Evidence map›Paper›PMID 41788546›Full record

ReviewFrontiers in neuroscience2026

Metabolic changes in mTOR pathway-associated cortical malformation.

Aditi Biswas, Philip H Iffland

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 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

2 authors.

Aditi BiswasDepartment of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, United States.
Philip H IfflandDepartment of Neurology, University of Maryland School of Medicine, Baltimore, MD, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malformations of cortical development (MCD) are a common cause of epilepsy, autism spectrum disorder (ASD), and intellectual disability (ID). A unifying mechanistic etiology for epilepsy, ASD, and ID has not been found due, in part, to the heterogeneity of MCD subtypes. However, changes in brain metabolism within MCD have emerged as a possible convergent mechanism across MCD that may have therapeutic potential. While there have been efforts to comprehensively describe known metabolic changes in other neurodevelopmental disorders, no such effort exists for MCD associated with mTOR pathway gene mutations (the most common cause of MCD; mTORopathies'). In this review, we detail finding related to mTORopathies that relate to dysfunctional brain metabolism including abnormal changes in macromolecule processing and mitochondrial metabolism. Further, we discuss cellular and molecular metabolic processes that may serve as key pathways in the development of MCD

Indexed as

brain developmentdevelopmental delayepilepsyintellectual disabilitymetabolismneurodevelopmental disordersseizures

Identifiers

PMID41788546
PMCPMC12957139

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.