ArticleExperimental neurology2021
Delayed onset of inherited ALS by deletion of the BDNF receptor TrkB.T1 is non-cell autonomous.
Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- TrkB Truncated Isoform Receptors as Transducers and Determinants of BDNF Functions.Frontiers in neuroscience · 2022Pooled it
- Disruption of BDNF signalling in neuropathologies.Biochemical Society transactions · 2026Review
- Ciliary neurotrophic factor slows axonal transport of signalling endosomes.Brain communications · 2026Article
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- Targeting brain-derived neurotrophic factor in the treatment of neurodegenerative diseases: A review.Neuroprotection (Chichester, England) · 2024Review
- Review
- Neurotrophic factors in the physiology of motor neurons and their role in the pathobiology and therapeutic approach to amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2023Review
- Amyotrophic Lateral Sclerosis Pathoetiology and Pathophysiology: Roles of Astrocytes, Gut Microbiome, and Muscle Interactions via the Mitochondrial Melatonergic Pathway, with Disruption by Glyphosate-Based Herbicides.International journal of molecular sciences · 2022Review
- BDNF-dependent modulation of axonal transport is selectively impaired in ALS.Acta neuropathologica communications · 2022Article
- Recent Advances on the Role of Brain-Derived Neurotrophic Factor (BDNF) in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- BDNF and Pro-BDNF in Amyotrophic Lateral Sclerosis: A New Perspective for Biomarkers of Neurodegeneration.Brain sciences · 2022Article
- Article
- The role of brain derived neurotrophic factor in central nervous system.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The pathophysiology of Amyotrophic Lateral Sclerosis (ALS), a disease caused by the gradual degeneration of motoneurons, is still largely unknown. Insufficient neurotrophic support has been cited as one of the causes of motoneuron cell death. Neurotrophic factors such as BDNF have been evaluated in ALS human clinical trials, but yielded disappointing results attributed to the poor pharmacokinetics and pharmacodynamics of BDNF. In the inherited ALS G93A SOD1 animal model, deletion of the BDNF receptor TrkB.T1 delays spinal cord motoneuron cell death and muscle weakness through an unknown cellular mechanism. Here we show that TrkB.T1 is expressed ubiquitously in the spinal cord and its deletion does not change the SOD1 mutant spinal cord inflammatory state suggesting that TrkB.T1 does not influence microglia or astrocyte activation. Although TrkB.T1 knockout in astrocytes preserves muscle strength and co-ordination at early stages of disease, its specific conditional deletion in motoneurons or astrocytes does not delay motoneuron cell death during the early stage of the disease. These data suggest that TrkB.T1 may limit the neuroprotective BDNF signaling to motoneurons via a non-cell autonomous mechanism providing new understanding into the reasons for past clinical failures and insights into the design of future clinical trials employing TrkB agonists in ALS.
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Registered trials
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