Memory function often declines with age, and is believed to deteriorate initially because of
changes in synaptic function rather than loss of neurons. Some individuals then go on to …

Abstract ALZHEIMER'S disease (AD) affects more than 30% of people over 80 years of
age1, 2. The aetiology and pathogenesis of this progressive dementia is poorly understood …

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects a large
proportion of the elderly population. Amyloid plaques, which are a neuro-pathological …

A PATHOLOGICAL hallmark of Alzheimer's disease is the deposition of amyloid fibrils in the
brain. The principal component of amyloid fibrils is β/A4 amyloid protein1, 2, which can be …

Abstract ALZHEIMER'S disease (AD) is the most common cause of progressive intellectual
failure in aged humans. AD brains contain numerous amyloid plaques surrounded by …

The amyloid-β peptide Aβ42 is known to be a primary amyloidogenic and pathogenic agent
in Alzheimer's disease. However, the role of Aβ43, which is found just as frequently in the …

Alzheimer's disease (AD) is a neurodegenerative condition, believed to be irreversible,
characterized by inexorable deterioration of memory and intellect, with neuronal loss …

The formation of fibrillar deposits of amyloid β protein (Aβ) in the brain is a pathological
hallmark of Alzheimer's disease1, 2 (AD). A central question is whether Aβ plays a direct role …

Studies of the molecular basis of Alzheimer's disease exemplify the increasingly blurred
distinction between basic and applied biomedical research. The four genes so far implicated …

Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor
protein (APP), presenilin 1 (PS1), and presenilin 2 (P52) genes1. The mutant APP K670N …