Gamma frequency entrainment attenuates amyloid load and modifies microglia
Open accessAbstract
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)1-40 and Aβ 1-42 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 1-40 and Aβ 1-42 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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By genetically engineering opsins into target neurons and controlling light, these neurons can be activated or inhibited, which is important for sensory and motor recovery and rehabilitation.
“By genetically engineering these proteins into target neurons and controlling the light around them, these neurons can be activated or inhibited, which is particularly important for sensory and motor recovery and rehabilitation.[555]”
From Flexible Electronics and Devices as Human–Machine Interfaces for Medical Robotics (2022) · cites this paper as [555]
The Methods (AAV vectors; Optogenetic stimulation protocol, page unavailable) describe expressing channelrhodopsin-2 in targeted mouse neurons and manipulating them with light. The paper supports light-driven activation, but does not establish light-driven inhibition or a role in sensory and motor recovery or rehabilitation; its Discussion instead concerns amyloid reduction in mouse models. (LLM, conf=0.87)
Experimental — accuracy not yet measuredOptogenetic stimulation is based on opsins that are light-sensitive and expressed only in certain cell types.
“Optogenetic stimulation is based on opsins that are sensitive to light signals and only expressed in certain types of cells.”
From Flexible Electronics and Devices as Human–Machine Interfaces for Medical Robotics (2022) · cites this paper as [555]
Gamma frequency modulation was beneficial in models with amyloid and/or tau pathology.
“Indeed, gamma frequency modulation was beneficial in models with amyloid and/or tau pathology54.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [54]
Gamma frequency modulation is beneficial in models with either amyloid and/or tau pathology.
“Indeed, gamma frequency modulation was found to be beneficial in models with either amyloid and/or tau pathology52”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [52]
These amyloid reductions accompany morphological changes, including enlarged soma and shortened processes filled with Aβ.
“Interestingly, entraining gamma oscillation at 40 Hz in 5xFAD mice induced amyloid reductions that were associated with an increase in microglial numbers and morphological changes such as soma enlargement and shortening of processes loaded with Aβ.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
These amyloid reductions accompany an increase in the number of microglia.
“Interestingly, entraining gamma oscillation at 40 Hz in 5xFAD mice induced amyloid reductions that were associated with an increase in microglial numbers and morphological changes such as soma enlargement and shortening of processes loaded with Aβ.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
Gamma oscillations are generated by local circuits of excitatory and fast-spiking inhibitory neurons that resonate at 20-50 Hz.
“Gamma oscillations arise from the activation of local circuits of excitatory and fast-spiking inhibitory neurons resonating at 20-50 Hz, and changes in gamma oscillation have been observed in neurological diseases (158).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
Altered gamma oscillations have been found in neurological disorders.
“Gamma oscillations arise from the activation of local circuits of excitatory and fast-spiking inhibitory neurons resonating at 20-50 Hz, and changes in gamma oscillation have been observed in neurological diseases (158).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
Driving gamma oscillations at 40 Hz in 5xFAD mice leads to reductions in amyloid.
“Interestingly, entraining gamma oscillation at 40 Hz in 5xFAD mice induced amyloid reductions that were associated with an increase in microglial numbers and morphological changes such as soma enlargement and shortening of processes loaded with Aβ.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
The expression of proinflammatory genes Il1b, Il6, and Cd11b and the antiinflammatory gene Igf1 remained unchanged.
“Notably, levels of proinflammatory genes (Il1b, Il6, Cd11b) and antiinflammatory genes (Igf1) were not changed (158), suggesting that it is possible to use immunomodulation to polarize microglia toward a beneficial activation state that is characterized by increased phagocytic activity without the induction of sustained inflammatory responses.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
Immunomodulation can shift microglia toward a beneficial activation state with increased phagocytic activity and without prolonged inflammatory responses.
“Notably, levels of proinflammatory genes (Il1b, Il6, Cd11b) and antiinflammatory genes (Igf1) were not changed (158), suggesting that it is possible to use immunomodulation to polarize microglia toward a beneficial activation state that is characterized by increased phagocytic activity without the induction of sustained inflammatory responses.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
RNA sequencing revealed higher expression of phagocytic genes, including Cd68, B2m, Icam, and Lyz2.
“RNA sequencing analysis showed an increase in phagocytic genes, such as Cd68, β 2 -microglobulin (B2m), Icam, and lysozyme 2 (Lyz2), and in the proliferation markers Csf1, Csf1r, and Csf2ra.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
RNA sequencing also showed higher expression of proliferation markers Csf1, Csf1r, and Csf2ra.
“RNA sequencing analysis showed an increase in phagocytic genes, such as Cd68, β 2 -microglobulin (B2m), Icam, and lysozyme 2 (Lyz2), and in the proliferation markers Csf1, Csf1r, and Csf2ra.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [158]
In mice, slow gamma frequency visual or audio input entrains neural firing to this frequency in the cortex and hippocampus and reduces Aβ pathology and microglial abnormalities.
“In mice, slow gamma frequency visual or audio input entrains neural firing to this frequency in the cortex and hippocampus and reduces Aβ pathology and microglial abnormalities [204, 205].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [204]
Transgenic mice with AD-like pathology have reduced gamma power, and in one model this reduction precedes cognitive impairment and amyloid plaque formation.
“Transgenic mice with AD-like pathology were found to have reduced gamma power that, in one model, precedes cognitive impairment and amyloid plaque formation [21,22].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [21]
Amyloid plaques were reduced when hippocampal PV-INs were made to produce gamma oscillations optogenetically.
“Interestingly, amyloid plaques were reduced when hippocampal PV-INs artificially produced gamma oscillations in optogenetics paradigms [21].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [21]
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- Authors
- Iaccarino, H. F., Singer, A. C., Martorell, A. J., Rudenko, A., Gao, F., Gillingham, T. Z., Mathys, H., Seo, J., Kritskiy, O., Abdurrob, F., Adaikkan, C., Canter, R. G., Rueda, R., Brown, E. N., Boyden, E. S., & Tsai, L.-H.
- Affiliations
- McGovern Institute for Brain Research (US)
- Massachusetts Institute of Technology (US)
- Massachusetts General Hospital (US)
- Broad Institute (US)
- Corresponding author
- Tsai, Li-Huei
- ORCID
- Venue
- Nature
- Published
- 2016-12-07
- Volume
- 540
- Issue
- 7632
- Pages
- 230-235
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC5656389
- OpenAlex
- W2560234750
- Cited by
- 1,328
- References
- 41
- Citations by year
- 2026: 169 · 2025: 191 · 2024: 172 · 2023: 160 · 2022: 147 · 2021: 150 · 2020: 131 · 2019: 85 · 2018: 76 · 2017: 42 · 2016: 2
- FWCI
- 54.95
- Type
- journal article
- Language
- en
- Update notices
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion)
- PMC
- Funders
- National Institute on Aging (RF1AG047661)
- National Eye Institute (R01EY023173)
- National Institute of General Medical Sciences (R01GM104948)
- National Institute of Neurological Disorders and Stroke (DP1NS087724)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- gamma oscillations, Alzheimer's disease, amyloid-beta, microglia, parvalbumin interneurons, optogenetics, amyloid plaques, 5xFAD mice, APP/PS1 mice, visual cortex, neurodegeneration
- MeSH terms
- Alzheimer Disease, Amyloid, Animals, Disease Models, Animal, Female, Interneurons, Light, Male, Parvalbumins, Peptide Fragments, Visual Cortex, Amyloid beta-Peptides, Microglia, Cell Shape, Mice, CA1 Region, Hippocampal, Plaque, Amyloid, Transcriptome, Optogenetics, Gamma Rhythm
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