Abstract
Alzheimer’s disease (AD) is a major cause of dementia in the elderly. Most patients are sporadic and develop the disease after 60 years of age. Senile plaques (SP), neurofibrillary tangles (NFT) and amyloid angiopathies are observed histopathologically and the deposition of β-amyloid protein is postulated to play a crucial role in the development of AD.1 Extensive genetic studies in this late-onset AD have failed to identify any consistent abnormalities in the gene encoding amyloid precursor protein (APP) so far, and the mechanism for deposition of β-amyloid is yet to be determined.
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Ueki, A. et al. (1995). Phenotypes and Genotypes of Apolipoprotein E in Japanese Patients with Late-Onset Sporadic Alzheimer’s Disease, Vascular Dementia, Down’s Syndrome or Parkinson’s Disease. In: Hanin, I., Yoshida, M., Fisher, A. (eds) Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 44. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9145-7_28
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