Evidence map›Paper›PMID 34712240›Full record

ArticleFrontiers in immunology2021

Topological Dissection of Proteomic Changes Linked to the Limbic Stage of Alzheimer's Disease.

Erika Velásquez, Beáta Szeitz, Jeovanis Gil, Jimmy Rodriguez, Miklós Palkovits, Éva Renner, Tibor Hortobágyi, Péter Döme, Fábio Cs Nogueira, György Marko-Varga and 2 more

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

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Recent update on the heterogeneity of the Alzheimer's disease spectrum.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
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

12 authors at 6 institutions in 3 countries.

Erika VelásquezSection for Clinical Chemistry, Department of Translational Medicine, Lund University, Skåne University Hospital Malmö, Malmö, Sweden.
Beáta SzeitzDivision of Oncology, Department of Internal Medicine and Oncology, Semmelweis University, Budapest, Hungary.
Jeovanis GilSection for Clinical Chemistry, Department of Translational Medicine, Lund University, Skåne University Hospital Malmö, Malmö, Sweden.
Jimmy RodriguezDivision of Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Miklós PalkovitsHuman Brain Tissue Bank, Semmelweis University, Budapest, Hungary.
Éva RennerHuman Brain Tissue Bank, Semmelweis University, Budapest, Hungary.
Tibor HortobágyiInstitute of Pathology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
Péter DömeDepartment of Psychiatry and Psychotherapy, Semmelweis University, Budapest, Hungary.
Fábio Cs NogueiraProteomics Unit, Department of Biochemistry, Institute of Chemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
György Marko-VargaDivision of Clinical Protein Science & Imaging, Department of Biomedical Engineering, Lund University, Lund, Sweden.
Gilberto B DomontProteomics Unit, Department of Biochemistry, Institute of Chemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Melinda RezeliDivision of Clinical Protein Science & Imaging, Department of Biomedical Engineering, Lund University, Lund, Sweden.
Semmelweis University · HULund University · SEUniversidade Federal do Rio de Janeiro · BRKarolinska Institutet · SESkåne University Hospital · SEUniversity of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder and the most common cause of dementia worldwide. In AD, neurodegeneration spreads throughout different areas of the central nervous system (CNS) in a gradual and predictable pattern, causing progressive memory decline and cognitive impairment. Deposition of neurofibrillary tangles (NFTs) in specific CNS regions correlates with the severity of AD and constitutes the basis for disease classification into different Braak stages (I-VI). Early clinical symptoms are typically associated with stages III-IV (i.e., limbic stages) when the involvement of the hippocampus begins. Histopathological changes in AD have been linked to brain proteome alterations, including aberrant posttranslational modifications (PTMs) such as the hyperphosphorylation of Tau. Most proteomic studies to date have focused on AD progression across different stages of the disease, by targeting one specific brain area at a time. However, in AD vulnerable regions, stage-specific proteomic alterations, including changes in PTM status occur in parallel and remain poorly characterized. Here, we conducted proteomic, phosphoproteomic, and acetylomic analyses of human postmortem tissue samples from AD (Braak stage III-IV, n=11) and control brains (n=12), covering all anatomical areas affected during the limbic stage of the disease (total hippocampus, CA1, entorhinal and perirhinal cortices). Overall, ~6000 proteins, ~9000 unique phosphopeptides and 221 acetylated peptides were accurately quantified across all tissues. Our results reveal significant proteome changes in AD brains compared to controls. Among others, we have observed the dysregulation of pathways related to the adaptive and innate immune responses, including several altered antimicrobial peptides (AMPs). Notably, some of these changes were restricted to specific anatomical areas, while others altered according to disease progression across the regions studied. Our data highlights the molecular heterogeneity of AD and the relevance of neuroinflammation as a major player in AD pathology. Data are available

Indexed as

AcetylationAgedAged, 80 and overAlzheimer DiseaseAntimicrobial PeptidesBrainDisease ProgressionEncephalitisFemaleHumansMaleMiddle AgedPeptidesPhosphorylationProteomeProteomicsAntimicrobial PeptidesPeptidesProteomeacetylomicsAlzheimer’s diseaselimbic stageneuroinflammationphosphoproteomicsproteomics

Identifiers

PMID34712240
PMCPMC8546208
OpenAlexW3206608762

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.