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Brain & Heart Oxidative stress and neurological disorders

a cascade of metabolic processes, ultimately resulting in outcomes. In addition, prolonged use of these drugs may
neuronal loss. 7 lead to side effects such as hallucinations, constipation,
mood swings, uncontrolled and involuntary movements,
8.1. Parkinson’s disease delusions, joint rigidity, and increased frequency of

The hallmark of Parkinson’s disease is the progressive loss tremors. Another class of drugs used in Parkinson’s
of dopaminergic neurons, particularly in the substantia therapy includes MAO inhibitors, which target
nigra region. Physiological changes associated with the enzymes involved in the metabolism of auto-oxidation
disease include resting tremors, slowing of voluntary of dopamine. Examples of these inhibitors include
movements (bradykinesia), muscle rigidity, mask-like rasagiline, selegiline, and safinamide, which can be
facial expression, and postural instability. Parkinson’s used either as an alternative to syndopa or levodopa or
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disease presents as a syndrome characterized by a range in combination with them. However, these drugs carry
of symptoms, including posture instability, depression, side effects such as nausea, vomiting, dizziness, fever,
impaired body equilibrium, and various other mental headaches, and vivid dreams. In addition to these
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health issues. Pathologically, the disease is marked by medications, other drugs may be employed in therapy to
the presence of Lewy bodies and the accumulation alleviate the side effects of levodopa. These drugs include
of various proteins such as α-synuclein, ubiquitin, clozapine and amitriptyline for addressing mental
and neurofilaments. Recent research suggests that an health issues, as well as rivastigmine and donepezil for
imbalance between oxidative stress and the antioxidant managing dementia.
defense mechanism may contribute to the etiology of
Parkinson’s disease. Studies have demonstrated the 8.2.2. Surgical therapy
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presence of oxidative markers in the cerebrospinal This procedure is effective in addressing various symptoms
fluid (CSF) and blood of Parkinson’s disease patients. of Parkinson’s disease, such as bradykinesia, tremors,
In addition, deficiencies in the mitochondrial complex instability in body postures, and rigidity in voluntary
system have been observed in these patients. This movements. It entails a neurosurgical intervention
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deficiency leads to an excessive production of ROS in primarily intended for patients with movement
the frontal cortex, fibroblasts, and platelets. Dopamine, disorders. These movement disorders mainly arise
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an unstable molecule, undergoes auto-oxidation, thereby from disorganized signals within the areas of the CNS
converting into dopamine quinones and free radicals. responsible for controlling movements. Conceptually,
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Under normal conditions, the concentration of dopamine this procedure operates similarly to a pacemaker for the
is regulated by the enzymatic activities of monoamine heart. Continuous pulses emitted from the neurostimulator
oxidase (MAO)-A and MAO-B. However, in Parkinson’s are transmitted through leads to the brain. This treatment
disease and aging, MAO concentration decreases in has been found beneficial for Parkinson’s disease patients,
glial cells, contributing to dopamine autoxidation. often leading to improvements in symptoms such as
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While the exact mechanism underlying oxidative stress tremors, stiffness, and bradykinesia. In addition, reports
and Parkinson’s disease pathology remains unknown, indicate that a deep brain stimulation (DBS) procedure
oxidative stress is recognized as a common mechanism can reduce the need for medication and improve symptom
that leads to cellular dysfunction and, eventually, cell management in patients. However, it is important to
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apoptosis. Treatment approaches primarily aim to provide note that Parkinson’s disease is a progressive disorder, and
symptomatic relief and include cell therapy, surgery, and while these treatments can alleviate symptoms, a complete
medication. cure is not currently attainable.

8.2. Treatment of Parkinson’s disease 8.2.3. Cell replacement therapy (CRT)
8.2.1. Pharmacological intervention Patients treated with levodopa and DBS may develop
Over the past 50 years, dopamine precursors in the problematic side effects such as speech problems,
form of syndopa, levodopa, or carbidopa have been hallucinations, and neuropsychiatric effects. Therefore,
used as symptomatic therapies for Parkinson’s disease. targeted therapies such as CRT are urgently needed.
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These supplements, such as l-dihydroxyphenylalanine CRT is used for long-term treatment of motor movements
(L-DOPA), serve as precursors of dopamine, which are by slowing down disease progression. It involves the use
absorbed into nerve cells in the brain and subsequently of cells such as neural stem cells, mesenchymal stem cells,
converted into dopamine. However, due to the and induced neural cells. While stem cells show promise in
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progressive nature of Parkinson’s disease, long-term use treatment, their use as a mainline treatment for Parkinson’s
of these medications may result in fluctuations in patient disease presents several challenges. Any type of graft or
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Volume 2 Issue 2 (2024) 9 doi: 10.36922/bh.2704