The cookie settings on this website are set to 'allow all cookies' to give you the very best experience. Please click Accept Cookies to continue to use the site.
Alzheimer’s Disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein components of these plaques are beta amyloid peptide (Aβ), 40, 42 or 43 amino acid residues peptide cleaved from amyloid precursor protein by β-secretase and γ-secretase. Increased release of Aβ42 or Aβ43, which have a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations ApoE alleles or may involve other undiscovered factors. Many researchers theorize that increased release of Aβ42/Aβ43 leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals.
Alzheimer’s Disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein components of these plaques are beta amyloid peptide (Aβ), 40, 42 or 43 amino acid residues peptide cleaved from amyloid precursor protein by β-secretase and γ-secretase. Increased release of Aβ42 or Aβ43, which have a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations ApoE alleles or may involve other undiscovered factors. Many researchers theorize that increased release of Aβ42/Aβ43 leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals.
