Therapeutic Modulation of HSF1-Dependent Gene Expression to Alleviate Motor Neuron Dysfunction in ALS

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating disease resulting from loss of motor neurons, leading to paralysis and eventually death. There are no effective therapies for ALS. The major disease hallmark found in the vast majority (>90%) of all ALS patients is called TDP-43, a protein that accumulates in the brain and spinal cord and is implicated in the death of neurons. Unfortunately, targeting or removing TDP-43 with drugs is not a logical step forward, as reducing overall TDP-43 levels can be quite toxic to cells, posing unique challenges in devising new therapies for the majority of sporadic ALS patients. Our recent work suggests that activation of HSF-1, a critical protein that controls the cells ability to refold toxic aggregates in the cell, is capable of preventing TDP-43 from accumulating and therefore may restore normal cellular function to diseased neurons that are affected by ALS. Therefore, we will test whether HSF-1 activator drugs represent a new avenue to explore for therapies that could prolong the survival of ALS patients. The implications of our study are very straightforward; preclinical testing of new drugs that slow disease progression by preventing TDP-43 accumulation could lead to new and effective ALS drugs. We made significant progress toward this goal already by showing that a particular drug, called HSF1A, which turns on HSF-1, is able to prevent TDP-43 from aggregating in cells grown in a dish. Now, our goal is to move this idea forward and test the extent that HSF1A produces a therapeutic response in animal models of ALS. Our study could dramatically accelerate the development of new drugs that act to disaggregate and therefore reduce toxic forms of TDP-43; these drugs could have a major impact on the field, as they represent potential therapies for the vast majority of patients currently afflicted by ALS.

Document Details

Document Type
DoD Grant Award
Publication Date
Nov 19, 2019
Source ID
W81XWH1910466

Entities

People

  • Todd J Cohen

Organizations

  • United States Army
  • University of North Carolina at Chapel Hill

Tags

Fields of Study

  • Biology
  • Medicine

Readers

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  • Molecular and Cellular Biology
  • Oncology