Accumulation of Alzheimer β-amyloid via Ganglioside Clusters
Alzheimer’s disease (AD) is the most common form of dementia. The pathological hallmarks of AD brains are extracellular senile plaques and intracellular neurofibrillary tangles. It is widely accepted that the amyloid β-peptide (Aβ), which exists in fibrillar forms as a major component of senile plaques, is central to the development of AD. Aβ is a peptide composed of 40–42 amino acids (Fig. 1) and generated from proteolytic cleavage of amyloid precursor protein by β- and γ-secretases. Aβ is present at a very low concentration (<10∞ M) in biological fluids, and its physiological role is unknown. According to the so-called Aβ hypothesis, the conversion of soluble, nontoxic Aβ to aggregated toxic Aβ rich in β-sheet structures ignites the neurotoxic cascade(s) of Aβ. However, it is not clear how soluble Aβ forms aggregates.
KeywordsLipid Raft Small Unilamellar Vesicle Nordihydroguaiaretic Acid Alzheimer Amyloid Extracellular Senile Plaque
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