ArticleJournal of neurology2018
Amyotrophic lateral sclerosis: the complex path to precision medicine.
Article in Journal of neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
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.
Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Divergence of cortical neurophysiology across different neurodegenerative disorders compared to healthy ageing.Progress in neurobiology · 2026Article
- Inverting the logic in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2025Article
- Asymmetry in amyotrophic lateral sclerosis: Clinical, neuroimaging and histological observations.Brain : a journal of neurology · 2025Review
- Extracellular vesicles in TDP-43 proteinopathies: pathogenesis and biomarker potential.Molecular neurodegeneration · 2025Review
- Drug repurposing in amyotrophic lateral sclerosis (ALS).Expert opinion on drug discovery · 2025Review
- Update on recent advances in amyotrophic lateral sclerosis.Journal of neurology · 2024Review
- The cortical neurophysiological signature of amyotrophic lateral sclerosis.Brain communications · 2024Article
- C9orf72-ALS human iPSC microglia are pro-inflammatory and toxic to co-cultured motor neurons via MMP9.Nature communications · 2023Article
- Advantages of routine next-generation sequencing over standard genetic testing in the amyotrophic lateral sclerosis clinic.European journal of neurology · 2023Article
- Granulocyte-colony stimulating factor (G-CSF): an emerging therapeutic approach for amyotrophic lateral sclerosis (ALS).Acta neurologica Belgica · 2023Review
- Primary care blood tests show lipid profile changes in pre-symptomatic amyotrophic lateral sclerosis.Brain communications · 2023Article
- Review
- "Walking a tightrope": A grounded theory approach to informal caregiving for amyotrophic lateral sclerosis.Health & social care in the community · 2022Article
- Modeling seeding and neuroanatomic spread of pathology in amyotrophic lateral sclerosis.NeuroImage · 2022Article
- Muscle cells of sporadic amyotrophic lateral sclerosis patients secrete neurotoxic vesicles.Journal of cachexia, sarcopenia and muscle · 2022Article
- Genetic testing in motor neurone disease.Practical neurology · 2022Review
- A novel variant inCold Spring Harbor molecular case studies · 2022Review
- Human stem cell models of neurodegeneration: From basic science of amyotrophic lateral sclerosis to clinical translation.Cell stem cell · 2022Review
- Higher blood high density lipoprotein and apolipoprotein A1 levels are associated with reduced risk of developing amyotrophic lateral sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2022Article
- Multicentre appraisal of amyotrophic lateral sclerosis biofluid biomarkers shows primacy of blood neurofilament light chain.Brain communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of the corticomotorneuronal network responsible for voluntary movement. There are well-established clinical, genetic and pathological overlaps between ALS and frontotemporal dementia (FTD), which together constitute the 'TDP-43 proteinopathies'. An ever-expanding list of genes in which mutation leads to typical ALS have implicated abnormalities in RNA processing, protein homoeostasis and axonal transport. How these apparently distinct pathways converge to cause the characteristic clinical syndrome of ALS remains unclear. Although there are major gaps in our understanding of the essential nature of ALS pathophysiology, the identification of genetic causes in up to 15% of ALS patients, coupled with advances in biotechnology and biomarker research provide a foundation for approaches to treatment based on 'precision medicine', and even prevention of the disease in pre-symptomatic mutation carriers in the future. Currently, multidisciplinary care remains the bedrock of management and this is increasingly being put onto an evidence-based footing.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.