Evidence map›Paper›PMID 35723096›Full record

ArticleJournal of Alzheimer's disease : JAD2022

Characterization of Early Alzheimer's Disease-Like Pathological Alterations in Non-Human Primates with Aging: A Pilot Study.

Hannah M Jester, Saahj P Gosrani, Huiping Ding, Xueyan Zhou, Mei-Chuan Ko, Tao Ma

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. A Perspective: Challenges in Dementia Research.Medicina (Kaunas, Lithuania) · 2022
    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

6 authors at 1 institution in 1 country.

Hannah M JesterDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Saahj P GosraniDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Huiping DingDepartment of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Xueyan ZhouDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Mei-Chuan KoDepartment of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Tao MaDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Wake Forest University · US

Funding

Isoform-specific roles of AMPK in synaptic failure and memory deficit in Alzheimer's DiseaseR01AG055581 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.9M
Role of protein synthesis in Alzheimers disease-associated impairments of synaptic plasticity and memoryR01AG056622 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.4M
NIA NIH HHS R01 AG055581NIA NIH HHS R01 AG056622
6 · The paper itself

Abstract

backgroundSporadic or late onset Alzheimer's disease (LOAD) is a multifactorial neurodegenerative disease with aging the most known risk factor. Non-human primates (NHPs) may serve as an excellent model to study LOAD because of their close similarity to humans in many aspects including neuroanatomy and neurodevelopment. Recent studies reveal AD-like pathology in old NHPs.

objectiveIn this pilot study, we took advantage of brain samples from 6 Cynomolgus macaques that were divided into two groups: middle aged (average age 14.81 years) and older (average age 19.33 years). We investigated whether AD-like brain pathologies are present in the NHPs.

methodsWe used immunohistochemical method to examine brain Aβ pathology and neuron density. We applied biochemical assays to measure tau phosphorylation and multiple signaling pathways indicated in AD. We performed electron microscopy experiments to study alterations of postsynaptic density and mitochondrial morphology in the brain of NHPs.

resultsWe found multiple AD-like pathological alteration in the prefrontal cortex (but not in the hippocampus) of the older NHPs including tau hyperphosphorylation, increased activity of AMP-activated protein kinase (AMPK), decreased expression of protein phosphatase 2A (PP2A), impairments in mitochondrial morphology, and postsynaptic densities formation.

conclusionThese findings may provide insights into the factors contributing to the development of LOAD, particularly during the early stage transitioning from middle to old age. Future endeavors are warranted to elucidate mechanisms underlying the regional (and perhaps cellular) vulnerability with aging and the functional correlation of such pathological changes in NHPs.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAgingAnimalsBrainDisease Models, AnimalHumansMiddle AgedPilot ProjectsPrimatestau Proteinstau ProteinsAgingAlzheimer’s diseaseAMPKmitochondrianon-human primatesynapses

Identifiers

PMID35723096
PMCPMC9378582
OpenAlexW4282825502

What OpenQuestion holds

Textmetadata
LicenceTDM
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.