Evidence map›Paper›PMID 42729803›Full record

ReviewFrontiers in genetics2026

Homeostatic conflict as a driver for brain aging.

Cristian A Wulkop-Gil, Michael Petrascheck

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Cristian A Wulkop-GilDepartment of Molecular and Cellular Biology, La Jolla, CA, United States.
Michael PetrascheckDepartment of Molecular and Cellular Biology, La Jolla, CA, United States.

Funding

Using geroscience to understand and treat Alzheimer's diseaseR01AG069206 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI MAHER, PAMELA ANNE · 2020 to 2024
$4.0M
Restoring neuronal degradative capacity as a therapeutic strategy to treat Prion DiseaseR01NS140965 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI SANDRA E Encalada, Michael Petrascheck · 2025 to 2026
$1.8M
A druggable mito-nuclear feedback mechanism that preserves mitochondrial and synaptic function in old-ageR01AG095974 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI Michael Petrascheck · 2025 to 2026
$1.7M
Contributions of cell type and exosome signaling to prodromal synaptic and circuit changes in Alzheimer's Disease modelsR01AG079517 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI Kristin Kay Baldwin, Michael Petrascheck · 2025 to 2026
$1.7M
Chemical modulation of proteostasis to promote longevity and healthy agingR37AG100304 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI Michael Petrascheck · 2026 to 2026
$645k
NIA NIH HHS R01 AG069206NIA NIH HHS R01 AG079517NIA NIH HHS R01 AG095974NIA NIH HHS R37 AG100304NINDS NIH HHS R01 NS140965
6 · The paper itself

Abstract

Mammalian tissue function depends on the balance between proliferative, mitotic cell populations and irreplaceable post-mitotic cells. Throughout life, aging progressively disrupts cell type balance and thus tissue function through opposing forces on different cell types. Aging promotes the aberrant proliferation or entry into pro-inflammatory senescent states of mitotic cells, while contributing to the functional erosion and, in vulnerable populations, loss of post-mitotic irreplaceable cells. The divergent age-associated vulnerabilities of mitotic and post-mitotic cells caused by aging generate a case of

Indexed as

agingcell type imbalancedementiaferroptosishomeostatic conflictneurodegenerationsenescencetherapeutic strategies

Identifiers

PMID42729803
PMCPMC13563124

What OpenQuestion holds

Textmetadata
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.