Evidence map›Paper›PMID 36641677›Full record

ArticleJournal of Alzheimer's disease : JAD2023

In-Depth Proteomic Analysis of De Novo Proteome in a Mouse Model of Alzheimer's Disease.

Xin Wang, Xueyan Zhou, Jingyun Lee, Cristina M Furdui, Tao Ma

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Plasma proteomic analysis identifies proteins and pathways related to Alzheimer's risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. 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

5 authors.

Xin WangDepartment of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Xueyan ZhouDepartment of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Jingyun LeeDepartment of Internal Medicine-Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Cristina M FurduiDepartment of Internal Medicine-Section on Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Tao MaDepartment of Internal Medicine, Gerontology and Geriatric Medicine, Wake Forest School of Medicine, Winston-Salem, NC, USA.

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Wake Forest University School of Medicine Alzheimer's Disease Research CenterP30AG072947 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SUZANNE CRAFT · 2021 to 2026
$24.3M
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
Targeting protein synthesis dysregulation in Down syndrome-associated cognitive impairment with agingR01AG073823 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Tao Ma · 2021 to 2026
$2.3M
NCI NIH HHS P30 CA012197NIA NIH HHS P30 AG072947NIA NIH HHS R01 AG055581NIA NIH HHS R01 AG056622NIA NIH HHS R01 AG073823
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the most common dementia syndrome in the elderly characterized by synaptic failure and unique brain pathology. De novo protein synthesis is required for the maintenance of memory and synaptic plasticity. Mounting evidence links impaired neuronal protein synthesis capacity and overall protein synthesis deficits to AD pathogenesis. Meanwhile, identities of AD-associated dysregulation of "newly synthesized proteome" remain elusive.

objectiveTo investigate de novo proteome alterations in the hippocampus of aged Tg19959 AD model mice.

methodsIn this study, we combined the bioorthogonal noncanonical amino acid tagging (BONCAT) method with the unbiased large-scale proteomic analysis in acute living brain slices (we name it "BONSPEC") to investigate de novo proteome alterations in the hippocampus of Tg19959 AD model mice. We further applied multiple bioinformatics methods to analyze in-depth the proteomics data.

resultsIn total, 1,742 proteins were detected across the 10 samples with the BONSPEC method. After exclusion of those only detected in less than half of the samples in both groups, 1,362 proteins were kept for further analysis. 37 proteins were differentially expressed (based on statistical analysis) between the WT and Tg19959 groups. Among them, 19 proteins were significantly decreased while 18 proteins were significantly increased in the hippocampi of Tg19959 mice compared to WT mice. The results suggest that proteins involved in synaptic function were enriched in de novo proteome of AD mice.

conclusionOur study could provide insights into the future investigation into the molecular signaling mechanisms underlying AD and related dementias (ADRDs).

Indexed as

Alzheimer DiseaseAnimalsDisease Models, AnimalHippocampusMiceMice, TransgenicProteomeProteomicsProteomeAgingAlzheimer’s diseasemass spectrometryprotein synthesisproteomics

Identifiers

PMID36641677
PMCPMC10016629

What Socratic 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 Socratic graph.