Peptide Tools to Study Alzheimer's Disease
About Alzheimer's Disease
Alzheimer's Disease is a neurodegenerative disease that typically begins after the age of 65 years and progresses until death. However, early-onset Alzheimer’s affects younger people, around 5% of people with Alzheimer’s are under 65.
Although the mechanisms are poorly understood, several hypotheses on the cause of Alzheimer's Disease exist. One of them is that an abnormally hyperphosphorylated tau protein initiates the disease. Another hypothesis states that the main pathogenic factor in Alzheimer's disease are amyloid plaques forming in the brain. Amyloid plaques are composed of regularly ordered amyloid fibers, a peptide fold also associated with protein misfolding diseases such as prion diseases.
Amyloid Beta Peptide
- Beta Amyloid A4 peptide (synonyms are Aβ, Abeta, Amyloid Beta)
- Several functions in healthy organisms, e.g. activation of kinases and cholesterol transport regulation
- Main component of amyloid plaques
- Arise from proteolytic processing of amyloid precursor protein (APP) involving sequential cleavages by ß- and γ-secretases
- Represent a mixture of peptides of different lengths (up to 43 amino acids)
- Pathological increase of ß/γ-secretase activities and diminished clearance rate initiate accumulation and aggregation of amyloid-ß peptides in the brain tissue of Alzheimer patients
- The two isoforms Aß(1-42) and Aß(1-43) tend to aggregate
- Resulting amyloid-ß peptide oligomers, fibrils and plaques disturb the neuronal network and show strong neurotoxic effects
- The exact biochemical pathways underlying the pathologic effects of amyloid-ß peptides are not quite understood
JPT's Peptide Tools to Study Alzheimer: