Article Synopsis
- Changes in gamma oscillations (20-50 Hz) are linked to various neurological disorders, but their connection to cellular issues is not well understood.
- In a mouse model of Alzheimer's, reduced gamma oscillations were observed before plaque formation and cognitive decline, and stimulating specific neurons at 40 Hz lowered amyloid-β levels.
- A non-invasive light-flickering treatment at 40 Hz effectively reduced amyloid levels in pre-plaque mice and plaque load in older mice, highlighting a new role for gamma rhythms in engaging brain responses to combat Alzheimer's-related pathology.
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Article Abstract
Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer's disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ) and Aβ isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ and Aβ levels in the visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate Alzheimer's-disease-associated pathology.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5656389 | PMC |
| http://dx.doi.org/10.1038/nature20587 | DOI Listing |
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