The pathophysiological process of Alzheimer’s disease (AD) is thought to begin many years
before the diagnosis of AD dementia. This long “preclinical” phase of AD would provide a …

To learn about the carboxy-terminal extent of amyloid g-protein (Ag) composition of senile
plaques (SPs) in the brain affected with Alzheimer’s disease (AD), we employed two end-…

The deposition of the abundant presynaptic brain protein α-synuclein as fibrillary aggregates
in neurons or glial cells is a hallmark lesion in a subset of neurodegenerative disorders. …

Background The accumulation of soluble and insoluble aggregated amyloid-beta (Aβ) may
initiate or potentiate pathologic processes in Alzheimer’s disease. Lecanemab, a humanized …

Mutations in presenilin genes account for the majority of the cases of the familial form of
Alzheimer's disease (FAD). Presenilin is essential for γ-secretase activity, a proteolytic activity …

Breakthroughs in molecular medicine have positioned the amyloid-β (Aβ) pathway at the
center of Alzheimer’s disease (AD) pathophysiology. While the detailed molecular mechanisms …

Lewy bodies (LBs) are hallmark lesions of degenerating neurons in the brains of patients
with Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Recently, a point …

Clinicopathologic correlation studies are critically important for the field of Alzheimer disease
(AD) research. Studies on human subjects with autopsy confirmation entail numerous …

A large body of evidence has implicated Aβ peptides and other derivatives of the amyloid
precursor protein (APP) as central to the pathogenesis of Alzheimer's disease (AD). However, …

Background Alzheimer's disease is characterized by amyloid-beta plaques, neurofibrillary
tangles, gliosis, and neuronal loss. Solanezumab, a humanized monoclonal antibody, …