Background Transgenic mice expressing disease-associated proteins have become
standard tools for studying human neurological disorders. Transgenes are often expressed …

Transient soluble oligomers of amyloid-β (Aβ) are toxic and accumulate early prior to
insoluble plaque formation and cognitive impairment in Alzheimer's disease (AD). Synthetic …

Alzheimer's disease (AD) constitutes the most prominent form of dementia among elderly
individuals worldwide. Disease modeling using murine transgenic mice was first initiated …

Abstract Background Recent research in Alzheimer's disease (AD) field has been focused
on the potential role of the amyloid-β protein that is derived from the transmembrane amyloid …

One of the major hallmarks of Alzheimer's disease (AD) is the extracellular deposition of
amyloid-β (Aβ) as senile plaques in specific brain regions. Clearly, an understanding of the …

Progress in understanding and treating Alzheimer's disease (AD) has been tremendously
bolstered by the era of transgenic models of AD. The identification of disease-causing …

Transgenic mice expressing in brain different mutant forms of the Amyloid Precursor Protein,
develop functional, cognitive and pathological defects which resemble or are reminiscent of …

The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's
disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue …

Transgenic mice expressing mutant human amyloid precursor protein (APP) develop an age-
dependent amyloid pathology and memory deficits, but no overt neuronal loss. Here, in mice …

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 …