The brain undergoes many gross and histopathologic changes with advancing age. Some of the changes seen with aging are also found in demented individuals, especially patients with Alzheimer's disease. The extent to which Alzheimer's disease and aging are truly different processes remains to be determined. The morphologic features that seem most clearly to distinguish between aging and Alzheimer's disease are the neurofibrillary tangles and senile plaques. The distinction can be further refined by determining the immunocytochemical and ultrastructural composition of the degenerating nerve processes in the neuritic plaques.
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http://dx.doi.org/10.1016/s0733-8619(05)70081-5 | DOI Listing |
Neurology
February 2025
Department of Neurology, Houston Methodist, TX, and Weill Cornell, New York, NY.
PLoS One
January 2025
Center for Innovation in Brain Science, University of Arizona Health Sciences, Tucson, Arizona, United States of America.
Translational validity of mouse models of Alzheimer's disease (AD) is variable. Because change in weight is a well-documented precursor of AD, we investigated whether diversity of human AD risk weight phenotypes was evident in a longitudinally characterized cohort of 1,196 female and male humanized APOE (hAPOE) mice, monitored up to 28 months of age which is equivalent to 81 human years. Autoregressive Hidden Markov Model (AHMM) incorporating age, sex, and APOE genotype was employed to identify emergent weight trajectories and phenotypes.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge CB2 1EW, United Kingdom.
The onset and development of Alzheimer's disease is linked to the accumulation of pathological aggregates formed from the normally monomeric amyloid-β peptide within the central nervous system. These Aβ aggregates are increasingly successfully targeted with clinical therapies at later stages of the disease, but the fundamental molecular steps in early stage disease that trigger the initial nucleation event leading to the conversion of monomeric Aβ peptide into pathological aggregates remain unknown. Here, we show that the Aβ peptide can form biomolecular condensates on lipid bilayers both in molecular assays and in living cells.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Introduction: Alzheimer's disease (AD) patients with higher educational attainment (EA) often exhibit better cognitive function. However, the relationship among EA status, AD pathology, structural brain reserve, and cognitive decline requires further investigation.
Methods: We compared cognitive performance across different amyloid beta (Aβ) positron emission tomography (A ±) statuses and EA levels (High EA/Low EA).
Adv Sci (Weinh)
January 2025
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China.
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Recent studies have identified a population of disease-associated astrocytes (DAA)-like astrocytes closely linked to amyloid deposition and tau pathology in an AD mouse model. However, the presence and role of these astrocytes in high-salt diet (HSD) models remain unexplored.
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