The relevance of BDNF for neuroprotection and neuroplasticity in multiple sclerosis
Open accessAbstract
Background: Neuroplasticity as a mechanism to overcome central nervous system injury resulting from different neurological diseases has gained increasing attention in recent years. However, deficiency of these repair mechanisms leads to the accumulation of neuronal damage and therefore long-term disability. To date, the mechanisms by which remyelination occurs and why the extent of remyelination differs interindividually between multiple sclerosis patients regardless of the disease course are unclear. A member of the neurotrophins family, the brain-derived neurotrophic factor (BDNF) has received particular attention in this context as it is thought to play a central role in remyelination and thus neuroplasticity, neuroprotection, and memory. Objective: To analyse the current literature regarding BDNF in different areas of multiple sclerosis and to provide an overview of the current state of knowledge in this field. Conclusion: To date, studies assessing the role of BDNF in patients with multiple sclerosis remain inconclusive. However, there is emerging evidence for a beneficial effect of BDNF in multiple sclerosis, as studies reporting positive effects on clinical as well as MRI characteristics outweighed studies assuming detrimental effects of BDNF. Furthermore, studies regarding the Val66Met polymorphism have not conclusively determined whether this is a protective or harmful factor in multiple sclerosis, but again most studies hypothesized a protective effect through modulation of BDNF secretion and anti-inflammatory effects with different effects in healthy controls and patients with multiple sclerosis, possibly due to the pro-inflammatory milieu in patients with multiple sclerosis. Further studies with larger cohorts and longitudinal follow-ups are needed to improve our understanding of the effects of BDNF in the central nervous system, especially in the context of multiple sclerosis.
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mTORC1 plays a critical role in local synaptic protein synthesis and cytoskeletal reorganization, such as actin polymerization, enabling formation and stabilization of new synaptic connections.
“mTORC1 plays a critical role in local synaptic protein synthesis and cytoskeletal reorganization, such as actin polymerization, enabling the formation and stabilization of new synaptic connections [90,91].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [91]
The Introduction’s “BDNF signaling pathways” section says mTORC1 induces translation of proteins related to synaptic formation and promotes outgrowth of cytoskeletal filaments and dendritic spines. It does not specify local synaptic synthesis or actin polymerization, or directly attribute stabilization of new synaptic connections to mTORC1. No page number is available in our copy. (LLM, conf=0.86)
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Pardossi, S., Fagiolini, A., & Cuomo, A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252313098 · Cited by 51 · see citing works
- Authors
- Maiworm, M.
- Affiliations
- University Hospital Frankfurt (DE)
- Corresponding author
- Maiworm, Michelle
- ORCID
- Maiworm, Michelle
- Venue
- Frontiers in Neurology
- Publisher
- Frontiers Media SA
- Published
- 2024-08-01
- Volume
- 15
- Pages
- 1385042-1385042
- ISSN
- 1664-2295 (ISSN-L)
- PMC
- PMC11325594
- OpenAlex
- W4401217265
- Cited by
- 27
- References
- 9
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 3
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
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- Locations
- Frontiers in Neurology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
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- Publication Server of Goethe University Frankfurt am Main (Goethe University Frankfurt) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Keywords
- brain-derived neurotrophic factor, multiple sclerosis, neuroplasticity, neuroprotection, remyelination, BDNF Val66Met polymorphism, neurotrophins, disability, anti-inflammatory activity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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