Evidence map›Paper›PMID 35784845›Full record

ReviewFrontiers in neuroscience2022

Brain Cell Type-Specific Nuclear Proteomics Is Imperative to Resolve Neurodegenerative Disease Mechanisms.

Ruth S Nelson, Eric B Dammer, Juliet V Santiago, Nicholas T Seyfried, Srikant Rangaraju

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Cell-specific protein expression in Alzheimer's disease prefrontal cortex.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Article
  4. Neurotrophic Effects ofInternational journal of molecular sciences · 2024
    Article
  5. In vivo validation of late-onset Alzheimer's disease genetic risk factors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  6. Article
  7. bioRxiv : the preprint server for biology · 2023
    Article
  8. Somatic mosaicism in the diseased brain.Molecular cytogenetics · 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

5 authors at 1 institution in 1 country.

Ruth S NelsonDepartment of Neurology, Emory University, Atlanta, GA, United States.
Eric B DammerDepartment of Biochemistry, Emory University, Atlanta, GA, United States.
Juliet V SantiagoDepartment of Neurology, Emory University, Atlanta, GA, United States.
Nicholas T SeyfriedDepartment of Biochemistry, Emory University, Atlanta, GA, United States.
Srikant RangarajuDepartment of Neurology, Emory University, Atlanta, GA, United States.
Emory University · US

Funding

Neuron and microglia-specific proteomic signatures of ERK mediated mechanisms of Alzheimer’s diseaseR01AG075820 · NIA · YALE UNIVERSITY · PI RANGARAJU, SRIKANT, SEYFRIED, NICHOLAS THOMAS · 2021 to 2025
$5.1M
Targeting Kv1.3 potassium channels for neuro-immunomodulation in Alzheimer's DiseaseR01NS114130 · NINDS · YALE UNIVERSITY · PI RANGARAJU, SRIKANT · 2020 to 2024
$3.1M
NIA NIH HHS R01 AG075820NINDS NIH HHS R01 NS114130
6 · The paper itself

Abstract

Neurodegenerative diseases (NDs) involve complex cellular mechanisms that are incompletely understood. Emerging findings have revealed that disruption of nuclear processes play key roles in ND pathogenesis. The nucleus is a nexus for gene regulation and cellular processes that together, may underlie pathomechanisms of NDs. Furthermore, many genetic risk factors for NDs encode proteins that are either present in the nucleus or are involved in nuclear processes (for example, RNA binding proteins, epigenetic regulators, or nuclear-cytoplasmic transport proteins). While recent advances in nuclear transcriptomics have been significant, studies of the nuclear proteome in brain have been relatively limited. We propose that a comprehensive analysis of nuclear proteomic alterations of various brain cell types in NDs may provide novel biological and therapeutic insights. This may be feasible because emerging technical advances allow isolation and investigation of intact nuclei from post-mortem frozen human brain tissue with cell type-specific and single-cell resolution. Accordingly, nuclei of various brain cell types harbor unique protein markers which can be used to isolate cell-type specific nuclei followed by down-stream proteomics by mass spectrometry. Here we review the literature providing a rationale for investigating proteomic changes occurring in nuclei in NDs and then highlight the potential for brain cell type-specific nuclear proteomics to enhance our understanding of distinct cellular mechanisms that drive ND pathogenesis.

Indexed as

Alzheimer's diseaseflow cytometryneurodegenerationnucleusproteomics

Identifiers

PMID35784845
PMCPMC9243337
OpenAlexW4282975769

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.