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Статті в журналах з теми "Olfactory disorders"
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Gaines, Alan. "Olfactory Disorders." American Journal of Rhinology & Allergy 27, no. 3_suppl (May 2013): S45—S47. http://dx.doi.org/10.2500/ajra.2013.27.3898.
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Gros, A., V. Manera, C. A. De March, N. Guevara, A. König, L. Friedman, P. Robert, J. Golebiowski, and R. David. "Olfactory disturbances in ageing with and without dementia: towards new diagnostic tools." Journal of Laryngology & Otology 131, no. 7 (April 20, 2017): 572–79. http://dx.doi.org/10.1017/s0022215117000858.
Повний текст джерелаАнотація:
AbstractBackground:Olfactory disorders increase with age and often affect elderly people who have pre-dementia or dementia. Despite the frequent occurrence of olfactory changes at the early stages of neurodegenerative disorders such as Alzheimer's disease, olfactory disorders are rarely assessed in daily clinical practice, mainly due to a lack of standardised assessment tools. The aims of this review were to (1) summarise the existing literature on olfactory disorders in ageing populations and patients with neurodegenerative disorders; (2) present the strengths and weaknesses of current olfactory disorder assessment tools; and (3) discuss the benefits of developing specific olfactory tests for neurodegenerative diseases.Methods:A systematic review was performed of literature published between 2000 and 2015 addressing olfactory disorders in elderly people with or without Alzheimer's disease or other related disorders to identify the main tools currently used for olfactory disorder assessment.Results:Olfactory disorder assessment is a promising method for improving both the early and differential diagnosis of Alzheimer's disease. However, the current lack of consensus on which tests should be used does not permit the consistent integration of olfactory disorder assessment into clinical settings.Conclusion:Otolaryngologists are encouraged to use olfactory tests in older adults to help predict the development of neurodegenerative diseases. Olfactory tests should be specifically adapted to assess olfactory disorders in Alzheimer's disease patients.
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Snow, James B. "Clinical Investigation of Disorders of Olfaction." American Journal of Rhinology 2, no. 4 (September 1988): 145–48. http://dx.doi.org/10.2500/105065888781692970.
Повний текст джерелаАнотація:
The receptor cells in the olfactory neuroepithelium are regularly replaced and, when injured, regenerate from basal cells and reestablish their central connections. This process of reconstitution occurs throughout the life span after mechanical, chemical, and infectious injury. The history and physical findings in association with the quantification of the olfactory loss allow an etiologic diagnosis in many patients. Olfactory losses can be categorized as transport or sensorineural defects. Therapy for transport olfactory losses is frequently effective in restoring the sense of smell. Reasonable strategies for treatment of patients with sensorineural olfactory losses remain limited.
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Ziuzia-Januszewska, Laura, and Marcin Januszewski. "Pathogenesis of Olfactory Disorders in COVID-19." Brain Sciences 12, no. 4 (March 27, 2022): 449. http://dx.doi.org/10.3390/brainsci12040449.
Повний текст джерелаАнотація:
Since the outbreak of the SARS-CoV-2 pandemic, olfactory disorders have been reported as a frequent symptom of COVID-19; however, its pathogenesis is still debated. The aim of this review is to summarize the current understanding of the pathogenesis of smell impairment in the course of COVID-19 and to highlight potential avenues for future research on this issue. Several theories have been proposed to explain the pathogenesis of COVID-19-related anosmia, including nasal obstruction and rhinorrhea, oedema of the olfactory cleft mucosa, olfactory epithelial damage either within the olfactory receptor cells or the supporting non-neural cells (either direct or immune-mediated), damage to the olfactory bulb, and impairment of the central olfactory pathways. Although the pathogenesis of COVID-19-related anosmia is still not fully elucidated, it appears to be mainly due to sensorineural damage, with infection of the olfactory epithelium support cells via the ACE1 receptor and disruption of the OE caused by immense inflammatory reaction, and possibly with direct olfactory sensory neurons infection mediated by the NRP-1 receptor. Involvement of the higher olfactory pathways and a conductive component of olfactory disorders, as well as genetic factors, may also be considered.
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Peyvandi, Aliasghar, Shahrokh Khoshsirat, Narges Bazgir, Amirreza Zaker, Azin Tahvildari, Somayeh Niknazar, Sara Mohammadi, and Mehri Salari. "Olfactory dysfunction as a diagnostic and prognostic marker for movement disorders." Annals of Movement Disorders 7, no. 3 (September 2024): 171–80. https://doi.org/10.4103/aomd.aomd_75_24.
Повний текст джерелаАнотація:
Abstract Olfactory dysfunction (OD) is a common nonmotor symptom observed in several movement disorders. The severity and pattern of olfactory impairment vary among these conditions. Notably, olfactory impairment often precedes the clinical diagnosis of movement disorders by several years, yet it remains frequently unrecognized by patients and physicians until formal olfactory tests are undertaken. This review focuses on exploring OD across various movement disorders. A systemic search strategy incorporating key terms such as movement disorders, dystonic disorders, tic disorders, parkinsonian disorders, parkinsonism, ataxia, essential tremors, drug-induced akathisia, and olfaction disorders was employed to query databases including Embase, Scopus, and PubMed. After excluding irrelevant articles, 99 studies were selected for comprehensive review. OD is a persistent feature across all movement disorders, with the exception of pseudo supranuclear palsy. Among these conditions, olfactory impairment is much more frequent and severe in patients with Parkinson’s disease. Incorporating olfactory testing into the diagnostic evaluation of at-risk individuals or patients with established movement disorders is recommended. These olfactory tests offer a practical, cost-effective, and convenient diagnostic tool that may aid in the early identification and management of these conditions.
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Lebedeva, G. V., M. V. Svistushkin, L. V. Selezneva, V. A. Kudryavtseva, K. K. Pogosyan, I. A. Zinchenko, and V. M. Svistushkin. "Possibilities of using the domestic olfactory test in the diagnosis of typical olfactory disorders." Russian Medical Inquiry 8, no. 8 (2024): 470–76. http://dx.doi.org/10.32364/2587-6821-2024-8-8-5.
Повний текст джерелаАнотація:
Background: the diagnosis of olfactory disorders remains a critical issue in clinical practice. Olfactory testing is the most commonly utilized diagnostic tool. Previously, we developed an olfactory test and validated it on healthy volunteers. Aim: to evaluate the diagnostic efficacy of a domestic olfactory test in detecting various olfactory disorders. Materials and Methods: this study included 100 patients presenting with typical olfactory disorders. Subjects were categorized into three groups: acute rhinosinusitis (AR) (n=50), polypous rhinosinusitis (PR) (n=25), and post-viral olfactory dysfunction (PVDO) (n=25). Olfactory function was assessed using the developed test and a visual analog scale (VAS) for comparative analysis. Olfactory threshold and odor discrimination ability were measured in all groups using the olfactory test. In the PR and PVDO groups, the assessment was conducted once on the examination day. In the AR group, assessments were performed twice: on the day of treatment and 14 days post-treatment. Results: olfactory dysfunction was detected in all groups. In the AR group, both the VAS and the domestic olfactory test indicated a decrease in olfactory threshold without changes in odor discrimination ability. Fourteen days post-treatment, improvements in olfactory threshold and odor discrimination were noted, although VAS scores demonstrated a decline. In the PR and PVDO groups, both VAS and the domestic olfactory test showed reductions in olfactory threshold and odor discrimination abilities. VAS results highly correlated with the olfactory threshold across all groups, and additionally with odor discrimination ability in the PVDO group. Conclusion: the study demonstrated the effectiveness of the domestic olfactory test in diagnosing typical olfactory disorders. KEYWORDS: olfaction, olfactory test, olfactory diagnostics, olfactory threshold, odor discrimination ability, acute rhinosinusitis, polypous rhinosinusitis, post-viral olfactory dysfunction, odor. FOR CITATION: Lebedeva G.V., Svistushkin M.V., Selezneva L.V., Kudryavtseva V.A., Pogosyan K.K., Zinchenko I.A., Svistushkin V.M. Possibilities of using the domestic olfactory test in the diagnosis of typical olfactory disorders. Russian Medical Inquiry. 2024;8(8):470–476 (in Russ.). DOI: 10.32364/2587-6821-2024-8-8-5.
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Langstaff, Lorna, Nisha Pradhan, Allan Clark, Duncan Boak, Mahmoud Salam, Thomas Hummel, and Carl M. Philpott. "Validation of the olfactory disorders questionnaire for English‐speaking patients with olfactory disorders." Clinical Otolaryngology 44, no. 5 (June 17, 2019): 715–28. http://dx.doi.org/10.1111/coa.13351.
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Park, Yong-Jin. "Treatment of the Olfactory Disorders." Journal of Clinical Otolaryngology Head and Neck Surgery 18, no. 1 (May 2007): 23–27. http://dx.doi.org/10.35420/jcohns.2007.18.1.23.
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Ryo, Yusuke, Mina Takeuchi, Naoko Ueda, Kazutaka Ohi, Hiroaki Kihara, Takamitsu Shimada, Takashi Uehara, and Yasuhiro Kawasaki. "Olfactory function in neuropsychiatric disorders." Psychiatry Research 252 (June 2017): 175–79. http://dx.doi.org/10.1016/j.psychres.2017.02.058.
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Sirota, P., D. Shamir, and E. Mitrany. "Olfactory sensitivity in eating disorders." Biological Psychiatry 39, no. 7 (April 1996): 572. http://dx.doi.org/10.1016/0006-3223(96)84195-3.
Повний текст джерелаДисертації з теми "Olfactory disorders"
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Morgan, Charlie David. "Olfactory event-related potentials in Alzheimer's disease /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9974114.
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Kamath, Vidyulata. "THE RELATIVE SENSITIVITY OF AN OLFACTORY IDENTIFICATION DEFICIT IN INDIVIDUALS WITH SCHIZOTYPAL PERSONALITY FEATURES." Master's thesis, University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3847.
Повний текст джерелаАнотація:
Olfactory identification deficits have received recent attention as a potentially useful endophenotype for schizophrenia. Examination of this deficit in individuals with schizotypal personality features (SPF) offers an alternative approach to multiple confounds present when examining individuals with schizophrenia. The aim of the current study was to compare the relative sensitivity of performance on measures of olfaction identification and sustained attention to the presence of SPF. Twenty-six undergraduates were defined as having SPF based on scoring in the top 10% of the Abbreviated Schizotypal Personality Questionnaire (SPQ-B; mean age 19.6, SD = 1.1; 62% female). These individuals were compared to twenty-six controls (scoring lower than half a standard deviation above the mean; mean age 19.8, SD = 1.6; 62% female). All participants were administered the Schizotypal Personality Disorder (SPD) section of the Structured Clinical Interview for DSM IV Axis II Personality Disorders (SCID-II). In addition, participants were administered the Brief Smell Identification Test (B-SIT) and a six-minute degraded-stimuli Continuous Performance Test (CPT). Group differences in performance indices of the CPT did not approach statistical significance. Similarly, there were no statistically significant group differences for males or females in performance on the B-SIT. Correlational analyses examined cognitive performance with a dimension score derived by summing quantitative ratings from the SPD items on the SCID-II. The SPD dimension score showed a statistically significant positive correlation with several performance indices of the CPT, including omission errors (rs(52) = .51, p < .001) and commission errors (rs(52) = .38, p < .005). In contrast, the B-SIT scores were not correlated with the SPD dimension score for males or females. Contrary to our hypothesis, results from the current study suggest that olfactory identification deficits may not represent a robust endophenotype consistently found in samples with schizotypal personality features. With regard to sustained attention, our differential findings suggest that schizotypal traits may be more adequately assessed through an interview by trained clinicians who use clinical judgment to determine the presence of phenotypic aspects of SPD (e.g., SCID-II), rather than relying on self-report measures (e.g., SPQ-B). Implications as well as limitations and future directions of these findings are discussed.M.S.
Department of Psychology
Sciences
Psychology PhD
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Todorovic, Michael. "Assessing the Role of the Oxidative Stress Response ‘Master Regulator’ Nrf2 in Parkinson’s Disease." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367349.
Повний текст джерелаАнотація:
Parkinson’s disease (PD) is a complex neurodegenerative disorder influenced by a combination of genetic and environmental factors. The molecular mechanisms that underlie PD are unknown. However, oxidative stress and impairment of antioxidant defence mechanisms have been implicated as major contributors to disease pathogenesis. Previously, we have reported a PD patient-derived cellular model, generated from biopsies of the olfactory mucosa, termed hONS cells. These cells have demonstrated disease-specific differences in gene expression and metabolic activity associated with the Nrf2-mediated antioxidant defence pathway.
To date, few studies have examined the role of the Nrf2 encoding gene, NFE2L2, in PD. This thesis comprehensibly assessed whether rare and common NFE2L2 genetic variations modify susceptibility to PD using a large Australian case-control sample (PD=1,338; controls=1,379). We employed a haplotype-tagging approach that identified an association with the tagging SNP rs2364725 and PD (OR = 0.849 (0.760-0.948), P = 0.004). Further genetic screening for rare variants in patient-derived cell lines produced no obvious pathogenic variants in the coding regions of NFE2L2. In addition, we were able to identify some age-at-onset modifying SNPs and replicate an ‘early-onset’ haplotype that contains a previously identified ‘functional promoter’ SNP (rs6721961).Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
Full Text
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Clevenger, Amy Christine. "Developing mouse models to understand olfactory deficits in schizophrenia /." Connect to full text via ProQuest. IP filtered, 2005.
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Clark, Jessica. "Effects of Sensory Ablation on the Young and Aged Ventriculo-Olfactory Neurogenic System." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/366315.
Повний текст джерелаАнотація:
Adult neurogenesis is a dynamic field of study, with potential for generating therapies for neurodegenerative disorders. The demonstration of adult brain neurogenesis strengthens the rationale for regenerative therapies for neurodegenerative disorders. The ‘ventriculo-olfactory neurogenic system’ (VONS) is used in the study neurogenesis, migration and differentiation of neural stem cells. Importantly, subventricular zone (SVZ) neuroblasts recapitulate a population of dopaminergic neurons within the olfactory bulb (OB), possibly the only population of dopaminergic interneurons, generated throughout adult life. This study aims to simulate a patho physiological model for olfactory epithelial cell turnover to demonstrate a link between the olfactory epithelium (OE) and cell proliferation in the SVZ.
In order to examine the relationship between the OE and the SVZ, an ablation protocol was generated. Using a double dose of methimazole, the OE was completely ablated leading to denervation of the olfactory bulb. This denervation resulted in an increase of astrocyte and microglial activity on day 11 which remained elevated up to day 21. This was accompanied by a significant decrease of tyrosine hydroxylase immunoreactivity in type I periglomerular cells on day 17. While there was a decrease in the type II periglomerular cells on day 17, this was shown to be not significant.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Henriksson, Jörgen. "Uptake of manganese and some other metals into the CNS via the olfactory pathway /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5447-6.pdf.
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Campabadal, Delgado Anna. "Idiopathic REM sleep behavior disorder and olfactory dysfunction in Parkinson's disease and premotor stages. MRI and neuropsychological studies." Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/671022.
Повний текст джерелаАнотація:
BACKGROUND:
The present Doctoral Thesis is focused on Rapid-eye-movement (REM) sleep behavior disorder (RBD) and olfactory dysfunction as biomarkers of Synucleinopathies, such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). RBD is a parasomnia characterized by loss of atonia during REM sleep that provokes dream-enacting behaviors. Clinically isolated RBD (IRBD) is considered a prodromal stage of alpha-Synucleinopathies since almost 75% of patients after 12 years of the disease develop a PD or atypical parkinsonism. Specifically, in a multicentric study,
56.5% of IRBD patients converted to parkinsonism as the first manifestation, while 43.5% developed dementia first. Subtle motor symptoms, hyposmia, and cognitive impairment are the best predictors of phenoconversion in IRBD.
OBJECTIVES AND HYPOTHESES:
The main objectives of this Thesis are: 1) To characterize structural and functional brain substrates underlying Idiopathic REM sleep behavior disorder as well as to relate these findings to cognitive performance; 2) To study olfactory dysfunction as a preclinical and clinical biomarker of alpha- Synucleinopathies, and its progression throughout the disease; 3) To investigate progressive brain degeneration throughout IRBD, and to investigate how these changes relate to cognitive decline.
The main hypotheses are:
1) IRBD will be characterized by specific changes in brain structure and functional connectivity that will be associate with olfactory and cognitive impairment,
2) IRBD patients will show structural brain changes over time and a cognitive decline superior to that seen in normal aging,
3) Smell dysfunction will be identified in IRBD and PD, and it is expected to progress slightly with the disease course.
MATERIAL AND METHODS:
This Doctoral Thesis is presented as a compendium of six studies that were carried out to achieve the above-mentioned objectives.
RESULTS:
In studies 1, 2, and 5, IRBD patients differed from controls in several cognitive domains, namely attention and executive functions, mental processing speed, verbal memory, and semantic fluency. Besides, studies 1 and 5 identified for first-time impairment in facial recognition and visuospatial functions. Contrary to our hypothesis in study 1, we did not find significant correlations between cognitive performance and brain atrophy. However, there was coherence between the structural changes detected by MRI and neuropsychological impairment. For instance, IRBD subjects had facial recognition impairment and cortical atrophy in the fusiform gyrus, a region that is known to be critical for such function. In the same way, patients showed memory impairment and hippocampal atrophy, a core structure for learning and memory. On the other hand, study
2 evidenced the potential role of altered brain functional connectivity in IRBD’s cognitive impairment. We found a positive correlation between mental processing speed and temporoparietal functional connectivity in the IRBD group. In study 5, we reported visual form discrimination decline in IRBD relative to normal aging after less than two years. More importantly, we identified that visual form discrimination worsening over time was explained by progressive reductions of the cortical thickness in the superior parietal.
CONCLUSIONS:
The present Doctoral Thesis has identified new cognitive deficits in IRBD patients and has shed some light on its progression throughout the course of the disease. In particular, our work has shown the importance of VS/VP functions as a measure able to identify cognitive changes across time in IRBD, and its potential in identifying those patients with progressive neurodegeneration in posterior cortices. Besides, we have exhaustively described the characteristics of severe and early olfactory dysfunction in IRBD and described for the first time its neuroanatomical correlates. The neuroimaging data from this Thesis points towards an early implication of the temporal-occipital-parietal cortices in IRBD. Additionally, our longitudinal work has shown that IRBD patients have brain degeneration of the occipitoparietal and orbitofrontal cortex over time, in line with the degenerative changes reported in PD and DLB. Abnormalities in such regions are supported by the association between impaired cognition and both functional and structural brain changes.
Cortical atrophy and disrupted cortico-cortical functional connectivity highlight that cortical degeneration and functional abnormalities already exist in patients with IRBD before they are diagnosed with DLB, PD, or MSA. Thus, suggesting that in prodromal PD, the alpha-synuclein pathology is already involving these structures earlier than would be expected according to the Braak degeneration model proposed form neuropathological data. Cortical atrophy and dysfunction may explain why some patients present neuropsychological impairment before the motor onset. We hope that our research will serve as a basis for further multicentric studies that confirm our findings, and to identify the optimal neuropsychological and neuroimaging markers for diagnostic, prognostic, and efficacy of future neuroprotective therapies.MARC TEÒRIC: La present Tesi Doctoral estudia el trastorn del comportament del son REM (RBD, per les seves sigles en anglès) i la disfunció olfactiva com a biomarcadors de les alfa- Sinucleinopaties, com ara la malaltia de Parkinson (PD, per les seves sigles en anglès), la demència per cossos de Lewy (DLB, per les seves sigles en anglès) i l’atròfia multisistèmica (MSA, per les seves sigles en anglès). El RBD és una parasòmnia caracteritzada per la pèrdua d’atonia durant el son REM que provoca episodis on els pacients mostren moviments que reflecteixen el contingut dels seus somnis. El RBD que es presenta clínicament aïllat (IRBD, per les seves sigles en anglès), es considera un estadi prodròmic de les Sinucleinopaties, doncs s’ha vist que gairebé el 75% dels pacients després de 12 anys amb diagnòstic d’IRBD acaben sent diagnosticats de malaltia de Parkinson o parkinsonismes atípics. Concretament, en un estudi multicèntric el 56.5% dels pacients amb IRBD varen desenvolupar parkinsonisme com a primera manifestació, mentre que el 43.5% va presentar demència en primer lloc. La simptomatologia motora, la hipòsmia i el deteriorament cognitiu han demostrat ser els millors predictors de conversió en aquests pacients. En aquest context, la comunitat científica ha demostrat un interès creixent en definir els canvis cognitius associats a l’IRBD. Els estudis publicats fins ara conclouen que entre el 15-50% dels pacients tenen deteriorament cognitiu lleu. Malgrat l’evidència ben documentada sobre la presència d’afectació neuropsicològica en pacients amb IRBD, cal una recerca addicional que valori de forma aïllada i específica les funcions visuoespacials i visuoperceptives (VS/VP), ja que l’alteració d’aquestes funcions és característica del perfil neuropsicològic dels pacients amb PD i DLB. Pel que fa al declivi cognitiu al llarg de la malaltia, encara hi ha una gran incertesa. OBJECTIUS I HIPÒTESIS: Els objectius principals d'aquesta Tesi són: 1 Caracteritzar els substrats cerebrals estructurals i funcionals subjacents a l’RBD, així com relacionar aquestes troballes amb el rendiment cognitiu, 2 Estudiar la disfunció olfactiva com a biomarcador clínic i preclínic de les alfa- Sinucleinopaties, i la seva progressió al llarg de la malaltia, 3 Investigar la degeneració cerebral progressiva al llarg de l’IRBD i com aquests canvis es relacionen amb el declivi cognitiu. Les principals hipòtesis són: 1 L'IRBD es caracteritzarà per canvis específics en l'estructura cerebral i la connectivitat funcional que estarà associada a un deteriorament olfactiu i cognitiu, 2 Els pacients amb IRBD mostraran canvis cerebrals estructurals amb el pas del temps i un declivi cognitiu superior a l’observat en l’envelliment normal, 3 S'espera identificar reducció de la capacitat olfactòria en l'IRBD i la PD, així com que progressi lleugerament amb el curs de la malaltia. MATERIAL I MÈTODES: La present Tesi Doctoral consta de sis estudis realitzats per donar resposta als objectius esmenats anteriorment. CONCLUSIONS: La present Tesi Doctoral ha identificat nous dèficits cognitius en pacients amb IRBD i ha perfilar la seva progressió al llarg de l’evolució de la malaltia. En particular, el nostre treball ha demostrat la importància de les funcions VS/VP com a mesura capaç d’identificar els canvis cognitius a través del temps en l’IRBD i el seu potencial per identificar aquells pacients amb neurodegeneració progressiva en el còrtex posterior. A més, hem descrit de forma exhaustiva les característiques de la disfunció olfactiva precoç i greu de l’IRBD i hem descrit per primera vegada els seus correlats neuroanatòmics.
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Godoy, Maria Dantas Costa Lima. "Acometimento do epitélio olfatório pela doença de Alzheimer: um estudo de correlação clínico-patológica." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-05102015-122610/.
Повний текст джерелаАнотація:
A doença de Alzheimer (DA) é caracterizada por declínio cognitivo e funcional progressivo e constitui-se como a forma mais prevalente de demência. O diagnóstico da DA é realizado atualmente, exclusivamente por meio de critérios clínicos. No entanto, a manifestação clínica da DA é precedida por um longo período assintomático, com depósito silencioso das proteínas tau e -amiloide no tecido cerebral. Evidências recentes demonstram que a mucosa olfatória, estrutura periférica e facilmente acessível também está acometida na DA, podendo representar um bom método de diagnóstico preciso e precoce desta moléstia. Os objetivos desse estudo consistem em correlacionar a prevalência das proteínas tau e -amiloide no epitélio olfatório (EO) com os estágios clínicos e neuropatológicos da doença e determinar a sensibilidade e especificidade dos achados no EO para o diagnóstico da DA em seus diferentes estágios de evolução. Para tal fim, é proposto estudo post-mortem, com avaliação de 92 tecidos cerebrais de indivíduos com idade igual ou superior a 50 anos, provenientes do Banco de Encéfalos Humanos do Grupo de Estudos em Envelhecimento Cerebral da Universidade de São Paulo, com coleta dos blocos de mucosa olfatória no momento da autópsia. A avaliação cognitiva foi realizada por meio de entrevista com informante de convívio próximo com o falecido, aplicando as escalas CDR e IQCODE. A avaliação neuropatológica do encéfalo e do EO foi realizada por meio de técnicas de . Os casos foram classificados mediante critério neuropatológico do CERAD e do estadiamento de Braak e Braak para DA. A presença de proteína tau e -amiloide no EO foi correlacionada com os parâmetros clínicos e neuropatológicos obtidos. A análise do EO da concha superior permitiu identificar as proteínas tau e -amiloide com sensibilidade alta, quando comparada com o diagnóstico neuropatológico (>80%) e clínico ( > 90%). Desta forma, a análise para as proteínas tau e - amiloide do epitélio olfatório pode representar um possível biomarcador para diagnóstico da DAAlzheimer\'s disease (AD) is characterized by a progressive functional and cognitive decline and is considered the most prevalent type of dementia. AD is diagnosed exclusively on the basis of clinical criteria. However, clinical symptoms of AD are preceded by a long asymptomatic period, with silent deposition of tau and amyloid proteins in brain tissue. Recent studies demonstrate the same findings in the olfactory epithelium, a ready accessible structure which could contribute to the precise and early diagnosis of AD. The objectives of the current study were to correlate the prevalence of tau and amyloid proteins distributed in several areas of the olfactory epithelium with clinical and neuropathological criteria used for the diagnosis of AD and to determine the sensitivity and specificity of the olfactory epithelium involvement for the diagnosis of AD. Ninety-two individuals, belonging to the Brazilian Brain Bank of the Aging Brain Study Group from University of São Paulo, whose blocks of olfactory mucosa were collected during autopsy, were tested. Cognitive data were gathered through an interview with a knowledgeable informant, using the CDR (Clinical Dementia Rating Scale) and the IQCODE (Informant Questionnaire on Cognitive Decline in the Elderly) scales. Neuropathological examination was carried out on the basis of accepted criteria, using immunohistochemistry. Neuropathological classification of AD was performed in accordance with the CERAD criteria and Braak & Braak staging. The presence of tau and amyloid protein deposits in the olfactory epithelium was compared with clinical and neuropathological parameters. Immunostaining of olfactory epithelium from the superior turbinate was able to identify tau protein and amyloid-? with high sensitivity when compared with neuropathological scales ( > 80%) and clinical classification of CDR ( > 90%). Thus, immunohistochemistry for tau and amyloid proteins of the olfactory epithelium may represent a potential biomarker for early diagnosis of AD
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Moussy, Erwan. "Remédiation olfactive connectée : impact sur la cognition et le bien-être." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10341.
Повний текст джерелаАнотація:
L’odorat remplit des fonctions fondamentales dans le quotidien à travers son implication dans la détection de dangers, la prise alimentaire et les relations sociales. Par conséquent, la perte partielle (hyposmie) ou totale (anosmie) d’odorat a un impact significatif sur les conditions de vie, en affectant la santé physique et mentale des personnes touchées. Un nombre important de personnes sont concernées par les troubles de l’odorat, nombre qui est amené à croitre dans le contexte post-crise sanitaire du COVID-19 et en raison du phénomène de vieillissement des populations. Malgré leurs importantes prévalences et conséquences, les troubles de l’odorat sont mal pris en charge à cause d’un double manque d’accès au diagnostic et de traitements efficaces. Parmi les stratégies de remédiation olfactive, l’entrainement olfactif a émergé comme une piste prometteuse mais il reste à être optimisé car son efficacité apparait variable selon les études. L’entrainement olfactif pourrait également présenter des bénéfices plus larges sur le fonctionnement cérébral, qui sont actuellement peu explorés. Ce travail de thèse propose de nouvelles stratégies de diagnostic et de remédiation innovantes pour améliorer la prise en charge des troubles de l’odorat. Il explore également l’intérêt de l’entrainement olfactif en tant que stratégie de promotion globale du bien-vieillir au niveau cérébral. Nous avons développé une nouvelle génération de tests olfactifs connectés, permettant une évaluation rapide et facile des capacités olfactives, plus compatible avec une utilisation en routine clinique que les tests psychophysiques existants. Basé sur un score d’identification et d’évaluation de l’intensité de 8 odeurs, ce test permet d’identifier avec fiabilité les personnes souffrant d’anosmie de diverses origines. Afin d’améliorer l’efficacité de l’entrainement olfactif, nous avons développé un protocole assisté par une plateforme numérique, permettant d’améliorer le suivi de l’entrainement et l’adhérence du patient. Nous avons également testé si l’augmentation de la fréquence d'exposition aux odeurs ou le renouvellement des odeurs durant l’entrainement olfactif permettraient d’améliorer la récupération olfactive. Chez des patients post-COVID-19 présentant des déficits olfactifs persistants, un entrainement olfactif de 3 mois permet une amélioration de la perception olfactive ainsi que de la qualité de vie (notamment du plaisir alimentaire). Toutefois, l’augmentation du nombre d’odeurs senties quotidiennement ne semble pas améliorer l’efficacité de cet entrainement olfactif. Un entrainement basé sur l’utilisation de produits odorants du domicile se révèle également efficace mais nécessite une vigilance particulière vis à vis de l’adhérence du patient. Nous avons ensuite testé l’intérêt d’un entrainement olfactif avec renouvellement des odeurs, chez des participants âgés avec ou sans troubles de l’odorat. Les résultats suggèrent une meilleure récupération olfactive des participants dysosmiques ayant suivi cet entrainement pendant 4 mois, comparés à ceux ayant suivi à un entrainement avec une seule et même odeur. Enfin, nous avons évalué les potentiels bénéfices de l’entrainement olfactif avec renouvellement des odeurs sur la cognition des participants âgés, ainsi que sur le bien-être, la qualité de vie et l’appréciation alimentaire. Nos résultats ne montrent pas d’amélioration significative de la cognition, mais un bénéfice sur les symptômes dépressifs des participants âgés, avec ou sans troubles de l’odorat. L’analyse de l’activité du système noradrénergique ne montre pas de modification suite à l’entrainement olfactif, suggérant que celui-ci ne contribue pas aux mécanismes sous-tendant les bénéfices de l’entrainement. L’ensemble de ce travail ouvre donc de nouvelles perspectives pour le diagnostic et la remédiation des déficits olfactifs. Il suggère également que l’utilisation des odeurs pour promouvoir le bien-vieillir cérébral reste à approfondirThe sense of smell fulfills fundamental functions in everyday life, through its involvement in danger detection, food intake and social relations. Consequently, partial (hyposmia) or total (anosmia) loss of smell has a significant impact on living conditions, affecting the physical and mental health of those affected. A significant number of people are affected by smell disorders, a number that is set to grow in the post COVID-19 health crisis context and due to the phenomenon of ageing populations. Despite their significant prevalence and consequences, olfactory disorders are poorly managed, lacking access to diagnosis and effective treatment. Among olfactory remediation strategies, olfactory training has emerged as a promising approach but remains to be optimized as its efficacy appears to vary from study to study. Olfactory training could also have wider benefits on brain function, which are currently little explored. This thesis proposes new and innovative diagnostic and remediation strategies to improve the management of olfactory disorders. It also explores the interest of olfactory training as a strategy to promote cerebral well-ageing. We developed a new generation of connected olfactory tests, enabling rapid and easy assessment of olfactory capacities, more compatible with routine clinical use than existing psychophysical tests. Based on an identification and perceived intensity score of 8 odors, this test can reliably identify people suffering from anosmia of various origins. In order to improve the effectiveness of olfactory training, we developed a protocol supported by a digital platform, enabling improved training follow-up and patient adherence. We also tested whether increasing the frequency of odor exposure or renewing odors during olfactory training would improve olfactory recovery. In post-COVID-19 patients with persistent olfactory deficits, 3 months of olfactory training led to an improvement in olfactory perception and quality of life (including food enjoyment). However, increasing the number of odors smelled daily does not seem to improve the effectiveness of olfactory training. A training based on the use of scented products from home also proved effective but required particular vigilance with regard to patient adherence. We then tested the interest of olfactory training with odor renewal, in elderly participants with or without olfactory disorders. The results suggest better olfactory recovery in dysosmic participants who underwent this training for 4 months, compared with those who underwent training with a single odor. Finally, we assessed the potential benefits of olfactory training with odor renewal on the cognition of elderly participants, as well as on well-being, quality of life and food appreciation. Our results show no significant improvement in cognition, but a benefit on depressive symptoms in elderly participants, with or without smell disorders. Analysis of noradrenergic system activity showed no change following olfactory training, suggesting that it does not contribute to the mechanisms underlying the benefits of training. Taken together, this work opens up new perspectives for the diagnosis and remediation of olfactory deficits. It also suggests that the use of odors to promote better brain aging remains to be further explored
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Tee, Jing Yang. "Olfactory Stem Cells as Disease Models for Schizophrenia." Thesis, Griffith University, 2019. http://hdl.handle.net/10072/388987.
Повний текст джерелаАнотація:
Schizophrenia is a strongly heritable multifactorial mental disorder that affects 1% of any population, but disease etiology is not yet fully understood. The limitations of using animal models, post-mortem brain studies and difficulty to obtain human brain biopsies have impeded the understanding of this disease from the biological perspective. There is a consensus, based on epidemiology and post-mortem human brains that schizophrenia is a neurodevelopmental disorder, but cellular and molecular mechanisms for this hypothesis are lacking. We have developed a model to address this using human olfactory neurosphere-derived (hONS) ‘stem’ cells, which were obtained non-invasively from human participants, expressed neural stem cell markers and allows comparative analyses of age- and sex-matched cell lines from patients diagnosed with schizophrenia with cell lines from healthy participants. Patient cells from various sources have a common dysregulation to gene pathway networks involved in axonal guidance, cell adhesion, cytoskeletal remodeling, focal adhesion signaling and reelin signaling - all important pathways that regulate cell migration.
A high throughput live cell tracking technique was developed to unbiasly quantify cell motility in vitro. At baseline on uncoated tissue culture plastic (TCP), patient cells moved longer distances than control cells. Patient cells were unable to respond to their microenvironment when increasing concentrations of well-defined ECM proteins were coated on TCP cell culture surfaces. This was despite patient cells expressing the necessary cell surface integrin receptors measured by flow cytometry, which meant they have the capacity to bind and recognize all tested ECM proteins. Patient cells have consistently lower levels of cytoskeletal proteins in filamentous actin (F-actin) and stable microtubules, which became more evident when cultured on ECM proteins. Despite being able to adjust their cell sizes and shapes, patient cells were consistently smaller than control cells. Focal adhesion kinase (FAK) levels were consistently lower in patient cells and they were unable to manufacture enough focal adhesions of the correct sizes upon contact with ECM proteins. These findings highlighted a global deficit to cell migration in schizophrenia that was not limited to just Fibronectin but also on all ECM proteins, which were caused by disease-dependent intracellular deficits in patient cell cytoskeleton and focal adhesions. Reelin is an important brain ECM protein that orchestrates neuronal migration during neurodevelopment and its expression is reduced in post-mortem brain tissues from patients with schizophrenia. In this study, reelin protein levels were also reduced in patient hONS cells compared to control cells. Despite having the capabilities to bind to reelin through expression of key reelin signaling pathway accessory protein Dab1 and reelin-binding receptors ApoER2 and VLDLR, patient cells were unable to respond to extracellular reelin. Patient cells were unable to adjust their movement track lengths when tracked on surfaces coated with full length reelin. Similar to our previous findings on other ECM proteins, patient cells had lower levels of F-actin and stable microtubules, and were consistently smaller in size compared to control cells. Our findings suggested that non-responsive cell migration deficits were caused by defective focal adhesion responses to extracellular reelin. Instead of producing more focal adhesions that were larger in response to reelin, patient cells reduced both the densities and sizes of their focal adhesions at the peripheral region of the cell where lamellipodia forms. This was the first study to demonstrate a biological link between reelin signaling and schizophrenia, with a focus on the effects of reelin on cell migration.
Published computer programs were used in silico to investigate the mechanistic components of cell migration and to further investigate reasons why patient cells were unable to respond to their ECM microenvironment. X-Y displacement coordinates for each individually tracked cell were analyzed by the DiPer and migration phase/cell turning analysis programs to compute cell movement variables in directionality, diffusivity, persistence and idling and turning. At baseline on TCP, patient cells did not move at the correct trajectories, failed to make directional changes, paused less and turned less when tracked for 24 h. When tracked on ECM proteins, it was difficult to pinpoint one explanation to explain our non-responsive cell migration findings as various mechanistic variables played a collective part to potentially give rise to the observed non-responsive cell migration phenotype. One explanation was that patient cells spent more time in persistent movement and were unable to make necessary changes to their directions. Another explanation was the unchanged cell pausing tendencies on Type I Collagen as a plausible explanation for observed non-responsive changes to motility on that ECM protein. The same in silico computational analyses showed that patient cells did not respond to extracellular reelin because they could not reduce the rate at which they changed the straightness of their movement trajectories. Patient cells were also unable to make well-timed changes to the direction of their movement trajectories by being more persistent in one direction for longer. Decreased densities and sizes of focal adhesions in patient cells upon contact with extracellular reelin resulted in patient cells not decreasing their turn angles, but instead made larger uncoordinated turns. The way that control cells responded negatively to extracellular reelin supported the hypothesis in the field that reelin acts as a “stop signal” for actively moving neuronal cells, which was disrupted in patient cells.
In conclusion, this thesis has uncovered a novel non-responsive cell migration phenotype in schizophrenia, which was broadly relevant on different ECM proteins, to suggest consistent defects in how patient cells respond to their surrounding microenvironment. Findings from this thesis also showed that observed cell migration deficits were caused by differences to intracellular components such as cell cytoskeleton and focal adhesions, coupled to previously published findings that FAK, integrin and actin signaling pathways were all dysregulated in schizophrenia. Using an analogy of patient cells as a moving vehicle, our findings showed a global defect to many parts of this faulty “vehicle”, such as defective “ignition” in FAK signaling, uncoordinated “wheels” in the lamellipodia and consistent faults to the “clutch” mechanism in the focal adhesions. All working in concert to cause patient cells to move in a less coordinated fashion and unable to make controlled mechanistic changes to their movement, causing them to ultimately lose their way.School of Environment and Sc
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Книги з теми "Olfactory disorders"
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Weiss, Logan E., and Jason M. Atwood. The biology of odors: Sources, olfaction, and response. Hauppauge, N.Y: Nova Science Publishers Inc., 2011.
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Hawkes, Christopher H. The neurology of olfaction. Cambridge: Cambridge University Press, 2009.
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Heinbockel, Thomas. Sino-Nasal and Olfactory System Disorders. Intechopen, 2020.
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Sino-Nasal and Olfactory System Disorders [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.80149.
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Olfactory cognition: From perception and memory to environmental odours and neuroscience. Amsterdam: John Benjamins Pub. Co., 2012.
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Phillips, Katharine A. Differentiating Body Dysmorphic Disorder from Normal Appearance Concerns and Other Mental Disorders. Edited by Katharine A. Phillips. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190254131.003.0018.
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This chapter discusses differentiation of body dysmorphic disorder (BDD) from disorders that may be misdiagnosed as BDD or that present differential diagnosis challenges: eating disorders, major depressive disorder, obsessive-compulsive disorder, trichotillomania (hair-pulling disorder), excoriation (skin-picking) disorder, illness anxiety disorder, social anxiety disorder, agoraphobia, panic disorder, generalized anxiety disorder, schizophrenia and other psychotic disorders, gender dysphoria, avoidant personality disorder, olfactory reference syndrome, and several other constructs. This chapter also discusses how to differentiate BDD from normal appearance concerns and from problematic preoccupation with obvious physical defects.BDD is commonly misdiagnosed as another mental disorder. Sometimes misdiagnosis occurs because patients are too embarrassed and ashamed to reveal their appearance concerns; in such cases, BDD symptoms that are more readily observable (such as social anxiety) may be assigned an incorrect diagnosis while BDD goes undetected. In other cases, BDD symptoms are recognized but are misdiagnosed as another disorder. BDD must be differentiated from other conditions so appropriate treatment can be instituted.
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Facial reactions in response to gustatory and olfactory stimuli in healthy adults, patients with eating disorders, and patients with attention-deficit hyperactivity disorder. Würzburg, Germany: Julius-Maximilians-Universität, 2010.
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Doty, Richard L., and Christopher H. Hawkes. Neurology of Olfaction. Cambridge University Press, 2009.
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Doty, Richard L., and Christopher H. Hawkes. Neurology of Olfaction. Cambridge University Press, 2009.
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Doty, Richard L., and Christopher H. Hawkes. Neurology of Olfaction. Cambridge University Press, 2009.
Знайти повний текст джерелаЧастини книг з теми "Olfactory disorders"
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Taha, Mohamed Shehata. "Olfactory Disorders." In Current Rhinology, 41–60. Cham: Springer Nature Switzerland, 2024. https://doi.org/10.1007/978-3-031-70077-4_2.
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Murphy, Claire. "Olfactory Impairment and Neurodegenerative Disorders." In Sensory Science and Chronic Diseases, 145–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-86282-4_7.
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Koçak, Tuğba, Aytuğ Altundağ, and Thomas Hummel. "Clinical Assessment of Olfactory Disorders." In All Around the Nose, 109–12. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21217-9_13.
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Rombaux, Philippe, Stephanie Collet, and Caroline Huart. "Assessment of Olfactory Function." In Nasal Physiology and Pathophysiology of Nasal Disorders, 403–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37250-6_30.
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Leonard, B. E., J. Butler, B. O’Neill, and W. T. O’Connor. "Bilaterally Olfactory Bulbectomized Rat Model of Depression." In New Directions in Affective Disorders, 13–16. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3524-8_3.
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Özdener-Poyraz, Ayşe Elif, and Mehmet Hakan Özdener. "Olfactory Impairement in Disease and Aging." In Nasal Physiology and Pathophysiology of Nasal Disorders, 403–17. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-12386-3_31.
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Holbrook, Eric H. "Clinical Assessment and Management of Olfactory Disorders." In Rhinology and Facial Plastic Surgery, 115–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-74380-4_10.
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Smith, David V., and Heather J. Duncan. "Primary Olfactory Disorders: Anosmia, Hyposmia, and Dysosmia." In Science of Olfaction, 439–66. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2836-3_16.
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Welge-Lüssen, Antje, and Markus Wolfensberger. "Olfactory Disorders following Upper Respiratory Tract Infections." In Taste and Smell, 125–32. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000093758.
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Avrunin, O. G., Y. V. Nosova, N. O. Shushlyapina, A. S. Zlepko, A. I. Bezuglyi, T. Zyska, and G. Ziyatbekova. "Formalization of the diagnosis of olfactory disorders." In Information Technology in Medical Diagnostics II, 23–30. London, UK; Boca Raton: CRC Press/Balkema, [2019] | Selected and extended conference papers from Polish, Ukranian and Kazakh scientists.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429057618-4.
Повний текст джерелаТези доповідей конференцій з теми "Olfactory disorders"
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Göktas, Ö., and C. Azar. "Olfactory and gustatory training in the treatment of olfactory disorders." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640845.
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Fernandes, Lucca Ferdinando Queiroz, Raiana Carol de Medeiros Dantas, Maria Clara Medeiros Araújo, and Lucas de Oliveira Araújo Andrade. "Non-motor clinical manifestations of Parkinson’s disease and its relevance in early diagnosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.100.
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Introduction: Parkinson’s disease is a progressive neurodegenerative disease that affects millions of people worldwide. Although Parkinson’s disease has traditionally been described as a disorder of the motor system, it is now recognized as a complex disease with several clinical features that include neuropsychiatric and non-motor manifestations. Studies show that 97% of patients with Parkinson’s disease report non-motor symptoms, in addition to motor symptoms, and some non-motor characteristics may appear before classic motor signs. Objectives: To list the main non-motor clinical manifestations of Parkinson’s disease and analyze its importance in establishing an accurate and early clinical diagnosis. Methods: This is an integrative review, carried out based on the search of scientific publications indexed in the datebase MEDLINE via PubMed, Lilacs and SciELO. At the end of the searches, 66 publications met the eligibility criteria and were selected to compose the study. Results: Within the non-motor clinical manifestations, there may be present: cognitive dysfunction and dementia, psychosis and hallucinations, mood disorders, sleep disorders, fatigue, autonomic dysfunction, olfactory dysfunction, gastrointestinal dysfunction, pain, sensory disorders and dermatological manifestations. Of these, olfactory dysfunction, constipation, depression and sleep disorders stand out because they often precede the motor symptoms of Parkinson’s disease. Conclusion: In this perspective, it is up to the general practitioner and the neurologist or geriatrician to carry out, whenever possible, screening tests to identify early changes that may precede Parkinson’s disease, guaranteeing patients an early multiprofessional treatment and consequently a better prognosis in the course of the disease.
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Pierchalla, Greta, Ulrike Förster-Ruhrmann, Heidi Olze, Uta Hoppmann, and Judith Bellmann-Strobl. "Investigation of olfactory disorders in patients with post-COVID fatigue syndrome." In 94th Annual Meeting German Society of Oto-Rhino-Laryngology, Head and Neck Surgery e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767135.
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Meshram, Dewanand, and Dipti Durgesh Patil. "Integrating Olfaction Technology and AI in Understanding Olfactory Dysfunction in Neurodegenerative Neuropsychiatric Disorders." In 2023 International Conference on Artificial Intelligence for Innovations in Healthcare Industries (ICAIIHI). IEEE, 2023. http://dx.doi.org/10.1109/icaiihi57871.2023.10489788.
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Shushliapina, Nataliia, Yuliia Svitlychna, and Yana Nosova. "Possibilities of Telemedicine Technologies in the Diagnosis and Rehabilitation of Olfactory Disorders in COVID-19." In 2021 IEEE 8th International Conference on Problems of Infocommunications, Science and Technology (PIC S&T). IEEE, 2021. http://dx.doi.org/10.1109/picst54195.2021.9772192.
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Weiler, Marina, Perla Moreno Castilla, Hannah Starnes, Edward Melendez, Kevin Stieger, Jeffrey Long, and Peter Rapp. "EFFECTS OF REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION IN AGED RATS DEPEND ON PRE-TREATMENT COGNITIVE STATUS: TOWARD INDIVIDUALIZED INTERVENTION FOR SUCCESSFUL COGNITIVE AGING." 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.rpda002.
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Background: Repetitive Transcranial Magnetic Stimulation (rTMS) has shown initial promise in combating age-related cognitive decline and dementia. The nature and severity of cognitive aging, however, varies markedly between individuals. Objective/Hypothesis: We hypothesized that the distinct constellation of brain changes responsible for individual differences in cognitive aging might influence the response to rTMS. Methods: Cognitive effects of rTMS were evaluated using a rat model of cognitive aging in which aged rats are classified as Aged-Impaired (AI) or -Unimpaired (AU) relative to young (Y) according to their performance in the Morris water maze. Several weeks later, following presentation of a sample odor in an olfactory recognition task, rats received either sham (Y, n = 9; AU, n = 8; AI, n = 9) or intermittent Theta Burst Stimulation (Y, n = 8; AU, n = 8; AI, n = 9). Memory was tested 24 hours later. Results: Recognition memory in the sham and stimulated conditions depended on pre-treatment cognitive status in the aged rats. Y and AU sham rats displayed robust odor recognition, whereas sham-treated AI rats exhibited no retention. In contrast, rTMS treated AI rats showed robust retention, comparable in magnitude to Y, whereas the AU stimulated scored at chance. Conclusion: Our results are consistent with a perspective that the unique neurobiology associated with variability in cognitive aging modulates the response to rTMS. Protocols with documented efficacy in young adults may have unexpected outcomes in aging or neurodegenerative conditions, requiring individualized approaches.
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Nunes, Alícia Malta Brandão. "COVID-19 and neuroinvasion: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.747.
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Background: Clinical practice throughout the pandemic has generated a debate about the existence of neurotropism and the neuropathogenic capacity of the new coronavirus. Medical professionals have noted that there is a wide spectrum of neurological manifestations associated with SARS-CoV-2 infections; from hyposmia to encephalopathy. The interaction of the viral protein spike (S) with the ACE2 gene present in endothelial and nerve cells and the cytokine storm triggered by COVID-19 are explanatory bases for a series of mechanisms proposed in recent literature. Objectives: To establish a direct connection, or not, between neurological manifestations and SARS-CoV-2 infection. Design and setting: Analysis of the current literature present in medical databases. Methods: To select the studies, the Medline (Pubmed), LILACS and SciELO databases were used with the keywords “neurology” and “covid” and “mechanism”. The search period for the articles covered the last 10 months (since June 2020). The selection and design criteria of the studies were descriptive, crosssectional, cohort, case report and randomized clinical study. Results: Thirty-eight articles with potential for inclusion were retrieved, but only seventeen of them declared no conflict of interest and answered the inclusion criteria and the guiding question, which consisted of assessing the association between neurological disorders and COVID-19. Conclusion: Eight studies defend the indirect invasion, due to the imaging exams presenting an olfactory bulb without any alteration. Through infection of the endothelial cells, vascular alterations and wear of the BBB by the cytokine storm. In parallel, the other nine studies advocate direct invasion, where the virus infects the olfactory bulb and reaches the rhinencephalon and midbrain through the axons, generating, for example, the lack of symptoms in the so-called happy hypoxia of the coronavirus. Neuroinvasion in COVID-19 is still unclear, but hypotheses show 2 possible pathways for the virus to access the CNS: hematogenous and retrograde neuronal pathways. To elucidate these pathogenic pathways, larger and more systematic studies will be needed.
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Hoover, Devin, Neelesh Parikh, James A. Espinosa, and Alan Lucerna. "Case Report: What’s That Smell? Olfactory Seizures." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. http://dx.doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.47_2024.
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We report a case of a 64-year-old male who presented with transient episodes of near syncope followed by a noxious odor and was diagnosed with olfactory seizures. The differential diagnosis for near syncope is broad. This case demonstrates that unusual olfactory symptoms can lead to a diagnosis of seizure disorder in the emergency department.
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Negoias, S., B. Meves, Y. Zang, A. Haehner, and T. Hummel. "Characteristics of olfactory disorder with and without reported flavor loss." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728857.
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Prashanth, R., S. Dutta Roy, P. K. Mandal, and S. Ghosh. "Parkinson's disease detection using olfactory loss and REM sleep disorder features." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944937.
Повний текст джерелаЗвіти організацій з теми "Olfactory disorders"
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Santos Sales, Déborah, Mariana Beiral Hammerle, Rayanne da Silva Souza, Patricia Gomes Pinheiro, Débora Viana Freitas, Ana Carolina F. Herzog, Daniel Lucas de L. S. Santos, et al. Long Covid-19 Syndrome: the Prevalence of Neuropsychiatric Symptoms in Patients with Olfactory Disorders. Progress in Neurobiology, December 2023. http://dx.doi.org/10.60124/j.pneuro.2023.30.01.
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Background: Among the frequently reported symptoms in long-term COVID-19 syndrome, we can highlight olfactory disorders depression, anxiety, and fatigue. OD can affect people's physical and mental health and can lead to neuropsychiatric symptoms. Objective: Determine the prevalence of symptoms of depression, anxiety, and fatigue in patients with olfactory disorders induced by long-term COVID-19; and investigate this impact on the quality of life. Methods: The study included 30 patients with confirmed long-term COVID-19, with persistent complaints of olfactory dysfunction. OD was evaluated by the connecticut smell test. Neuropsychiatric disorders were evaluated by the fatigue severity and hospital anxiety and depression scales. Quality of life was accessed using the SF-36. Results: 70% of the patients had different degrees of hyposmia and 20% had anosmia. The most prevalent symptom was depression with 66.7% of the sample. More than half of patients also had symptoms of anxiety and fatigue (53,3% both). The most affected dimensions of SF-36 were emotional, vitality, role physical and mental health (36.6 ± 44.0, 44.3 ± 28.7, 47.5 ± 42.7, 49.8 ± 24.7 respectively). There was a moderate negative correlation between symptoms of depression and the physical role and mental health dimension. There was a moderate negative correlation between anxiety and general health, vitality, social functioning, and mental health dimensions. Symptoms of fatigue obtained a moderate negative correlation in the physical function dimension. Conclusion: The prevalence of symptoms of depression, anxiety and fatigue is high in patients with olfactory disorders induced by long-term COVID-19, with a negative impact on the quality of life of these patients, highlighting the role emotional aspect.