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S3–01–02: Detecting change in Alzheimer's disease brains
Author(s) -
Fox Nick
Publication year - 2006
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.2006.05.161
Subject(s) - atrophy , entorhinal cortex , medicine , temporal lobe , pathology , alzheimer's disease , hippocampus , neuroscience , disease , psychology , epilepsy , psychiatry
not available. S3-01-05 MONITORING DRUG STUDIES IN DEMENTIA WITH IMAGING Jeremie Pariente, INSERM, Unknown, France. Contact e-mail: Jeremie.Pariente@toulouse.inserm.fr Abstract not available.not available. S3-01-06 TRACERS FOR MONITORING CEREBRAL AMYLOID Bengt Langstrom, Uppsala University, Uppsala, Sweden. Contact e-mail: bengt.langstrom@pet.uu.se Abstract not available.not available. TUESDAY, JULY 18, 2006 SYMPOSIA S3-02 DISEASE MECHANISMS (APOE) S3-02-01 A -PEPTIDES A 40 AND A 42 ARE PHYSIOLOGICAL REGULATORS OF CHOLESTEROL AND SPHINGOLIPID HOMEOSTASIS Tobias Hartmann, University of Heidelberg, Heidelberg, Germany. Contact e-mail: tobias.hartmann@zmbh.uni-heidelberg.de During the past decade multiple links between Alzheimer’s disease (AD), cholesterol and other lipids have been noticed. Two independent regulatory cycles that control cholesterol and sphingomyelin lipid homeostasis. Surprisingly, these feed-back cycles utilize as central enzymatic events APP processing and A release. The molecular pathways involved reveal a physiological function for A 40 which down regulates cholesterol de novo synthesis, and A 42 which activates sphingomyelin degrading enzymes (SMases). This biological function of APP processing ultimately results in keeping the molar ratio between the typical raft lipids cholesterol and sphingomyelin constant during steady state conditions. At the same time the molecular independency of these cycles sets a necessary condition to allow adjustments at a subcellular level, e.g. during neuronal differentiation or synaptic plasticity. Similar changes are observed in case of FAD-presenilin mutations. These mutations induce a shift in the ratio of S46 Symposia S3-02: Disease Mechanisms (APOE)