Evidence map›Paper›PMID 42745993›Full record

ReviewMolecular neurodegeneration advances2026

Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?

Silas A Buck, Sidharth S Madhavan, Laurie H Sanders

Abstract readReview
In one paragraph

Review in Molecular neurodegeneration advances, 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

3 authors.

Silas A BuckDepartments of Neurology and Pathology, Duke University School of Medicine, Durham, NC 27710 USA.
Sidharth S MadhavanDepartments of Neurology and Pathology, Duke University School of Medicine, Durham, NC 27710 USA.
Laurie H SandersDepartments of Neurology and Pathology, Duke University School of Medicine, Durham, NC 27710 USA.

Funding

BEHAVIOR AND PHYSIOLOGY IN AGINGT32AG000029 · NIA · DUKE UNIVERSITY · PI Maria Marquine · 1985 to 2026
$9.3M
Mechanisms of mitochondrial genome integrity in familial and idiopathic Parkinson's diseaseR01NS119528 · NINDS · DUKE UNIVERSITY · PI SANDERS, LAURIE H · 2020 to 2024
$2.9M
NIA NIH HHS T32 AG000029NINDS NIH HHS R01 NS119528
6 · The paper itself

Abstract

Many neurodegenerative diseases are characterized by pathological protein aggregation in the brain. Alzheimer's disease displays amyloid-β and tau inclusions in the form of amyloid-β plaques and tau neurofibrillary tangles. Synucleinopathies comprise Parkinson's disease and Dementia with Lewy bodies, which are classified by α-synuclein depositions in the form of Lewy bodies, as well as multiple system atrophy, which displays glial cytoplasmic α-synuclein inclusions. Tar DNA binding protein 43 (TDP-43) inclusions are observed in amyotrophic lateral sclerosis and frontotemporal lobar dementia with TDP-43 inclusions. A separate subgroup of frontotemporal lobar dementias, including Pick's disease, progressive supranuclear palsy and corticobasal degeneration, are characterized by disease-specific patterns of tau pathology and are termed primary tauopathies. Despite these classifications, it is not often appreciated that neurodegenerative diseases commonly display amyloid-β, tau, α-synuclein, and/or TDP-43 co-pathologies not typically associated with that specific disease's pathophysiology. Additionally, Graphical abstract:

Indexed as

Alzheimer’s diseaseAmyloidAmyotrophic lateral sclerosisCo-pathologyGranulovacuolar degeneration bodiesLewy body diseaseSynucleinTauTauopathyTDP-43

Identifiers

PMID42745993
PMCPMC13574929

What OpenQuestion holds

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Registered trials

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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.