Pathogenic Mechanism of Alzheimer's Disease.
- Author:
Seol Heui HAN
1
Author Information
1. Department of Neurology, Konkuk University Hospital, 143-792, Seoul, Korea. alzdoc@kuh.ac.kr
- Publication Type:Review
- Keywords:
Alzheimer's disease;
Etiopathogenesis;
Amyloid cascade hypothesis;
Risk factors;
Thera peutic targets
- MeSH:
Alzheimer Disease*;
Blood Pressure;
Cerebral Cortex;
Diet;
Education;
Genetic Loci;
Hippocampus;
Interpersonal Relations;
Memory;
Molecular Biology;
Neocortex;
Neurodegenerative Diseases;
Neurofibrillary Tangles;
Neurons;
Penetrance;
Plaque, Amyloid;
Risk Factors
- From:Hanyang Medical Reviews
2006;26(1):4-13
- CountryRepublic of Korea
- Language:English
-
Abstract:
Alzheimer's disease (AD) is regarded as a prototype of the neurodegenerative disorder characterized by progressive memory impairment and multiple cognitive deficits in mid- to late- life. Its pathological hallmarks consist of neuritic plaques and neurofibrillary tangles in the cerebral cortex, accompanied by neuronal loss. These neuropathological findings are prominent in the temporal neocortex and hippocampus. There are a small proportion of AD cases (10%) that appear to be transmitted as pure autosomal dominant Mendelian traits with age-dependent, but, high penetrance. Molecular genetic studies on pedigrees with the latter type of familial Alzheimer's disease (FAD) with molecular genetic tools has led to the discovery of four different genetic loci associated with inherited susceptibility to AD. It is generally suggested that late-onset AD is caused by a complex set of genetic and environmental factors, such as diet, blood pressure, education, social interaction, and others. In this communication, some of the known risk factors relevant to etiopathogenesis of AD to date will be briefly reviewed.
