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Plasma ADAM10 Levels and Their Association with Alzheimer's Disease Diagnosis in Older Adults with Fewer Years of Formal Education.
Dement Geriatr Cogn Disord
June 2024
Department of Gerontology, Federal University of São Carlos, São Carlos, Brazil,
Article Synopsis
- Low educational attainment may increase the risk of developing Alzheimer's disease (AD), and the enzyme ADAM10 could serve as a crucial blood biomarker for diagnosing Mild Cognitive Impairment (MCI) and AD in older adults.
- Researchers evaluated cognition through standardized tests and analyzed plasma ADAM10 levels in participants, finding significant differences in cognitive performance and health characteristics between those with MCI and AD.
- Elevated plasma ADAM10 levels were linked to a higher likelihood of being diagnosed with MCI and AD, suggesting its potential as a valuable biomarker for assessing cognitive health in individuals with low educational attainment.
Association Between Persistent Treatment of Alzheimer's Dementia and Osteoporosis Using a Common Data Model.
Dement Neurocogn Disord
October 2023
Kangwon National University School of Medicine, Chuncheon, Korea.
Background And Purpose: As it becomes an aging society, interest in senile diseases is increasing. Alzheimer's dementia (AD) and osteoporosis are representative senile diseases. Various studies have reported that AD and osteoporosis share many risk factors that affect each other's incidence.
View Article and Find Full Text PDFSARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes.
Metabolites
November 2022
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre 90035-003, Brazil.
The main neuropathological feature of Alzheimer's disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases. Although the relationship between these two amyloid disorders is obvious, this does not make CAA a characteristic of AD, as 40% of the non-demented population presents this derangement.
View Article and Find Full Text PDFAll the Tau We Cannot See.
Annu Rev Med
January 2023
Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts, USA; email:
Alzheimer's disease (AD) was described in 1906 as a dementing disease marked by the presence of two types of fibrillar aggregates in the brain: neurofibrillary tangles and senile plaques. The process of aggregation and formation of the aggregates has been a major focus of investigation ever since the discoveries that the tau protein is the predominant protein in tangles and amyloid β is the predominant protein in plaques. The idea that smaller, oligomeric species of amyloid may also be bioactive has now been clearly established.
View Article and Find Full Text PDFDissecting the Crosstalk between Endothelial Mitochondrial Damage, Vascular Inflammation, and Neurodegeneration in Cerebral Amyloid Angiopathy and Alzheimer's Disease.
Cells
October 2021
Alzheimer's Center at Temple, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Alzheimer's disease (AD) is the most prevalent cause of dementia and is pathologically characterized by the presence of parenchymal senile plaques composed of amyloid β (Aβ) and intraneuronal neurofibrillary tangles of hyperphosphorylated tau protein. The accumulation of Aβ also occurs within the cerebral vasculature in over 80% of AD patients and in non-demented individuals, a condition called cerebral amyloid angiopathy (CAA). The development of CAA is associated with neurovascular dysfunction, blood-brain barrier (BBB) leakage, and persistent vascular- and neuro-inflammation, eventually leading to neurodegeneration.
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