Cited by 1,022Alzheimer's disease research and treatmentsNeural dynamics and brain functionNeuroscience and Neuropharmacology Research

Network abnormalities and interneuron dysfunction in Alzheimer disease

Open access
Palop, Jorge J., Mucke, Lennart·2016·Nature reviews. Neuroscience

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nrn.2016.141

Cites

261 of 261 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

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
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
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review