Evidence map›Paper›PMID 41293526›Full record

ArticleArXiv2025

Advancing Risk Gene Discovery Across the Allele Frequency Spectrum.

Madison Caballero, Behrang Mahjani

Abstract readPreprint
In one paragraph

Article in ArXiv, 2025. 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

5 · Who and what money

Authors and funding

2 authors.

Madison CaballeroSeaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Behrang MahjaniSeaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Funding

Moderate effect size genes in autism spectrum disorderR01MH139952 · NIMH · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MAHJANI, BEHRANG · 2025 to 2025
$845k
NIMH NIH HHS R01 MH139952
6 · The paper itself

Abstract

The discovery of genetic risk factors has transformed human genetics, yet the pace of new gene identification has slowed despite the exponential expansion of sequencing and biobank resources. Current approaches are optimized for the extremes of the allele frequency spectrum: rare, high-penetrance variants identified through burden testing, and common, low-effect variants mapped by genome-wide association studies. Between these extremes lies variants of intermediate frequency and effect size where statistical power is limited, pathogenicity is often misclassified, and gene discovery lags behind empirical evidence of heritable contribution. This "missing middle" represents a critical blind spot across disease areas, from neurodevelopmental and psychiatric disorders to cancer and aging. In this review, we organize strategies for risk gene identification by variant frequency class, highlighting methodological strengths and constraints at each scale. We draw on lessons across fields to illustrate how innovations in variant annotation, joint modeling, phenotype refinement, and network-based inference can extend discovery into the intermediate range. By framing the frequency spectrum as a unifying axis, we provide a conceptual map of current capabilities, their limitations, and emerging directions toward more comprehensive risk gene discovery.

Indexed as

complex disordersGenetic architecturerisk gene discovery

Identifiers

PMID41293526
PMCPMC12642764

What OpenQuestion 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 OpenQuestion graph.