Evidence map›Paper›PMID 41419490›Full record

Articlenpj aging2025

Age-related nigral downregulation of the Parkinson's risk factor FAM49B primes human microglia for inflammaging.

Jacqueline Martin, Guan-Ju Lai, Christopher Y Park, Colista West, Trevor Van Brunt, Samarah Ahmed, Saheed Lawal, Maya Dickson, Taylor Russo, Wendy Akmentin and 6 more

Abstract read
In one paragraph

Article in npj aging, 2025. 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

16 authors.

Jacqueline Martin *Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Guan-Ju Lai *Department of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Christopher Y Park *Flatiron Institute, Simons Foundation, New York, NY, USA.
Colista WestDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Trevor Van BruntDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Samarah AhmedDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Saheed LawalDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Maya DicksonDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Taylor RussoDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Wendy AkmentinDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Molly WeinerPerelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
Zachary B HobelDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Benjamin KolisnykLaboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY, USA.
Joshua L PlotkinDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA.
Olga G TroyanskayaFlatiron Institute, Simons Foundation, New York, NY, USA.
Markus RiesslandDepartment of Neurobiology and Behavior, Stony Brook University, Stony Brook, NY, USA. markus.riessland@stonybrook.edu.

Funding

Molecular Assessment of Cause and Consequence of Cellular Senescence in Diverse Midbrain Cell Types in Parkinson's DiseaseR01NS124735 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI Markus Riessland · 2022 to 2026
$2.0M
NINDS NIH HHS 1R01NS124735NINDS NIH HHS R01 NS124735
6 · The paper itself

Abstract

Parkinson's Disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), which is associated with changes in microglia function. While age remains the biggest risk factor, the underlying molecular cause of PD onset and its concurrent neuroinflammation are not well understood. Many identified PD risk genes have been directly linked to dopamine neuron impairment, while others are linked to immune cell function. In this study, we found that the PD risk gene FAM49B is critically expressed in microglia of the human SNpc and is downregulated with age and PD. We utilized human and murine microglia cells to demonstrate the role of FAM49B in regulating fundamental microglial functions such as cytoskeletal maintenance, migration, surface adherence, energy homeostasis, autophagy, and, importantly, inflammatory response. Downregulation of microglial FAM49B, as observed in the SNpc of aging individuals, led to significant alterations in these cellular functions, which are associated with increased microglial activation. Thus, our study highlights novel cell-type-specific roles of FAM49B and provides a potential mechanism for susceptibility to neuroinflammation, and reactive gliosis observed in both PD and normal aging.

Identifiers

PMID41419490
PMCPMC12764901

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.