ReviewBrain : a journal of neurology2020
Decoding the relationship between ageing and amyotrophic lateral sclerosis: a cellular perspective.
Review in Brain : a journal of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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.
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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.
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Who cites it
56 citing papers in PubMed, 87 citations in OpenAlex.
- Molecular signatures of selective motor neuron vulnerability in old age.Experimental physiology · 2026Article
- Drug screen and machine learning predict neuroprotective agents in a preclinical human model of childhood dementia.Nature communications · 2026Article
- Intron retention in health and amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Review
- Fiber type specific tibialis anterior muscle atrophy and oxidative capacity reduction is contemporaneous with death of larger lumbar motor neurons in old rats.Physiological reports · 2026Article
- Impact of G-quadruplex RNA oxidation on its conformational dynamics and interaction with ALS-associated TDP-43.Scientific reports · 2026Article
- Impact of weight loss and disease progression on survival in ALS: insights from a multidisciplinary care center.Arquivos de neuro-psiquiatria · 2025Article
- Programmable self-replicating JEV nanotherapeutics redefine RNA delivery in ALS.Communications biology · 2025Review
- The myokine FGF21 associates with enhanced survival in ALS and mitigates stress-induced cytotoxicity.Aging · 2025Article
- Aging on Chip: Harnessing the Potential of Microfluidic Technologies in Aging and Rejuvenation Research.Advanced healthcare materials · 2025Review
- Review
- Neural Excitatory/Inhibitory Imbalance in Motor Aging: From Genetic Mechanisms to Therapeutic Challenges.Biology · 2025Review
- Blm10-Based Compounds Add to the Knowledge of How Allosteric Modulators Influence Human 20S Proteasome.ACS chemical biology · 2025Article
- Serine metabolism in aging and age-related diseases.GeroScience · 2025Review
- The role of autophagy in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).Autophagy reports · 2025Review
- Muscle-specific Bet1L knockdown induces neuromuscular denervation, motor neuron degeneration, and motor dysfunction in a rat model of familial ALS.Frontiers in neuroscience · 2025Article
- The emerging role of cellular senescence in amyotrophic lateral sclerosis.Frontiers in neuroscience · 2025Review
- Racial and ethnic disparities in ALS: a longitudinal electronic health records study.Therapeutic advances in neurological disorders · 2025Article
- Current aspects of targeting cellular senescence for the therapy of neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Dysregulated FOXO1 activity drives skeletal muscle intrinsic dysfunction in amyotrophic lateral sclerosis.Acta neuropathologica · 2024Article
- From inflammatory signaling to neuronal damage: Exploring NLR inflammasomes in ageing neurological disorders.Heliyon · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
With an ageing population comes an inevitable increase in the prevalence of age-associated neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), a relentlessly progressive and universally fatal disease characterized by the degeneration of upper and lower motor neurons within the brain and spinal cord. Indeed, the physiological process of ageing causes a variety of molecular and cellular phenotypes. With dysfunction at the neuromuscular junction implicated as a key pathological mechanism in ALS, and each lower motor unit cell type vulnerable to its own set of age-related phenotypes, the effects of ageing might in fact prove a prerequisite to ALS, rendering the cells susceptible to disease-specific mechanisms. Moreover, we discuss evidence for overlap between age and ALS-associated hallmarks, potentially implicating cell type-specific ageing as a key contributor to this multifactorial and complex disease. With a dearth of disease-modifying therapy currently available for ALS patients and a substantial failure in bench to bedside translation of other potential therapies, the unification of research in ageing and ALS requires high fidelity models to better recapitulate age-related human disease and will ultimately yield more reliable candidate therapeutics for patients, with the aim of enhancing healthspan and life expectancy.
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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.