A Newer Therapeutic Strategies For Alzheimer's Disease.
- Author:
Seol Heui HAN
1
Author Information
1. Department of Neurology, Chungbuk National University Hospital, Korea. shhan@med.chungbuk.ac.kr
- Publication Type:Review
- Keywords:
Alzheimer's disease;
Amyloid precursor protein;
Presenilin;
Apolipoprotein E;
A betavaccine;
Secretase inhibitor
- MeSH:
Alzheimer Disease*;
Amyloid beta-Peptides;
Amyloid Precursor Protein Secretases;
Brain;
Gliosis;
Immunization;
Neurofibrillary Tangles;
Neurons;
Plaque, Amyloid;
Presenilins
- From:Journal of the Korean Neurological Association
2001;19(6):559-565
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Alzheimer's disease (AD) is characterized pathologically by cholinergic deficits, extracelluar amyloid deposit, intra-neuronal neurofibrillary tangles, gliosis and neuronal and synaptic loss. The primary therapeutic approach has been cholinergic augumentation by chlolinesterase inhibitors, which at best modestly improve cognitive function. Several recent advances have provided new insights and possibilities in defining therapeutic targets for AD. Research on the underlying pathophysiological dysfunction finally disclose more disease specific processes. Of particular importance is the identification and characterization of the secretases involved in endoproteolytic processing of beta-amyloid precursor protein, the precursor of the amyloid beta-peptide (A beta). It is generally accepted that A beta has pivotal role in the pathogenesis of AD, and that reducing brain A beta levels may be a disease modifying strategy. By inhibiting one or both amyloidogenic secretase and immunization with A beta, neuropathological features of AD can be prevented or alleviated.
