Brain-derived neurotrophic factor in neurodegenerative diseases
Abstract
Changes in the levels and activities of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), have been described in a number of neurodegenerative disorders, including Huntington disease, Alzheimer disease and Parkinson disease. It is only in Huntington disease, however, that gain-of-function and loss-of-function experiments have linked BDNF mechanistically with the underlying genetic defect. Altogether, these studies have led to the development of experimental strategies aimed at increasing BDNF levels in the brains of animals that have been genetically altered to mimic the aforementioned human diseases, with a view to ultimately influencing the clinical treatment of these conditions. In this article, we will review the current knowledge about the involvement of BDNF in a number of neurodegenerative diseases, with particular emphasis on Huntington disease, and will provide the rationale for and discuss the problems in proposing BDNF treatment as a beneficial and feasible therapeutic approach in the clinic.
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Decreased BDNF levels, especially in older adults, may lead to compromised memory, neurodegeneration, and cognitive impairments found in Alzheimer's disease.
“Furthermore, decreased BDNF levels, especially in older adults, may lead to compromised memory, neurodegeneration, and various other cognitive impairments found in Alzheimer's disease (for review, see Zuccato and Cattaneo, 2009).”
From Exercise-Mediated Neurogenesis in the Hippocampus via BDNF (2018) · cites this paper as Zuccato and Cattaneo, 2009
Neurodegenerative and neuropsychiatric diseases may be partially caused by defects in synaptic plasticity associated with insufficient neuronal supply of BDNF and other neurotrophic factors.
“Furthermore, it was shown that neurodegenerative and neuropsychiatric diseases may be partially caused by defects in synaptic plasticity associated with the insufficient neuronal supply of BDNF and other neurotrophic factors [11,12,13].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [11]
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“Reduced striatal BDNF has been shown in both HD patients (Ferrer et al., 2000) and transgenic models of HD (Zuccato and Cattaneo, 2009).”
- Authors
- Zuccato, C., & Cattaneo, E.
- Affiliations
- University of Milan (IT)
- Corresponding author
- Cattaneo, Elena
- Venue
- Nature Reviews Neurology
- Published
- 2009-06
- Volume
- 5
- Issue
- 6
- Pages
- 311-322
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- OpenAlex
- W1996893328
- Cited by
- 947
- References
- 9
- Citations by year
- 2026: 28 · 2025: 35 · 2024: 56 · 2023: 67 · 2022: 58 · 2021: 55 · 2020: 64 · 2019: 46 · 2018: 57 · 2017: 60 · 2016: 53 · 2015: 51 · 2014: 59 · 2013: 62 · 2012: 67
- FWCI
- 5.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- brain-derived neurotrophic factor, neurotrophic factors, neurodegenerative diseases, Huntington's disease, Alzheimer's disease, Parkinson's disease
- MeSH terms
- Animals, Humans, Models, Biological, Brain-Derived Neurotrophic Factor, Neurodegenerative Diseases, PubMed
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