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P2–007: Apoptosis induced by overexpression of APP requires its localization to mitochondria
Author(s) -
Wilkins Heather,
Marquardt Kristin,
Linseman Daniel
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2013.05.649
Subject(s) - mitochondrion , apoptosis , microbiology and biotechnology , neurotoxicity , programmed cell death , amyloid precursor protein , amyloid beta , oxidative stress , intracellular , chemistry , biology , amyloid (mycology) , alzheimer's disease , biochemistry , pathology , peptide , medicine , inorganic chemistry , disease , organic chemistry , toxicity
Levels of Tn were higher in later stages of the disease in cortex but not hippocampus, indicating that levels may be highest prior to end-stage neuronal loss. Conclusions: The reason for increased Tn expression in AD has not yet been clarified, but we suggest that it may indicate an abnormality in the biosynthesis of Core 1 O-glycans, which initiates neuronal dysfunction and consequently the formation of plaques and tangles and neuronal death. Alterations in galactosyl transferase activity is being investigated.