AI Article Synopsis
- * Targeting an enzyme called glutamate carboxypeptidase II (GCPII) to boost NAAG levels is considered a potential treatment approach for Alzheimer's disease.
- * Research findings reveal discrepancies between brain NAAG levels in humans and commonly used mouse models of Alzheimer's, questioning the reliability of these models for predicting human outcomes.
Article Abstract
Studies over the past two decades report significant reductions in brain N-acetylaspartyl glutamate (NAAG) levels in neurodegenerative diseases with associated cognitive impairment, including Alzheimer's disease (AD). Because NAAG is cleaved by glutamate carboxypeptidase II (GCPII), restoration of brain NAAG levels via GCPII inhibition is a potential therapeutic strategy for AD. Herein, studies were conducted to identify an appropriate murine model of AD that recapitulates human brain NAAG changes in order to preclinically evaluate the therapeutic benefit of GCPII inhibition. Our opposing findings of brain NAAG changes in human and mouse AD highlights the limited predictive value of AD mouse models.
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| http://dx.doi.org/10.3233/JAD-181251 | DOI Listing |
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