Among the proteins implicated in age?related neurodegeneration, TDP?43 has taken on growing importance: its misfolding and mislocalization are now linked to frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and are estimated to be present in more than half of Alzheimer’s cases. Faster cognitive decline, greater brain atrophy, and worsening memory loss are all associated with TDP-43.
Now, researchers at the University of California, San Diego (UCSD), are testing a gene?therapy strategy designed not to remove TDP?43, but to help neurons withstand its toxicity. In a study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, the team reports that systemic delivery of a gene called SynCav1 to brain cells protected cognition and preserved neuronal structure in a mouse model of TDP?43 proteinopathy. The study is titled, “Systemic delivery of synapsin-promoted caveolin-1 overexpression ameliorates pathological TDP-43–induced cognitive decline and neurodegenerative changes.”
The…
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