Hippocampal hyperglutamatergic signaling matters: Early targeting glutamate neurotransmission as a preventive strategy in Alzheimer's disease: An Editorial Highlight for "Riluzole attenuates glutamatergic tone and cognitive decline in AβPP/PS1 mice" on page 513

This Editorial highlights a remarkable study in the current issue of the Journal of Neurochemistry in which Hascup and coworkers provide novel data showing that riluzole, an anti-glutamatergic drug, may be a promising early intervention strategy for Alzheimer's disease (AD), aimed at restoring...

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Bibliographic Details
Published in:Journal of neurochemistry 2021-02, Vol.156 (4), p.399-402
Main Author: Gulyaeva, Natalia V
Format: Article
Language:English
Subjects:
Accumulation
Age
Alzheimer Disease - drug therapy
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Amyloid beta-Protein Precursor - genetics
Amyloid beta-Protein Precursor - metabolism
Animals
Cognitive ability
Cognitive Dysfunction
Glutamatergic transmission
Glutamic Acid
Hippocampus
Hippocampus - metabolism
Humans
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurodegenerative diseases
Neurotransmission
Presenilin 1
Riluzole - pharmacology
Riluzole - therapeutic use
Strategy
Synaptic Transmission
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Summary:This Editorial highlights a remarkable study in the current issue of the Journal of Neurochemistry in which Hascup and coworkers provide novel data showing that riluzole, an anti-glutamatergic drug, may be a promising early intervention strategy for Alzheimer's disease (AD), aimed at restoring glutamate neurotransmission prior to amyloid beta (Aβ) plaque accumulation and cognitive decline. The mice APP/PS1, a model of AD, initially are cognitively normal but have elevated glutamate release in the hippocampus at 2-4 months of age. They begin showing cognitive decline and Aβ plaque accumulation at approximately 6-8 months of age, and show obvious AD neuropathology and cognitive impairment at 10-12 months. The riluzole treatment over 4 months (at 2-6 months of age) targeting early changes in glutamatergic neurotransmission prevents cognitive decline observed at 12 months of age and restores glutamatergic neurotransmission. This is one of the most convincing preclinical evidence supporting the idea of targeting glutamate neurotransmission in patients at risk for AD and to use riluzole for this purpose.
ISSN:0022-3042
1471-4159
DOI:10.1111/jnc.15238