Evidence map›Paper›PMID 42139290›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer's disease model.

Aanishaa Jhaldiyal, Manisha Kumari, Lauren C Guttman, Trupti Tripathi, Mohammed Repon Khan, Justin Wang, Devanik Biswas, Abhishek Pasupuleti, Akansha Aggarwal, Shraddha Pandya and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. 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
–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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer's disease model.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Aanishaa Jhaldiyal *Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-0620-7390
Manisha Kumari *Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-6956-6032
Lauren C GuttmanNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0001-5221-4236
Trupti TripathiNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0009-0001-6763-4222
Mohammed Repon KhanNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Justin WangNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0003-1973-3258
Devanik BiswasNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Abhishek PasupuletiNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Akansha AggarwalNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Shraddha PandyaNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0009-0009-0203-3950
Shih-Ching ChouNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Nikhil PanickerNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Abhay MonghekarDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Marilyn AlbertDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-8167-8985
Lynn M BekrisDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA 98104.
James B LeverenzLou Ruvo Center for Brain Health, Neurological Institute, Cleveland Clinic, Cleveland, OH 44195.ORCID 0000-0002-0896-0749
Tae-In KamNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-7241-4902
Ted M DawsonNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-6459-0893
Valina L DawsonNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.ORCID 0000-0002-2915-3970

Funding

Project 2 MeasurementU19AG033655 · NIA · JOHNS HOPKINS UNIVERSITY · PI Arnold Bakker · 2014 to 2026
$51.5M
Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI Corinne Pettigrew · 2020 to 2026
$29.3M
Gasdermin-D tags mitochondria to serve as mobile propagators of inflammatory responsesR35GM162199 · NIGMS · CLEVELAND CLINIC LERNER COM-CWRU · PI Nikhil Panicker · 2026 to 2026
$432k
Alzheimer's Association (AA) Zenith AwardEdward N. and Della L. Thome Memorial Foundation (Thome Memorial Foundation) n/aHHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS) NS067525HHS | NIH | National Institute on Aging (NIA) AG085688HHS | NIH | National Institute on Aging (NIA) U19AG033655NIA NIH HHS P30 AG066507NIA NIH HHS U19 AG033655NIGMS NIH HHS R35 GM162199
6 · The paper itself

Abstract

Poly(ADP-ribose) (PAR) polymerase 1 (PARP1) has been implicated in DNA damage responses and neuroinflammation in Alzheimer's disease (AD), yet its role in amyloid-beta (Aβ) pathology remains unclear. Here, we show that PARP1 activation drives Aβ pathology and neurodegeneration. Using a sensitive enzyme-linked immunosorbent assay, we observed significantly elevated PAR levels in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) and AD compared to controls. In vitro, oligomeric Aβ

Indexed as

Alzheimer DiseaseCognitive DysfunctionPoly (ADP-Ribose) Polymerase-1Amyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesDisease Models, AnimalDNA DamageFemaleHumansMaleMiceMice, KnockoutMice, TransgenicPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesPARP1 protein, humanParp1 protein, mousePeptide FragmentsPoly (ADP-Ribose) Polymerase-1Alzheimer’s diseaseamyloid beta (Aβ)neurodegenerationPARPpoly(ADP-ribose) (PAR)

Identifiers

PMID42139290
PMCPMC13187709

What OpenQuestion holds

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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.