Subjects Affected by Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) Elevated Brain-Derived Neurotrophic Factor (BDNF) Serum Levels

INTRODUCTION: Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) are neurodegenerative disorders with marked neuronal dysfunction and damage, accompanied by the accumulation of abnormal alpha-synuclein. Identifying the proteins involved in their specific neurodegenerative processes is important to understand shared or disease-specific mechanisms of neurodegeneration. Recent investigations into these disorders have revealed intriguing alterations in the functionality of neurotrophic factors, including and predominantly the Brain-Derived Neurotrophic Factor (BDNF). Thus, the aim of this study was to investigate the BDNF serum levels in two cohorts of DLB and MSA patients and compare them to those of healthy individuals. Investigating serum BDNF concentrations in these conditions may provide insights into aspects of the underlying mechanisms of neurodegeneration. METHODS: Serum BDNF concentrations were determined using commercial enzyme-linked immunosorbent assays. All serum samples were tested in duplicate, and the reported BDNF concentrations were ng/ml. RESULTS: The findings demonstrated a significant increase in serum BDNF levels in both DLB and MSA patients versus healthy subjects. DISCUSSION: This increase may represent a compensatory neuroprotective response to ongoing neuronal damage or a reflection of disease-related pathophysiological mechanisms involving altered BDNF regulation. CONCLUSION: These findings contribute to a growing body of evidence implicating neurotrophic fac-tor dysregulation in the pathogenesis of α-synucleinopathies. Moreover, the findings highlight BDNF as a potential therapeutic target and a candidate adjunct biomarker for diagnosis, monitoring disease activity, or treatment response. Additional experiments will clarify this causal relationship and the utility of BDNF-based interventions in modifying the disease trajectories in DLB and MSA.

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Publication Details

Journal
Current Neuropharmacology
Published
2026-04-16
DOI
https://doi.org/10.2174/011570159x448255260220084137
Primary Topic
Nerve injury and regeneration
Type
article
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article

Subjects Affected by Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) Elevated Brain-Derived Neurotrophic Factor (BDNF) Serum Levels

Zuzana Nedelská, Francesco Angelucci, Vanesa Jurášová, Jakub Hort et al.
Current Neuropharmacology
Nerve injury and regeneration
article

Subjects Affected by Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) Elevated Brain-Derived Neurotrophic Factor (BDNF) Serum Levels

Zuzana Nedelská, Francesco Angelucci, Vanesa Jurášová, Jakub Hort, Daniela Imal
article en

Abstract

INTRODUCTION: Dementia with Lewy Bodies (DLB) and Multiple System Atrophy (MSA) are neurodegenerative disorders with marked neuronal dysfunction and damage, accompanied by the accumulation of abnormal alpha-synuclein. Identifying the proteins involved in their specific neurodegenerative processes is important to understand shared or disease-specific mechanisms of neurodegeneration. Recent investigations into these disorders have revealed intriguing alterations in the functionality of neurotrophic factors, including and predominantly the Brain-Derived Neurotrophic Factor (BDNF). Thus, the aim of this study was to investigate the BDNF serum levels in two cohorts of DLB and MSA patients and compare them to those of healthy individuals. Investigating serum BDNF concentrations in these conditions may provide insights into aspects of the underlying mechanisms of neurodegeneration. METHODS: Serum BDNF concentrations were determined using commercial enzyme-linked immunosorbent assays. All serum samples were tested in duplicate, and the reported BDNF concentrations were ng/ml. RESULTS: The findings demonstrated a significant increase in serum BDNF levels in both DLB and MSA patients versus healthy subjects. DISCUSSION: This increase may represent a compensatory neuroprotective response to ongoing neuronal damage or a reflection of disease-related pathophysiological mechanisms involving altered BDNF regulation. CONCLUSION: These findings contribute to a growing body of evidence implicating neurotrophic fac-tor dysregulation in the pathogenesis of α-synucleinopathies. Moreover, the findings highlight BDNF as a potential therapeutic target and a candidate adjunct biomarker for diagnosis, monitoring disease activity, or treatment response. Additional experiments will clarify this causal relationship and the utility of BDNF-based interventions in modifying the disease trajectories in DLB and MSA.

Current NeuropharmacologyVol. 24
Charles University (CZ), University Hospital in Motol (CZ), University Hospital Brno (CZ), St. Anne's University Hospital Brno (CZ)
Openalex Percentile: Top 13%
Nerve injury and regeneration
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