Evidence map›Paper›PMID 39741782›Full record

ReviewBrain communications2025

Can brain network connectivity facilitate the clinical development of disease-modifying anti-Alzheimer drugs?

Lorenzo Pini, Simone Lista, Alessandra Griffa, Gilles Allali, Bruno P Imbimbo

Abstract readReview
In one paragraph

Review in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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  12. Sleep on it!Brain communications · 2025
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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

5 authors.

Lorenzo PiniDepartment of Neuroscience, Università degli Studi di Padova, 35121 Padova, Italy.
Simone Listai+HeALTH Strategic Research Group, Department of Health Sciences, Miguel de Cervantes European University (UEMC), Valladolid 47012, Spain.ORCID https://orcid.org/0000-0001-6804-7858
Alessandra GriffaDepartment of Clinical Neurosciences, Leenaards Memory Center, Lausanne University Hospital and University of Lausanne, Montpaisible 16, 1011 Lausanne, Switzerland.ORCID https://orcid.org/0000-0003-1923-1653
Gilles AllaliDepartment of Clinical Neurosciences, Leenaards Memory Center, Lausanne University Hospital and University of Lausanne, Montpaisible 16, 1011 Lausanne, Switzerland.ORCID https://orcid.org/0000-0002-4455-6719
Bruno P ImbimboDepartment of Research and Development, Chiesi Farmaceutici, 43122 Parma, Italy.ORCID https://orcid.org/0000-0002-0327-7262

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The preclinical phase of Alzheimer's disease represents a crucial time window for therapeutic intervention but requires the identification of clinically relevant biomarkers that are sensitive to the effects of disease-modifying drugs. Amyloid peptide and tau proteins, the main histological hallmarks of Alzheimer's disease, have been widely used as biomarkers of anti-amyloid and anti-tau drugs. However, these biomarkers do not fully capture the multiple biological pathways of the brain. Indeed, robust amyloid-target engagement by anti-amyloid monoclonal antibodies has recently translated into modest cognitive and clinical benefits in Alzheimer's disease patients, albeit with potentially life-threatening side effects. Moreover, targeting the tau pathway has yet to result in any positive clinical outcomes. Findings from computational neuroscience have demonstrated that brain regions do not work in isolation but are interconnected within complex network structures. Brain connectivity studies suggest that misfolded proteins can spread through these connections, leading to the hypothesis that Alzheimer's disease is a pathology of network disconnectivity. Based on these assumptions, here we discuss how incorporating brain connectivity outcomes could better capture global brain functionality and, in conjunction with traditional Alzheimer's disease biomarkers, could facilitate the clinical development of new disease-modifying anti-Alzheimer's disease drugs.

Indexed as

anti-amyloidanti-taudisease-modifying drugsfunctional MRIneurodegeneration

Identifiers

PMID39741782
PMCPMC11686405

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.