ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2026
Genetic frontotemporal degeneration across the lifespan? A critical appraisal of the neurodevelopmental hypothesis.
Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Potential neurodevelopmental effects of genetic frontotemporal degeneration (FTD)-related variants have been postulated by observational studies over the past 25 years. Recent data from large FTD cohort studies have delineated biological and phenotypic characteristics of presymptomatic stages of disease, with some genetic variants showing effects even in young adults. However, human data on whether differences exist in youth are not yet available. This review critically appraises evidence from preclinical and human studies regarding the potential roles of FTD-associated genetic variants in neurodevelopment. We focus on the three major contributing pathogenic variant groups: chromosome 9 open reading frame 72 (C9orf72), progranulin (GRN), and microtubule-associated protein tau (MAPT). No causal evidence has been reported that supports the neurodevelopmental hypothesis in genetic FTD despite converging correlational findings. Theories are raised behind potential connections between neurodevelopmental and neurodegenerative processes in FTD. Understanding potential cellular and network responses to the presence of FTD genetic variants in early life may inform novel approaches to therapeutic development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.