Evidence map›Paper›PMID 42561134›Full record

ArticleHuman molecular genetics2026

Clinical genome sequencing in neurodegenerative diseases-outcome in the first 500 patients.

Emma Ehn, Håkan Thonberg, Inger Nennesmo, Anna Lindstrand, Malin Kvarnung, Caroline Graff

Abstract read
In one paragraph

Article in Human molecular genetics, 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

6 authors.

Emma EhnDivision for Neurogeriatrics, Centre for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, H1 Neurobiology, Care Sciences and Society, H1 Neurogeriatrics, 171 77 Stockholm, Sweden.ORCID 0009-0001-6181-7562
Håkan ThonbergKarolinska University Hospital Solna, Department of Clinical Genetics and Genomics, Karolinska Universitetslaboratoriet, Gävlegatan 68, 171 76 Stockholm, Sweden.
Inger NennesmoDepartment of Oncology-Pathology, Karolinska Institutet, OnkPat, 171 77 Solna, Sweden.
Anna LindstrandKarolinska University Hospital Solna, Department of Clinical Genetics and Genomics, Karolinska Universitetslaboratoriet, Gävlegatan 68, 171 76 Stockholm, Sweden.
Malin KvarnungKarolinska University Hospital Solna, Department of Clinical Genetics and Genomics, Karolinska Universitetslaboratoriet, Gävlegatan 68, 171 76 Stockholm, Sweden.
Caroline GraffDivision for Neurogeriatrics, Centre for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, H1 Neurobiology, Care Sciences and Society, H1 Neurogeriatrics, 171 77 Stockholm, Sweden.ORCID 0000-0002-9949-2951

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases (NDDs) are clinically and genetically heterogeneous, requiring neuropathology or molecular testing for a definitive diagnosis. Clinical whole genome sequencing (WGS) enables comprehensive variant calling across flexible gene lists that can be tailored to the clinical presentation. By allowing simultaneous detection of single-nucleotide variants, copy-number variants, structural variants, and repeat expansions, WGS has the potential to improve diagnostic yield, facilitate genetic counseling and support clinical trial inclusion. This study assesses the diagnostic performance of WGS in individuals with NDD. WGS in 500 individuals representing a wide spectrum of NDDs identified a disease-causing variant in 61 cases, resulting in a diagnostic yield of 12%. These variants were found in 16 different genes, with C9orf72 being the most prevalent. Repeat expansions represented the largest variant class, accounting for 35 of 61 LP/P cases (57%); most of which were C9orf72 expansions (31/35). In the largest phenotype groups, frontotemporal dementia (FTD) had the highest diagnostic yield (19%) followed by amyotrophic lateral sclerosis (ALS, 13%), whereas an underlying monogenic cause was expectedly low in Alzheimer disease (AD, 4%). A positive family history was present in the majority (74%) of FTD, ALS, combined ALS-FTD and AD cases with an LP/P finding. Clinical WGS provides a clear diagnostic advantage in NDDs marked by substantial clinical and genetic overlap. WGS enables comprehensive variant detection and mapping of genotype-phenotype relationships across the disease continuum. In FTD and ALS, these results support universal access to genetic testing independent of age at onset or family history.

Indexed as

Neurodegenerative DiseasesWhole Genome SequencingAdultAgedAlzheimer DiseaseAmyotrophic Lateral SclerosisC9orf72 ProteinDNA Copy Number VariationsDNA Repeat ExpansionFemaleFrontotemporal DementiaGenetic Predisposition to DiseaseHumansMaleMiddle AgedPhenotypeC9orf72 ProteinC9orf72 protein, humanneurodegenerationNeurogeneticsrare variantswhole genome sequencing

Identifiers

PMID42561134
PMCPMC13648039

What OpenQuestion holds

Textmetadata
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.