Evidence map›Paper›PMID 35501886›Full record

ArticleTranslational neurodegeneration2022

Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer's disease.

Christopher Daniel Morrone, Aaron Yenhsin Lai, Jossana Bishay, Mary Elizabeth Hill, JoAnne McLaurin

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Stable neuronal representations underlie cognitive resilience to Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  9. High-caloric intake rescues early symptomatic AD-induced hippocampal neurovascular coupling deficits.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  11. Beyond binary classification: Comparing three region-based multi-phase Aβ staging systems.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

5 authors at 1 institution in 1 country.

Christopher Daniel MorroneBiological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada. morrone.cdm@gmail.com.ORCID 0000-0002-5887-2691
Aaron Yenhsin LaiBiological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada.ORCID 0000-0001-5188-0034
Jossana BishayBiological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada.
Mary Elizabeth HillBiological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada.
JoAnne McLaurinBiological Sciences, Sunnybrook Research Institute, Toronto, ON, M4N 3M5, Canada.ORCID 0000-0002-7428-9105
Sunnybrook Health Science Centre · CA

Funding

CSVD and AD: the drivers of late life dementiaR01AG057665 · NIA · SUNNYBROOK RESEARCH INSTITUTE · PI MCLAURIN, JOANNE, STEFANOVIC, BOJANA · 2018 to 2022
$1.6M
NIA NIH HHS R01 AG057665NIH HHS R01 AG057665-02
6 · The paper itself

Abstract

backgroundPatient-to-patient variability in the degree to which β-amyloid, tau and neurodegeneration impact cognitive decline in Alzheimer's disease (AD) complicates disease modeling and treatment. However, the underlying mechanisms leading to cognitive resilience are not resolved. We hypothesize that the variability in cognitive function and loss relates to neuronal resilience of the hippocampal GABAergic network.

methodsWe compared TgF344-AD and non-transgenic littermate rats at 9, 12, and 15 months of age. Neurons, β-amyloid plaques and tau inclusions were quantified in hippocampus and entorhinal cortex. Somatostatin (SST) and parvalbumin (PVB) interneurons were traced to examine hippocampal neuroplasticity and cognition was tested in the Barnes maze.

resultsThe 9-month-old TgF344-AD rats exhibited loss of neurons in the entorhinal cortex and hippocampus. Hippocampal neuronal compensation was observed in 12-month TgF344-AD rats, with upregulation of GABAergic interneuronal marker. By 15 months, the TgF344-AD rats had robust loss of excitatory and inhibitory neurons. β-Amyloid and tau pathology accumulated continuously across age. SST interneurons exhibited tau inclusions and atrophy from 9 months, whereas PVB interneurons were resilient until 15 months. The hippocampal PVB circuit underwent neuroplastic reorganization with increased dendritic length and complexity in 9- and 12-month-old TgF344-AD rats, before atrophy at 15 months. Strikingly, 12-month-old TgF344-AD rats were resilient in executive function and cognitive flexibility. Cognitive resilience in TgF344-AD rats occurred as maintenance of function between 9 and 12 months of age despite progressive spatial memory deficits, and was sustained by PVB neuroplasticity.

conclusionsOur results demonstrate the inherent neuronal processes leading to cognitive maintenance, and describe a novel finding of endogenous cognitive resilience in an AD model.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAtrophyCognitionDisease Models, AnimalHumansNeuronal PlasticityParvalbuminsPlaque, AmyloidRatsRats, Inbred F344Rats, TransgenicSomatostatinAmyloid beta-PeptidesParvalbuminsSomatostatinAlzheimer’s diseaseBarnes mazeCognitive resilienceGABAergic interneuronHippocampusNeuronal compensationParvalbuminSomatostatinTgF344-AD rat

Identifiers

PMID35501886
PMCPMC9063209
OpenAlexW4225323985

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.