Yeung, Jason HyKwakowsky, Andrea2025-01-122025-01-122023-10Neural Regeneration Research 18(10):p 2196-2197, October 20231673-5374https://hdl.handle.net/2292/71032Alzheimer’s disease (AD) is the leading neurodegenerative disorder globally. Despite this, there is minimal effective therapeutics proven to reduce or prevent the progression of this disease. Glutamate is the main excitatory neurotransmitter within the central nervous system and plays a crucial role in neuronal and synaptic functions. As such, the glutamatergic system is finely regulated within normal physiology, with multiple mechanisms to prevent excessive or insufficient glutamatergic receptor activation. This perspective article aims to highlight pertinent findings regarding metabotropic glutamate receptor (mGluR) expression and function in the AD brain, with a particular focus on the mGluR1α variant and its functional significance, concluding with a discussion regarding its potential as a therapeutic target in future AD studies.PrintItems in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher.https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm3214 Pharmacology and Pharmaceutical Sciences32 Biomedical and Clinical SciencesNeurodegenerativeAlzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD)AgingAlzheimer's DiseaseDementiaBrain DisordersNeurosciencesAcquired Cognitive Impairment2.1 Biological and endogenous factorsScience & TechnologyLife Sciences & BiomedicineCell BiologyNeurosciences & Neurology1109 Neurosciences3209 NeurosciencesMetabotropic glutamate receptor 1 alpha: a unique receptor variant with variable implications for Alzheimer's disease pathogenesisJournal article10.4103/1673-5374.369109Copyright: Neural Regeneration Research1876-7958NeuralRegenRes_2023_18_10_2196_369109Attribution-NonCommercial-ShareAlike 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-sa/4.0/