[Abstract Title]. - Society for Neuroscience

here, the anterior piriform, posterior piriform and entorhinal cortices, revealing four major
properties beyond their spontaneous occurrence: broadband frequency (often up to 80-100 Hz); a
brief (~250 ms) duration; near synchrony across even widely separated brain regions (often
appearing within 5-6 ms of one another); and either bursty (two or more occurring on the same
LFP channel less than 250 ms apart) or singular occurrences.
We will present the findings of SFB activity across the extended olfactory circuit in two studies
using a different species: mice. The first study demonstrated the occurrence of SFBs in normal
adult mice as well as in juveniles, with properties extremely similar to those seen in rats. The
second study, in progress at the time of abstract submission, is comparing young htau
Alzheimer‟s model mice and normal controls. We hypothesize that the SFB metric will suggest
early reductions in long-range coherence, prior to prevalent tau pathology in the neocortex and
hippocampus, and well before neurofibrillary tangles are present.
Disclosures: J. Robson, None; N. Esiobu, None; R. Hermer-Vazquez, None; A. Brown,
None; L.L. Hermer-Vazquez, None.
Poster
245. Tau and Alzheimer's disease
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 245.10/O4
Topic: C.01.h. Tau
Support: The Alzheimer's Association
Title: Does retromer deficiency observed in Alzheimer‟s disease affect Tau phosphorylation?
Authors: A. S. BENDER, E. PLANEL, K. DUFF, *S. A. SMALL;
Taub Instt Res. & Alzh Dis & Aging Brain, Columbia Univ, Col. Physicians & Sur, New York,
NY
Abstract: Gene-expression and genetic studies have implicated the retromer sorting pathway in
late-onset Alzheimer‟s disease. Previous studies in animal models have shown that retromer
deficiency observed in Alzheimer‟s disease can cause hippocampal dysfunction, Abeta
accumulation, and neurodegeneration. Nevertheless, whether retromer deficiency causes tau
hyperphosphorylation, a key histological feature of the disease, remains unknown.
We have begun addressing this question by using monoclonal antibody PHF1 to examine brain
extracts of genetically-modified retromer-deficient mice, heterozygote knockouts for VPS26. In
our first analysis we found no abnormalities in tau phosphorylation in whole brain extracts of
retromer-deficient mice. Guided by recent studies suggesting that the retromer is differentially