SPOP loss of function protects against tauopathy.

The pathological accumulation of the microtubule binding protein tau drives age-related neurodegeneration in a variety of disorders, collectively called tauopathies. In the most common tauopathy, Alzheimer's disease (AD), the accumulation of pathological tau strongly correlates with cognitive decline. The underlying molecular mechanisms that drive neurodegeneration in tauopathies remain incompletely understood and no effective disease modifying pharmacological interventions currently exist.

Association of Two Opposing Responses Results in the Emergence of a Novel Conditioned Response.

Recent studies examining association of opposing responses, contrasting emotional valences, or counter motivational states have begun to elucidate how learning and memory processes can translate to clinical therapies for trauma or addiction. In the current study, association of opposing responses is tested in . Due to its relatively simple and well-described nervous system, it was hypothesized that association of two oppositional stimuli presented in a delayed conditioning protocol would strengthen the behavioral response to the first stimulus (alpha conditioning).

Loss of aly/ALYREF suppresses toxicity in both tau and TDP-43 models of neurodegeneration.

Neurodegenerative diseases with tau pathology, or tauopathies, include Alzheimer's disease and related dementia disorders. Previous work has shown that loss of the poly(A) RNA-binding protein gene sut-2/MSUT2 strongly suppressed tauopathy in Caenorhabditis elegans, human cell culture, and mouse models of tauopathy. However, the mechanism of suppression is still unclear.