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Advanced Neurology Exercise modulated Vitamin D and HDL in epilepsy

to normal children. Moreover, a significant correlation Seizure attacks are known to activate apoptotic pathways
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was observed between inadequate Vitamin D levels and in various brain areas. 44,45 Both intrinsic and extrinsic
adverse lipid metabolism in obese pediatric patients. factors contribute to the regulation of the apoptosis
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Among male adolescents, those deficient in Vitamin D signaling pathway. Activation of the Vitamin D receptor
exhibited lower serum HDL levels compared to those with has been shown to decrease the level of cleaved caspase-3
sufficient Vitamin D. Our findings indicate that regular following traumatic brain injury, and the expression of
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physical exercise may have a significant beneficial impact Vitamin D receptor in the hippocampus plays an important
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on the lipid profiles, potentially by modulating Vitamin D role in cell survival through the calcium buffering system.
deficiency. In addition, pretreatment with Vitamin D has been
3
reported to improve mesencephalic neuron survival in the
These findings are particularly relevant in the context
of neurological health, as both lipids and Vitamin D are pathological condition induced by 6-hydroxydopamine
administration. Vitamin D is also known to protect
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crucial in maintaining brain function and protecting the hippocampus through its anti-inflammatory and
neurons from damage. Exercise-induced regulation of antioxidant properties. The anti-inflammatory properties
lipid metabolism, especially the increase of HDL, might of Vitamin D reduce neuronal loss and the risk of dementia
contribute to reducing neuroinflammation, oxidative stress, and Alzheimer’s disease by modulating pro-inflammatory
and neuronal damage involved in the pathophysiology of cytokines such as interleukin 6 and tumor necrosis factor
epilepsy. In parallel, our findings suggest that exercise alpha in the hippocampus. In addition, Vitamin D has
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could be an effective strategy for mitigating the adverse been shown to protect neurons by reducing oxidative stress
3
effects of Vitamin D deficiency, a condition that is widely factors such as catalase enzyme. 50
observed in individuals with epilepsy.
Further evidence on the neuroprotective role of HDL
Furthermore, physical activity might play an
important role in the prevention and management of derives from in vitro studies involving astrocytes, the most
abundant glial cells in the CNS, which play a critical role in
Vitamin D deficiency in individuals undergoing long- maintaining neuronal homeostasis and responding to injury.
term treatment with antiepileptic drugs. Long-term It has been demonstrated that the incubation of astrocytes
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administration of antiepileptic drugs interferes with the with HDL isolated from human plasma significantly enhances
metabolism of Vitamin D, leading to suboptimal serum their viability in the presence of toxic concentrations of
levels and potentially exacerbating bone fragility, immune divalent copper ions in the culture medium. 51
dysfunction, and neuronal vulnerability. By enhancing the
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synthesis of Vitamin D through increased sun exposure and This finding is particularly noteworthy because
optimizing overall metabolic health, exercise might help to copper, while essential in trace amounts for enzymatic
counteract some of the negative effects of antiepileptic drugs. activity, becomes neurotoxic at high levels and contributes
These dual effects – improving lipid profiles and restoring to oxidative stress, mitochondrial dysfunction, and
Vitamin D levels – suggest that exercise could be a simple inflammatory factors commonly implicated in seizure
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and accessible therapeutic intervention for individuals with pathology and neurodegenerative diseases. HDL, through
epilepsy, enhancing their overall well-being and potentially its antioxidant property and lipid-transporting capacity,
improving their neurological outcomes. may protect against this toxicity, thereby preserving
astrocyte function under stress conditions. 52
4.3. Neuroprotective effect of exercise
In contrast, prolonged exposure to elevated levels of
Epileptic seizure attacks have been reported to induce LDL, particularly in the oxidized form, has been associated
neural cell damage. To assess the neuroprotective effects with detrimental effects on the brain. Studies have shown
of certain supplements, such as Nigella sativa and that chronic high LDL concentrations aggravated the
astaxanthin, researchers have commonly used the PTZ deposition of beta-amyloid in brain tissue, a process central
kindling models. 39,40 This model has been shown to cause to the pathogenesis of Alzheimer’s disease. Furthermore,
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neural cell damage in various brain regions. 41,42 LDL has been implicated in compromising the integrity of
Dark cells are considered a valid histological marker the blood–brain barrier, a selectively permeable structure
for assessing neuronal damage in the brain. In this study, that protects the brain from circulating toxins and immune
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we observed a significant decrease in the number of dark cells. Damage to the blood–brain barrier might permit
cells in epileptic rats that underwent physical activity. the infiltration of pro-inflammatory mediators, further
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These findings indicate that exercise may have a moderate exacerbating neuronal damage.
neuroprotective effect by improving neural cell survival in Moreover, astrocytes subjected to oxygen-glucose
epileptic rats. deprivation – a well-established in vitro model that

Volume 4 Issue 3 (2025) 83 doi: 10.36922/an.8347