Chunk #19 — Introduction — Rationale for the present study: Mechanisms of Alzheimer’s disease identified as upstream regulators of alcohol-sensitive protein networks in C57BL/6J mice
are increasing in a compensatory fashion in response to both the detrimental consequences of alcohol and of increasing levels of AB in the brain. Likewise, total levels of CRMP2 may be blunted in the alcohol-drinking mice because more of the protein may be phosphorylated and starting to aggregate with Tau and AB proteins. Both heat shock and CRMP proteins appear to react quickly to stress and chronic alcohol drinking and given their link to AD pathology, they may be useful early biomarkers for AD-like pathology associated with alcohol use or abuse.
