Information

Name

Binder, Lester (Skip), PhD

Title

Abbott Labs/Burnham Professor of Genetic and Molecular Medicine

Email

l-binder@northwestern.edu

Office Phone

312-503-0823

Office Fax

312-503-7912

Department

Cellular and Molecular Biology

Office

Tarry 8-733 Chicago

Areas of Research

Cell Biology, Neurobiology of Disease

NU Scholar Profile

http://www.scholars.northwestern.edu/expert.asp?u_id=180

Recent Publications on PubMed

http://www.ncbi.nlm.nih.gov/pubmed?term=Binder%2C%20Lester%5BFull%20Author%20Name%5D&cmd=DetailsSearch

Current Research

Current Research

We study the role of microtubule-associated proteins (MAPs) in the normal and diseased nervous system. Most of our work has focused on tau, a protein thought to stabilize axonal microtubules, but that is also present in other cellular and subcellular compartments in the central nervous system. The functions of this extra-microtubule tau is not known although its association with ribosomes in neurons and astrocytes and with the rRNA gene clusters in nuclei and on chromosomes of dividing cells suggests some role in protein synthesis. We have also documented tau’s presence in oligodendrocytes, perhaps associated with membrane vesicles, suggesting yet another function for this fascinating molecule.

Interest in tau is great in the medical community because we and others have shown that it is the major protein species in the paired helical filaments (PHFs). These filaments comprise the fibrillar pathologies found in the brains of patients with Alzheimer’s Disease. Furthermore, many forms of human Frontal Lobe Dementias, that are characterized by tau filamentous inclusions, are caused by autosomal dominant mutations in tau. Using cellular, molecular and immunological techniques, my lab studies the mechanism of tau filament formation in vitro and in vivo and seeks to determine the functional consequences of tau polymerization to the neurodegenerative cascade.

The characteristic neurofibrillar pathologies of AD contain tau truncated at Asp421. The CA1 hippocampal region from a patient with AD was analyzed by immunohistochemistry by using TauC3 (A) and Tau5 (B) mAbs. NFT and dystrophic neurites forming neuritic plaques (NP), two hallmark pathologic features of AD, are indicated. (Bars = 50 ┬Ám.)