang Fang, Guozhen Zhao, and Bo Ji. The comparative efficacy and safety of acupuncture for mild and moderate Alzheimer's disease: A systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0014.

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Review question / Objective: According to the current randomized clinical trials (RCT) of acupuncture therapy for Alzheimer's disease (AD), to evaluate their methodology, the quality of evidence and the report are evaluated and summarize evidence of important outcomes of randomized clinical trials. We aim to provide accurate clinical decision-making for acupuncture treatment of Alzheimer's disease. Condition being studied: According to the current randomized clinical trials (RCT) of acupuncture therapy for Alzheimer's disease (AD), to evaluate their methodology, the quality of evidence and the report are evaluated and summarize evidence of important outcomes of randomized clinical trials. We aim to provide accurate clinical decision-making for acupuncture treatment of Alzheimer's disease.
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