Mechanisms of Cortical Excitability Changes in Frontotemporal Degeneration Onset

Abstract

Head injuries, including combat-related trauma like TBI, increase lifetime risk of acquired dementias, including Frontotemporal Degeneration (FTD). A major pathological mechanism of dementias like FTD is misfolding and aggregation of Tau isoforms. But there is not yet an effective treatment targeting Tau aggregation that addresses clinical symptoms or slows disease progression. Early pathological changes include hyperexcitability and increased seizure incidence, which precede substantial Tau aggregation and FTD diagnosis. There is a significant knowledge gap about how changes in circuits lead to hyperexcitability. Understanding the pathogenesis in the cortical circuit might help identify potential therapeutic targets to treat or slow the progression of FTD. We hypothesize that pre-tangle mutant Tau induces circuit changes, resulting in weakened inhibition or increased neuronal excitability in specific circuit components. Our specific aims test this hypothesis. To model FTD, we will express a mutant Tau isoform (P301L) in a mouse model to dissect cell-type specific circuitry. This approach allows use of transgenic lines to fluorescently label and manipulate targeted neuron populations, allowing the study of mutant Tau effects in specific connections. Use of viral vectors also allows the study of direct effects on neuronal circuits in defined cortical areas, eliminating the need to control for compensatory mechanisms as intransgenic mutant Tau mice and enabling control of the onset time of mutant Tau expression. Stereotaxic injections of viral vectors expressing mutant Tau will be made in the primary motor cortex (M1), a brain region whose general circuit connectivity is understood. We will measure changes in inhibitory connection strength as well as intrinsic excitability by targeted whole-cell recordings in mouse brain slice.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2022
Accession Number
AD1172663

Entities

People

  • Bryan M Hooks
  • Roman Goz

Organizations

  • University of Pittsburgh

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Cells
  • Chemical Synthesis
  • Combat Injuries
  • Data Analysis
  • Diseases And Disorders
  • Experimental Design
  • Head Injuries
  • Health Services
  • Inhibition
  • Maryland
  • Medical Personnel
  • Neurons
  • Patent Applications
  • Professional Development
  • Therapy
  • Universities

Fields of Study

  • Biology

Readers

  • Molecular Genetics
  • Neuroscience
  • Trauma Surgery or Emergency Medicine.