Journal
ACTA NEUROPATHOLOGICA
Volume 119, Issue 5, Pages 523-541Publisher
SPRINGER
DOI: 10.1007/s00401-010-0679-9
Keywords
Amyloid; Synapse; Tau; Head injury; Endosome; Dementia pugilistica
Categories
Funding
- National Institutes of Health [AG028174, AG027140]
- Alzheimer's Association
- Zenith award
- NATIONAL INSTITUTE ON AGING [K02AG028174, R01AG027140] Funding Source: NIH RePORTER
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The aberrant accumulation of aggregated beta-amyloid peptides (A beta) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of A beta has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby A beta is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracellular A beta have been viewed as the most important pathogenic form of A beta in AD. More recently, the intraneuronal accumulation of A beta has been described in the brain, although technical considerations and its relevance in AD have made this a controversial topic. Here, we review the emerging evidence linking intraneuronal A beta accumulation to the development of synaptic pathology and plaques in AD, and discuss the implications of intraneuronal beta-amyloid for AD pathology, biology, diagnosis and therapy.
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