Evidence map›Paper›PMID 41827903›Full record

ReviewCells2026

Role of Alpha-Synuclein in Frontotemporal Dementia: Narrative Review.

Anastasia Bougea

Abstract readReview
In one paragraph

Review in Cells, 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

1 author.

Anastasia Bougea1st Department of Neurology, Medical School, National and Kapodistrian University of Athens, 11528 Athens, Greece.ORCID 0000-0003-3006-8711

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFrontotemporal dementia (FTD) is traditionally classified based on the accumulation of either tau or TDP-43 proteins; however, the presence of alpha-synuclein (α-Syn) in these patients is increasingly recognized as a critical factor driving disease progression.

methodsA comprehensive narrative review of recent clinical, neuropathological, and biochemical studies was conducted, focusing on cases of FTLD-synuclein and the occurrence of alpha-syn as a co-pathology in more common FTD variants.

resultsCurrent evidence indicates that α-syn often co-aggregates with tau and TDP-43 via "cross-seeding" mechanisms, significantly accelerating neuronal loss and contributing to clinical heterogeneity. Although FTLD-synuclein is a rare, distinct subtype that mimics atypical multiple system atrophy, secondary α-syn pathology is common and strongly correlates with rapid cognitive decline. Furthermore, existing diagnostic biomarkers typically fail to detect this pathological overlap, which may explain the limited efficacy in protein-specific clinical trials.

conclusionsα-Syn is a major, yet under-recognized, catalyst of neurodegeneration within the FTD spectrum. The findings emphasize the need for future therapeutic and diagnostic strategies to adopt multi-target approaches, addressing the synergistic toxicity of multiple protein aggregates rather than isolating single protein in isolation.

Indexed as

alpha-SynucleinFrontotemporal DementiaAnimalsDNA-Binding ProteinsHumanstau Proteinsalpha-SynucleinDNA-Binding Proteinstau Proteinsalpha-synucleinbiomarkersco-pathologycross-seedingfrontotemporal dementiaFTLD-synucleinneurodegenerationproteinopathytauTDP-43

Identifiers

PMID41827903
PMCPMC12984503

What Socratic 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 Socratic graph.