Sidney Strickland

Sidney Strickland Rockefeller University
Vice President for Educational Affairs
Homepage
PhD , University of Michigan (1972)

Compare

vs.

Go

Research Summary

The brain is critically dependent on sufficient blood flow. Dr. Strickland’s laboratory investigates how dysfunction of the circulatory system contributes to neurological diseases, such as Alzheimer’s disease, in humans and mice.

Neurological disorders of the central nervous system represent profound medical problems worldwide. For example, Alzheimer’s disease affects millions of people and has severe physical, psychological, and financial consequences. By studying patients and mouse models with neurological diseases, Dr. Strickland is working to elucidate the molecular mechanisms by which neural function is disrupted.

In investigating neurovascular dysfunction, the Strickland lab studies the mechanisms underlying the pathogenesis of Alzheimer’s disease. Cerebrovascular defects contribute to the progression of Alzheimer’s pathology, and members of the lab are using transgenic mouse models of Alzheimer’s to evaluate blood-brain barrier damage and the roles that blood clot formation and degradation play in this disease. Their research has determined that the amyloid-β peptide, which is considered to be a causative factor in Alzheimer’s, interacts with fibrinogen to promote irregular fibrin accumulation in the brain and increase brain inflammation. This peptide also hinders blood clot degradation, which could compromise blood flow, exacerbate inflammation, and lead to neuronal death. These results suggest that fibrin and the mechanisms involved in its accumulation and clearance may present novel therapeutic targets for slowing the progression of Alzheimer’s disease.

The Strickland lab has also recently found that amyloid-β can activate coagulation Factor XII (FXII) in the plasma of both Alzheimer’s disease patients and mouse models. The activation of FXII initiates fibrin clotting as well as inflammatory processes, both of which are recognized pathologies in Alzheimer’s disease. Promotion of FXII activation by amyloid-β could help explain the association between Alzheimer’s disease and vascular diseases. This knowledge may ultimately identify new pathogenic mechanisms that could disrupt neuronal function, aiding in the discovery of novel diagnostic and therapeutic approaches.

Dr. Strickland is a faculty member in the David Rockefeller Graduate Program and the Tri-Institutional M.D.-Ph.D. Program.

Similar Researchers

Columbia University
New York, NY
Profile
Percentiles
Citations
11st
Papers
6th
Funding
39th
Channels, Receptors, Tools & Methods, Ion Channels, Molecular Biophysics
Columbia University
New York, NY
Profile
Percentiles
Citations
7th
Papers
16th
Funding
42nd
Synapses & Circuits, Neuroscience, Transcriptional Regulation, Signal Transduction, Developmental Biology...
New York University
New York, NY
Profile
Percentiles
Citations
8th
Papers
6th
Funding
48th
Nucleic Acids, Transcriptional Regulation, Aging & Dementia, Genomics & Genetics, Cancer
New York University
New York, NY
Profile
Percentiles
Citations
24th
Papers
21st
Funding
50th
Neuroscience, Signal Transduction, Developmental Biology, Cell Specification & Differentiation
New York University
New York, NY
Profile
Percentiles
Citations
2nd
Papers
6th
Funding
44th
Cancer, Mouse Biology, Renal Biology

Percentiles

Citations*
15th
Papers*
10th
Funding
65th
Efficiency
15th

Today's Citations vs.
Paper Publication Year*

-

Funding by Source
2012-2015

-
*Cited papers in our current database **Coming soon