Lab Home | Phone | Search
Center for Nonlinear Studies  Center for Nonlinear Studies
 Home 
 People 
 Current 
 Affiliates 
 Alumni 
 Visitors 
 Students 
 Research 
 ICAM-LANL 
 Quantum 
 Publications 
 Publications 
 2007 
 2006 
 2005 
 2004 
 2003 
 2002 
 2001 
 2000 
 <1999 
 Conferences 
 Workshops 
 Sponsorship 
 Talks 
 Colloquia 
 Colloquia Archive 
 Seminars 
 Postdoc Seminars Archive 
 Quantum Lunch 
 CMS Colloquia 
 Q-Mat Seminars 
 Q-Mat Seminars Archive 
 Archive 
 Kac Lectures 
 Dist. Quant. Lecture 
 Ulam Scholar 
 Colloquia 
 
 Jobs 
 Students 
 Summer Research 
 Student Application 
 Visitors 
 Description 
 Past Visitors 
 Services 
 General 
 PD Travel Request 
 
 History of CNLS 
 
 Maps, Directions 
 CNLS Office 
 T-Division 
 LANL 
 
Monday, March 24, 2014
3:00 PM - 4:00 PM
CNLS Conference Room (TA-3, Bldg 1690)

Colloquium

A Black Hole of Memory: Cytoskeletal Collapse in Late Stages of Alzheimer’s Disease?

Daniel Cox
University of California, Davis

In the late stages of Alzheimer’s disease, the tau proteins that serve to nucleate, stabilize, and crosslink microtubules in the axons of nerve cells are degraded. The customary view is that the removal of taus can allow for the catastrophic dynamical instability of microtubules in which depolymerization of tubulin monomers overwhelms polymerization and the microtubules vanish. We offer an alternative perspective, that removal of taus essentially corresponds to a problem of rigidity percolation with the added feature of a depletion force induced by the taus themselves. We show with a combination of 2D projected simulations and analytic arguments that there is an irreversible first order collapse when too many taus are removed, driven by the attractive depletion force, loosely analogous to gravitational collapse. The values of tau density and entropic spring constants are such to make this likely dominate over the dynamic instability for a wide range of tau occupancies. If correct, these arguments point to kinase phosphorylation as the main mechanism of tau degradation. We discuss possible experimental tests of this on cultured neurons and whether “white matter” volume loss observed by functional MRI in afflicted patients can be attributed to this phenomenon. Clearly this collapse represents a “Point of No Return” signpost in disease progression and therapeutic intervention.

*Work supported by US NSF Grants DMR-1207624 and DMR-0844115 in collaboration with A. Sendek, H.R. Fuller, N.E. Hall, and R.R.P. Singh.

Host: Lena Lopatina