2025-06-18
Neurodegeneration: the shadow of a deficiency?
Neurology
#Alzheimer #MS #Parkinson #ALS #VitaminD
Neurodegenerative diseases such as multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) represent a major global public health challenge. Their prevalence is steadily increasing, notably due to demographic aging. These conditions are characterized by a progressive, irreversible, and often multifocal loss of neurological functions, leading to cognitive, motor, sensory, or respiratory deficits depending on the disease.
Current treatments may alleviate certain symptoms or slow the disease’s course, but they do not stop neurodegeneration. Their effectiveness remains limited, varies between patients, and is often accompanied by side effects. Moreover, the lack of reliable biomarkers complicates personalized care. These limitations highlight the urgent need for new approaches, more specifically targeted at the root causes of the disease.
In this context, interest in modifiable environmental factors, such as vitamin D, has grown significantly. Vitamin D has been shown to play a key role in immunomodulation, neuroprotection, and cellular regulation through its nuclear receptor (VDR), which is present in many regions of the central nervous system. Its potential role in preventing or slowing neurodegenerative processes makes it a strong candidate for risk modulation strategies or therapeutic adjuvants.
This study was initiated to assess the potential role of vitamin D in the progression of MS, AD, PD, and ALS. The objective is to better understand the underlying mechanisms, to take stock of the current state of clinical knowledge, and to identify the gaps that need to be filled for future integration into personalized therapeutic strategies.
In multiple sclerosis (MS), numerous observational studies show an association between low vitamin D levels and an increased risk of onset or relapse. Immunomodulatory mechanisms are involved. Vitamin D inhibits pro-inflammatory Th1 and Th17 responses while promoting regulatory T cells. Some data suggest that higher intakes could reduce the frequency of relapses and slow the progression of disability.
In Alzheimer’s disease (AD), experimental data are also encouraging. Vitamin D appears to play a role in beta-amyloid clearance, protection against oxidative stress, and improvement of synaptic plasticity. These effects are mediated by the expression of VDR in the hippocampus, a key region for memory. However, clinical trials conducted so far have produced variable results, often limited by methodological biases and small sample sizes.
In Parkinson’s disease (PD), vitamin D may exert a neuroprotective effect on dopaminergic neurons in the substantia nigra. It appears to reduce neuroinflammation, improve motor function in animal models, and its deficiency is frequently observed in patients with Parkinson’s. Although some studies suggest a link between deficiency and clinical worsening, the evidence remains insufficient for concrete therapeutic recommendations.
Finally, in amyotrophic lateral sclerosis (ALS), the literature is more limited but nonetheless suggestive. Several studies have observed lower serum levels of vitamin D in affected patients, sometimes associated with faster disease progression or reduced survival. Vitamin D may act by modulating oxidative stress, regulating intracellular calcium, and providing protective effects on motor neurons. Preclinical studies have shown functional improvement in ALS mouse models treated with vitamin D. However, clinical trials remain rare, with preliminary results needing confirmation in larger and better-controlled cohorts.
Neurodegenerative diseases are characterized by a progressive, irreversible, and often multifocal loss of neurons in the central nervous system. This degeneration leads to major functional impairment—cognitive, motor, or sensory—with a profound impact on patients’ quality of life. In a therapeutic context still largely limited to symptom management, where curative interventions are lacking, identifying modifiable environmental factors that can influence the disease’s course has become a major objective.
Beyond its classic role in calcium homeostasis, vitamin D appears to be a potential modulator of neuroinflammation, neuronal plasticity, and brain aging. This review confirms that chronic deficiency could contribute to the progression of diseases like MS, Alzheimer’s, or Parkinson’s through immune and neurotoxic mechanisms.
However, available data remain fragmented, particularly for Alzheimer’s and Parkinson’s, and the effects of supplementation are still debated. Randomized controlled trials are few, often small in scale, and marked by methodological heterogeneity. More rigorous research is needed to clarify optimal dosages, target populations, and relevant therapeutic windows. The integration of vitamin D into preventive or therapeutic strategies for neurodegenerative diseases must rely on robust data, but this avenue deserves increased attention.
Neurodegenerative diseases such as multiple sclerosis (MS), Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) represent a major global public health challenge. Their prevalence is steadily increasing, notably due to demographic aging. These conditions are characterized by a progressive, irreversible, and often multifocal loss of neurological functions, leading to cognitive, motor, sensory, or respiratory deficits depending on the disease.
Current treatments may alleviate certain symptoms or slow the disease’s course, but they do not stop neurodegeneration. Their effectiveness remains limited, varies between patients, and is often accompanied by side effects. Moreover, the lack of reliable biomarkers complicates personalized care. These limitations highlight the urgent need for new approaches, more specifically targeted at the root causes of the disease.
In this context, interest in modifiable environmental factors, such as vitamin D, has grown significantly. Vitamin D has been shown to play a key role in immunomodulation, neuroprotection, and cellular regulation through its nuclear receptor (VDR), which is present in many regions of the central nervous system. Its potential role in preventing or slowing neurodegenerative processes makes it a strong candidate for risk modulation strategies or therapeutic adjuvants.
This study was initiated to assess the potential role of vitamin D in the progression of MS, AD, PD, and ALS. The objective is to better understand the underlying mechanisms, to take stock of the current state of clinical knowledge, and to identify the gaps that need to be filled for future integration into personalized therapeutic strategies.
Less sunlight, more neurons at risk?
In multiple sclerosis (MS), numerous observational studies show an association between low vitamin D levels and an increased risk of onset or relapse. Immunomodulatory mechanisms are involved. Vitamin D inhibits pro-inflammatory Th1 and Th17 responses while promoting regulatory T cells. Some data suggest that higher intakes could reduce the frequency of relapses and slow the progression of disability.
Read next: Progressive MS: could the placenta pave the way?
In Alzheimer’s disease (AD), experimental data are also encouraging. Vitamin D appears to play a role in beta-amyloid clearance, protection against oxidative stress, and improvement of synaptic plasticity. These effects are mediated by the expression of VDR in the hippocampus, a key region for memory. However, clinical trials conducted so far have produced variable results, often limited by methodological biases and small sample sizes.
Read next: Genes and Alzheimer’s: the key to the mystery?
In Parkinson’s disease (PD), vitamin D may exert a neuroprotective effect on dopaminergic neurons in the substantia nigra. It appears to reduce neuroinflammation, improve motor function in animal models, and its deficiency is frequently observed in patients with Parkinson’s. Although some studies suggest a link between deficiency and clinical worsening, the evidence remains insufficient for concrete therapeutic recommendations.
Read next: MoCA boosted, brain relieved!
Finally, in amyotrophic lateral sclerosis (ALS), the literature is more limited but nonetheless suggestive. Several studies have observed lower serum levels of vitamin D in affected patients, sometimes associated with faster disease progression or reduced survival. Vitamin D may act by modulating oxidative stress, regulating intracellular calcium, and providing protective effects on motor neurons. Preclinical studies have shown functional improvement in ALS mouse models treated with vitamin D. However, clinical trials remain rare, with preliminary results needing confirmation in larger and better-controlled cohorts.
Read next: ALS: exercise on prescription?
Vitamin D: a path still to be validated
Neurodegenerative diseases are characterized by a progressive, irreversible, and often multifocal loss of neurons in the central nervous system. This degeneration leads to major functional impairment—cognitive, motor, or sensory—with a profound impact on patients’ quality of life. In a therapeutic context still largely limited to symptom management, where curative interventions are lacking, identifying modifiable environmental factors that can influence the disease’s course has become a major objective.
Beyond its classic role in calcium homeostasis, vitamin D appears to be a potential modulator of neuroinflammation, neuronal plasticity, and brain aging. This review confirms that chronic deficiency could contribute to the progression of diseases like MS, Alzheimer’s, or Parkinson’s through immune and neurotoxic mechanisms.
However, available data remain fragmented, particularly for Alzheimer’s and Parkinson’s, and the effects of supplementation are still debated. Randomized controlled trials are few, often small in scale, and marked by methodological heterogeneity. More rigorous research is needed to clarify optimal dosages, target populations, and relevant therapeutic windows. The integration of vitamin D into preventive or therapeutic strategies for neurodegenerative diseases must rely on robust data, but this avenue deserves increased attention.
Read next: Vitamin D deficiency: a risk for the mind?
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Neurodegeneration: the shadow of a deficiency?
#Alzheimer #MS #Parkinson #ALS #VitaminD <br><br><br>
