FOR IMMEDIATE RELEASE
Tuesday, May 4, 2004
CONTACT:
Floyd E. Bloom, M.D.
Founding Chief Executive Officer
(858) 677-0466
Neurome announces publication of research
findings on Alzheimer’s disease in the Proceedings of
the National Academy of Sciences
Findings conclude that substantial neuronal
pathology is evident well before amyloid accumulation occurs.
LA JOLLA, CA - Neurome, Inc. recently completed the third
phase of its analysis of Elan’s mouse model of Alzheimer’s
disease (AD), which is to be published today in the Proceedings
of the National Academy of Sciences of the United States of
America (PNAS), Vol. 101, No. 18 p.p.7141-7146 (2004). The
paper by Chi-Cheng Wu et al. is entitled “Selective
vulnerability of dentate granule cells prior to amyloid deposition
in PDAPP mice: Digital morphometric analyses” and is
also available in the online edition of PNAS at www.pnas.org.
Using a specific, high-throughput technique to visualize
neurons in their entirety and Neurome’s proprietary
microscopy software, individual neurons from the brains of
these mice expressing the gene associated with familial Alzheimer’s
disease were reconstructed and analyzed in 3-D. The analysis
revealed a specific form of cellular pathology of nerve cells
in the region of the hippocampus that earlier Neurome work
had shown to be affected before amyloid deposits could be
seen. The findings in this new paper suggest that the reduced
volume in the dentate gyrus region of the hippocampus is the
consequence of an extensive loss of dendrites – the
long, branching extensions from a nerve cell that receive
synaptic inputs – in this same region.
Normally, a healthy nerve cell has many dendrites. Neurome’s
quantitative analysis of the structural differences among
individual nerve cells in the brains of these mice provides
evidence for selective vulnerability of a specific sub-type
of nerve cells in the dentate gyrus prior to any amyloid deposition.
Furthermore, the location of these nerve cells correlates
perfectly with circuits known to be the most vulnerable to
degeneration in human Alzheimer’s disease, and provides
support for previous reports of consequent volume loss in
this same brain region of the transgenic mouse model of Alzheimer’s
disease. This finding further supports Neurome’s previous
findings suggesting that early intervention will be required
to halt the degenerative cascade that occurs in Alzheimer’s
disease. In addition, the identification of the vulnerable
cell class in this mouse model provides an ideal target for
measuring the success of experimental therapeutics.
The paper is co-authored by Faisal Chawla (Neurome), Dora
Games, Ph.D. (Elan Pharmaceuticals), Russell E. Rydel, Ph.D.
(Elan Pharmaceuticals), Stephen Freedman, Ph.D. (Elan Pharmaceuticals),
Dale Schenk, Ph.D. (Elan Pharmaceuticals), Warren G. Young,
Ph.D. (Neurome), John H. Morrison, Ph.D. (Neurome and Mount
Sinai School of Medicine) and Floyd E. Bloom, M.D. (Neurome
and The Scripps Research Institute).
“These new findings are doubly interesting to us,”
said Floyd E. Bloom, M.D., Founding CEO and Chairman of the
Board of Neurome and Chairman of the Department of Neuropharmacology
at The Scripps Research Institute. “Firstly, they validate
precisely our earlier reports that at 90 days of age, long
before amyloid deposits can be visualized, the dentate gyrus
of the transgenic mouse model of Familial Alzheimer’s
disease shows significant pathology in exactly the locations
where amyloid will deposit much later in the mouse’s
life.“
“Secondly,” continued Dr. Bloom, “the new
data will allow us to focus on these vulnerable cells and
further increase our analytical speed in future trials of
any therapeutic interventions we may be called upon to evaluate.”
Alzheimer’s disease is a progressive, neurodegenerative
disease of the brain characterized by memory loss, language
deterioration, impaired visuospatial skills, poor judgment,
indifferent attitude, but preserved motor function. Symptoms
of Alzheimer’s disease usually manifest after age sixty-five;
however, onset may occur as early as age forty, appearing
first as memory decline and, over several years, destroying
cognition, personality, and ability to function. There is
no known cure for Alzheimer’s disease, which affects
at least 20 million people worldwide.
About Neurome
Neurome, Inc. performs contract brain research for pharmaceutical
and biotechnology companies while at the same time pursuing
its own in-house and collaborative research protocols. Neurome
develops standardized, quantitative databases that accurately
depict and integrate gene expression patterns in the three-dimensional
context of the brain’s structures, circuits, and cells,
and deploys these databases in primary research directed toward
the discovery and development of gene targets for enhancement
of brain function and treatment of brain-based disease. The
data collected from these efforts will populate an evolving,
comprehensive database available by subscription and useful
on a broad level for analyses of mouse models of brain function
and disease. The application of the Neurome technologies provides
rigorous, quantitative data that are optimally suited to the
measurement of subtle cell-type specific shifts in gene expression,
as well as progression and prevention of degenerative events
affecting specific cell classes and brain regions. For more
information, please visit Neurome’s website at www.neurome.com.
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