Evidence map›Paper›PMID 39968697›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

GABAergic modulation of beta power enhances motor adaptation in frontotemporal lobar degeneration.

Laura E Hughes, Natalie E Adams, Matthew A Rouse, Michelle Naessens, Alexander Shaw, Alexander G Murley, Thomas E Cope, Negin Holland, David Nesbitt, Duncan Street and 2 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. GABAergic modulation of beta power enhances motor adaptation in frontotemporal lobar degeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Article
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

12 authors.

Laura E HughesDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Natalie E AdamsDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Matthew A RouseMedical Research Council Cognition and Brain Sciences Unit, Cambridge, UK.
Michelle NaessensDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Alexander ShawPsychology Department, University of Exeter, Exeter, UK.
Alexander G MurleyDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Thomas E CopeDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Negin HollandDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
David NesbittMedical Research Council Cognition and Brain Sciences Unit, Cambridge, UK.
Duncan StreetDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
David J WhitesideDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.

Funding

Department of Health NIHR203312Holt Fellowship, Association of British Neurologists, and the Patrick Berthoud TrustMedical Research Council MC_UU_00030/14Medical Research Council MR/T033371/1NIHR Cambridge Biomedical Research Centre NIHR203312NIHR Cambridge Clinical Research FacilityWellcome TrustWellcome Trust 220258
6 · The paper itself

Abstract

introductionWe examined how abnormal prefrontal neurophysiology and changes in gamma-aminobutyric acid-ergic (GABAergic) neurotransmission contribute to behavioral impairments in disorders associated with frontotemporal lobar degeneration (FTLD).

methodsWe recorded magnetoencephalography during an adaptive visuomotor task from 11 people with behavioral-variant frontotemporal dementia, 11 with progressive supranuclear palsy, and 20 age-matched controls. We used tiagabine, a gamma-aminobutyric acid (GABA) re-uptake inhibitor, as a pharmacological probe to assess the role of GABA during motor-related beta power changes.

resultsTask impairments were associated with diminished movement-related beta power. Tiagabine facilitated partial recovery of behavioral impairments and neurophysiology, moderated by executive function, such that the greatest improvements were seen in those with higher cognitive scores. The right prefrontal cortex was revealed as a key site of drug interaction. DISCUSSION: Behavioral and neurophysiological deficits can be mitigated by enhancement of GABAergic neurotransmission. Clinical trials are warranted to test for enduring clinical benefits from this restorative-psychopharmacology strategy. HIGHLIGHTS: Event-related beta power changes during movement can be altered by the GABA reuptake inhibitor, tiagabine. In people with behavioral-variant frontotemporal dementia and progressive supranuclear palsy, tiagabine enhanced beta modulation and concurrently improved task performance, dependent on baseline cognition, and diagnosis. The effects of the drug suggest a GABA-dependent beta-related mechanism that underlies adaptive motor control. Restoring selective deficits in neurotransmission is a potential means to improve behavioral symptoms in patients with dementia.

Indexed as

Beta RhythmFrontotemporal Lobar Degenerationgamma-Aminobutyric AcidAgedExecutive FunctionFemaleHumansMagnetoencephalographyMaleMiddle AgedPrefrontal CortexSupranuclear Palsy, ProgressiveTiagabinegamma-Aminobutyric AcidTiagabinebeta powerFTLDGABAmagnetoencephalographymotor adaptationtiagabine

Identifiers

PMID39968697
PMCPMC7617437

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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.