Alzheimer's Disease and Apoptosis.
- Author:
Young Hoon KIM
;
Young Kyung KIM
;
Sun Hee KIM
;
Sang Kyeng LEE
;
Sung Su KIM
;
Hye Sun KIM
;
Cheol Hyoung PARK
;
Sung Jin JEONG
;
Yoo Hun SUH
- Publication Type:Original Article
- Keywords:
Apoptosis;
Alzheimer's disease;
beta-Amyloid protein;
Amyloid precursor protein;
Presenilin 1;
Presenilin 2
- MeSH:
Alzheimer Disease*;
Amyloid beta-Peptides;
Animals;
Apoptosis*;
Brain;
Cell Death;
Chromatin;
DNA Damage;
DNA Fragmentation;
Membranes;
Mice;
Mice, Transgenic;
Neurons;
Oxidative Stress;
Presenilin-1;
Presenilin-2;
Risk Factors
- From:Journal of the Korean Society of Biological Psychiatry
1998;5(1):66-70
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Apoptosis is a form of cell death in which the cells shrink and exhibit nuclear chromatin condensation and DNA fragmentation, and yet maintain membrane integrity. Many lines of evidence have shown that brain neurons are vulnerable to degeneration by apoptosis. Also it has been suggested that apoptosis is one of the mechanism contributing neuronal loss in Alzheimer's disease(AD), since the conditions in the disease(A beta peptide, oxidative stress, low energy metabolism) are the inducers that activate apoptosis. Indeed some neurons in vulnerable regions of the AD brain show DNA damage, chromatin condensation, and apoptic bodies. Consistently, mutations in AD causative genes(Amyloid precursor protein, Presenilin-1 and Presenilin-2) increase A beta peptide1-42(Abeta1-42) and sensitize neuronal cell to apoposis. However, several lines of evidence have shown that the location of neuronal loss and A beta peptide deposition is not correlated in AD brain and transgenic mice brain over-expressing Abeta1-42. Taken together, these data may indicated that A beta peptide(and other causative factors of AD) can interact with other cellular insults or risk factors to exacerbate pathological mechansim of AD through apoptosis. Thus, this review discusses possible role and mechanism of apoptosis in AD.
