Alzheimer’s Disease Brain Deficits Reversed in Mouse Model By Yale School of Medicine

Alzheimer’s Disease Brain Deficits Reversed in Mouse Model By Yale School of Medicine
STEP in Alzheimer'sResearchers at Yale School of Medicine have discovered a new drug compound with the capacity to reverse the brain deficits of Alzheimer's disease (AD) in an animal model. In this month’s issue of PLoS Biology, in an article entitled, "Inhibitor of the Tyrosine Phosphatase STEP Reverses Cognitive Deficits in a Mouse Model of Alzheimer's Disease," researchers revealed that TC-2153 inhibits the negative effects of STEP (Striatal-Enriched protein tyrosine Phosphatase), a neuron-specific phosphatase that regulates several other proteins, and a key player in the regulation of learning and memory. Different studies have reported an overactivation of STEP in several neuropsychiatric and neurodegenerative disorders, leading to disrupted synaptic strengthening, a process required to turn short-term memories into long-term memories. Thus, the enhanced levels of STEP in the brain are likely to contribute to the cognitive deficits observed in Alzheimer’s. The investigators engineered mice that develop AD and are deficient in STEP, observing that these animals can restore the levels of glutamate receptors on synaptosomal membranes and improve cognitive function, suggesting STEP as a novel therapeutic target for AD. A large-scale scan was then preformed to identify and characterize small-molecule STEP inhibitors, finding TC-2153 (benzopenta
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