Evidence map›Paper›PMID 36460716›Full record

ArticleCommunications biology2022

Reduced excitatory neuron activity and interneuron-type-specific deficits in a mouse model of Alzheimer's disease.

Moustafa Algamal, Alyssa N Russ, Morgan R Miller, Steven S Hou, Megi Maci, Leon P Munting, Qiuchen Zhao, Dmitry Gerashchenko, Brian J Bacskai, Ksenia V Kastanenka

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. How Do Amyloid Pathology and Aberrant Neuronal Activity Disrupt Plasticity and Memory in Alzheimer's Disease?The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026
    Review
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  6. Review
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  8. Excitation-inhibition homeostasis in Alzheimer's disease: a selective multiscale review of mechanisms, sex differences, and therapeutic opportunities.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Bidirectional Relationship Between Epilepsy and Alzheimer's Disease.Current neurology and neuroscience reports · 2025
    Review
  15. Article
  16. Article
  17. Article
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  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Moustafa AlgamalDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.ORCID 0000-0002-6215-0122
Alyssa N RussDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.ORCID 0000-0002-6353-139X
Morgan R MillerDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.ORCID 0000-0002-3740-8144
Steven S HouDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Megi MaciDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Leon P MuntingDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Qiuchen ZhaoDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Dmitry GerashchenkoHarvard Medical School/VA Boston Healthcare System, West Roxbury, MA, USA.
Brian J BacskaiDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA. BBACSKAI@mgh.harvard.edu.ORCID 0000-0002-2584-6702
Ksenia V KastanenkaDepartment of Neurology, MassGeneral Institute of Neurodegenerative Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA. KKASTANENKA@mgh.harvard.edu.ORCID 0000-0002-3727-0317
Harvard University · US

Funding

Slow-wave activity as a modifier of the progression of neurodegeneration in Alzheimer's diseaseRF1AG061774 · NIA · HARVARD MEDICAL SCHOOL · PI BACSKAI, BRIAN J, GERASHCHENKO, DMITRY · 2019 to 2021
$3.7M
Elucidating circuit disruptions in Alzheimer's diseaseR01AG066171 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI KASTANENKA, KSENIA V. · 2020 to 2024
$2.9M
Alzheimer's Association AARG-18-52336NIA NIH HHS R01 AG066171NIA NIH HHS RF1 AG061774NIA NIH HHS RF1AG061774
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by progressive memory loss and cognitive decline. These impairments correlate with early alterations in neuronal network activity in AD patients. Disruptions in the activity of individual neurons have been reported in mouse models of amyloidosis. However, the impact of amyloid pathology on the spontaneous activity of distinct neuronal types remains unexplored in vivo. Here we use in vivo calcium imaging with multiphoton microscopy to monitor and compare the activity of excitatory and two types of inhibitory interneurons in the cortices of APP/PS1 and control mice under isoflurane anesthesia. We also determine the relationship between amyloid accumulation and the deficits in spontaneous activity in APP/PS1 mice. We show that somatostatin-expressing (SOM) interneurons are hyperactive, while parvalbumin-expressing interneurons are hypoactive in APP/PS1 mice. Only SOM interneuron hyperactivity correlated with proximity to amyloid plaque. These inhibitory deficits were accompanied by decreased excitatory neuron activity in APP/PS1 mice. Our study identifies cell-specific neuronal firing deficits in APP/PS1 mice driven by amyloid pathology. These findings highlight the importance of addressing the complexity of neuron-specific deficits to ameliorate circuit dysfunction in Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloidosisAmyloidogenic ProteinsAnimalsDisease Models, AnimalInterneuronsMiceNeuronsPlaque, AmyloidAmyloidogenic Proteins

Identifiers

PMID36460716
PMCPMC9718858
OpenAlexW4310555362

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.