Stereo Investigator Aids in Researching Familial Alzheimer’s Disease

Alzheimer’s disease is the most common form of dementia. Most cases occur in people over 65, and are not genetically inherited. Roughly five percent of Alzheimer’s patients suffer from familial Alzheimer’s disease (FAD), an uncommon form that tends to strike sooner, and is related to a genetic predisposition – most commonly, a mutation in the presenilin 1 gene (PS1).

A recent study, led by Dr. Miguel A. Gama Sosa of the Mount Sinai School of Medicine in New York, shows that the mutated PS1 gene contributes to the vascular pathology of familial Alzheimer’s disease.

During the course of their research, Dr. Gama Sosa’s team used Stereo Investigator for the stereologic analyses of transgenic mouse brains.

“We quantified the density, area and length of the vasculature in the hippocampus of mice that express a mutation associated with familial Alzheimer’s disease,” explained coauthor Dr. Gregory A. Elder of the James J. Peters Veterans Affairs Medical Center in the Bronx.

“We found [Stereo Investigator] easy to use and adaptable to the requirements of the study,” he added.

Read “Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer’s Disease Mutations” at the American Journal of Pathology.

{Image: Anti collagen IV-peroxidase staining of the hippocampal vasculature of a 26 month-old transgenic mouse expressing a human presenilin 1 (PSEN1) transgene harboring the M146V mutation associated with familial Alzheimer’s disease (FAD). Present are vascular abnormalities including string, tortuous and double-barreled vessels.  In addition many vessels are irregular with decreased diameters. – Courtesy of Miguel Gama-Sosa Ph.D.}

Miguel A. Gama Sosa, Rita De Gasperi, Anne B. Rocher, Athena Ching-Jung Wang,  William G.M. Janssen, Tony Flores, Gissel M. Perez, James Schmeidler, Dara L. Dickstein, Patrick R. Hof, and Gregory A. Elder (2010), “Age-Related Vascular Pathology in Transgenic Mice Expressing Presenilin 1-Associated Familial Alzheimer’s Disease Mutations.” American Journal of Pathology, 176:353-368

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