Network abnormalities and interneuron dysfunction in Alzheimer disease
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The function of neural circuits and networks can be controlled, in part, by modulating the synchrony of their components' activities. Network hypersynchrony and altered oscillatory rhythmic activity may contribute to cognitive abnormalities in Alzheimer disease (AD). In this condition, network activities that support cognition are altered decades before clinical disease onset, and these alterations predict future pathology and brain atrophy. Although the precise causes and pathophysiological consequences of these network alterations remain to be defined, interneuron dysfunction and network abnormalities have emerged as potential mechanisms of cognitive dysfunction in AD and related disorders. Here, we explore the concept that modulating these mechanisms may help to improve brain function in these conditions.
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Synaptogenic mechanisms of AD cognitive decline-network activation and deactivation deficits, abnormal oscillatory rhythmic activity, and network hypersynchrony-account for AD-related synaptic failure.
“From a functional standpoint, synaptogenic mechanisms of AD cognitive decline–that is, network activation and deactivation deficits, abnormal oscillatory rhythmic activity, and network hypersynchrony–account for AD-related synaptic failure (120–122).”
From The β-Secretase BACE1 in Alzheimer’s Disease (2021) · cites this paper as [121]
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- Authors
- Palop, J. J., & Mucke, L.
- Affiliations
- Gladstone Institutes (US)
- Corresponding author
- Palop, Jorge J.
- Mucke, Lennart
- Venue
- Nature reviews. Neuroscience
- Published
- 2016-11-10
- Volume
- 17
- Issue
- 12
- Pages
- 777-792
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC8162106
- OpenAlex
- W2549366107
- Cited by
- 1,022
- References
- 261
- Citations by year
- 2026: 132 · 2025: 132 · 2024: 118 · 2023: 118 · 2022: 123 · 2021: 119 · 2020: 108 · 2019: 73 · 2018: 61 · 2017: 36
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Alzheimer's Association (IIRG-13-284779)
- Bristol-Myers Squibb
- National Institutes of Health (AG011385)
- National Institute on Aging (R37AG011385, R01AG047313, R01AG011385, RF1AG053981)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, cognitive impairment, neural circuits, therapeutic target, brain atrophy, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Animals, Brain, Cognition Disorders, Humans, Interneurons, Nerve Net, Neural Pathways
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