ArticlemicroPublication biology2025
Expression of polyglutamine repeats at the pathogenic threshold modestly enhances tau neurotoxicity and protein accumulation in
Article in microPublication biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CAG repeat expansions within the HTT gene cause Huntington's disease (HD), a devastating neurodegenerative disease characterized by progressive movement, cognitive, and behavioral symptoms. These expansions result in the expression and accumulation of neurotoxic poly-glutamine (polyQ). Disease initiation depends on the length of the expansion, with fewer than 35 repeats of polyQ typically not pathogenic, while 40 or greater repeats almost always result in HD. Longer expansions correlate with earlier onset of disease; however, there may be other factors that contribute to disease initiation or progression, particularly in individuals with repeat lengths close to or below the 40 repeat length pathogenic threshold. Aggregates of the protein tau are a frequent co-pathology in HD and may modify disease presentation. To examine relationships between tau and polyQ
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