The pathogenesis of Alzheimer's disease is highly complex. While several pathologies
characterize this disease, amyloid plaques, composed of the β-amyloid peptide are hallmark …

The amyloid β protein (Aβ) is derived from β‐amyloid precursor protein (APP). Cleavage of
APP by β‐secretase generates a C‐terminal fragment (APPCTFβ or C99), which is …

Various environmental and genetic factors influence the onset and progression of
Alzheimer's disease (AD). Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis …

The molecular mechanism underlying the pathogenesis of the majority of cases of sporadic
Alzheimer's disease (AD) is unknown. A history of stroke was found to be associated with …

The fetal basis of adult disease (FeBAD) hypothesis states that many adult diseases have a
fetal origin. According to FeBAD, injury or environmental influences occurring at critical …

Classic cardio-metabolic risk factors such as hypertension, stroke, diabetes, and
hypercholesterolemia all increase the risk of Alzheimer's disease. We found increased …

Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ)
peptide as neuritic plaques in the brain. The short Aβ peptide is derived from the large …

Amyloid β (Aβ) damages neurons and triggers microglial inflammatory activation in the
Alzheimer disease (AD) brain. BACE1 is the primary enzyme in Aβ generation …

Summary Cyclin-dependent kinase 5 (cdk5) has been implicated in Alzheimer's disease
(AD) pathogenesis. Here, we demonstrate that overexpression of p25, an activator of cdk5 …

Oxidative damage to DNA has been associated with neurodegenerative diseases.
Developmental exposure to lead (Pb) has been shown to elevate the Alzheimer's disease …