J Korean Soc Biol Psychiatry.  1998 Jun;5(1):66-70.

Alzheimer's Disease and Apoptosis

• Kim YH
• Kim YK
• Kim SH
• Lee SK
• Kim SS
• Kim HS
• Park CH
• Jeong SJ
• Suh YH

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.

MeSH Terms

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
Amyloid beta-Peptides
Chromatin
Presenilin-1
Presenilin-2