Parkinson's Disease: Is It a Toxic Syndrome?

El-Hak, Seham A. Gad; Ghanem, Ahmed N; Abdel-Ghaffar, Hassan; Dakroury, Sahar El; Salama, Mohamed

doi:10.1155/2010/103094

Cited by 4 publications

(3 citation statements)

References 90 publications

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“…The process of production of lewy bodies is confirmed by scientists as subordinate to the refractive proteolytic pathway that causes an unusual breakdown or increased production subjected to genetic mutations. It is confirmed that alpha-synuclein modifies dopamine biosynthesis and negatively controls the dopamine transporter system 18,19 . Apart from the mechanisms mentioned above, other various routes are expected to be involved.…”

Section: Pathogenesis Of Pdmentioning

confidence: 88%

“…The complex 1 deficiency understood as the uninterrupted relation between mitochondrial dysfunction and PD in SNPc; this deficiency was also successively observed in skeletal muscles and platelets. DA neurons being more susceptible to oxidative stress resulted in the association of auto-oxidation and DA metabolism, a rise in iron and a fall in total glutathione levels was seen along with mitochondrial complex 1 inhibition that led to surpassing the oxidative capability of DA cells, eventually causing cell death 18 .…”

Section: Pathogenesis Of Pdmentioning

confidence: 99%

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Untitled

2022

IJPSR

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Parkinson"s disease is the second most common progressive, age-linked neurodegenerative disorder. The sporadic form of the disease is usually idiopathic, where mitochondrial dysfunction is its major hallmark. Mitochondria are multifunctional dynamic organelles that carry out major cellular functions that get damaged by reactive oxygen species, deposition of lewy bodies, dopaminergic neuronal cell death, mitochondrial DNA mutations, and imbalance in fission/fusion that ultimately weakens mitophagy. In this review, the updated key roles and mechanisms of mitochondrial dysfunction structurally and functionally in the pathogenesis of sporadic Parkinson"s disease are discussed to understand the process of neurodegeneration. Research Data from numerous studies confirm mitochondrial dysfunction being the Basis of the disease. Here, we briefly bring the overview of illicit drug administration, oxidative stress, mitochondrial DNA mutations, mitochondrial genome mutations, alpha-synuclein aggregation, mitochondrial dynamics-fission and fusion, and the impairment of mitophagy in the disease pathogenesis. In conclusion, understanding mitochondrial dysfunction and its pathways can be a major target in treatment and prevention of Parkinson"s disease. INTRODUCTION:Parkinson"s disease (PD) was first started in an essay on "shaking palsy" by James Parkinson in 1817. In the beginning, it was discussed as "paralysis agitans" but Later was acknowledged as "maladie de Parkinson" or simply Parkinson"s disease by Charcot in 19 th century 1 . It has approximately 3-7% of lifetime risk after Alzheimer"s disease and is an age-linked progressive condition that is expected to increase exponentially in the elderly population.

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Section: Pathogenesis Of Pdmentioning

confidence: 88%

Section: Pathogenesis Of Pdmentioning

confidence: 99%

Untitled

2022

IJPSR

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“…The misfolded protein behaves like a template inducing conformational change in the wild type proteins causing a cross-reaction and leading to neurodegeneration. Histologically, there is neuronal loss in the substantia nigra pars compacta along with compensatory astrocytic and microglial proliferation and biochemically there is loss of dopaminergic termini in the striatum [21]- [23].…”

Section: Introductionmentioning

confidence: 99%

The Development of Treatment for Parkinson’s Disease

Yadav¹,

Li²

2015

APD

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Parkinson's disease (PD) is a slowly progressive, age-related, second most common neurodegenerative disorder after Alzheimer's disease of unknown etiology. Dopamine replacement therapies were introduced five decades ago and still remain the mainstay of treatment for Parkinson's disease. However, with long-term treatment with L-dopa, more than 50% of patients were found to develop motor response complications approximately after 4-5 years of initiation of continuous treatment, in 80% of patients treated for 10 years, and in nearly 100% patients with young-onset disease. The complications of long-term treatment with levodopa include-motor fluctuations, dyskinesias, and nonmotor fluctuations are such as mood disturbance, cognitive dysfunction, dysautonomia and pain. Till date, there are various therapeutic approaches having been developed for the treatment of advanced PD comprising Pharmacotherapy, neurotrophic factors, surgical procedures such as DBS, cell-based therapies and gene therapies. The pharmacological and surgical therapies are only aiming to improve the symptoms of PD, but none are proven to have a significant effect on the underlying disease process with respect to either slowing disease progression or restoring the affected dopaminergic neurons. Although there is no cure for PD, Gene based therapy has significant prospective advantages over the conventional treatment modalities for PD, as it could theoretically be used to preserve or restore dopaminergic neurons affected by PD through the action of neurotrophic factors or alternatively increase the availability of enzymes required for dopamine synthesis. All commonly employed PD therapies focus on the amelioration of symptoms and do not cure disease. In this review only we summarize the newer therapeutic strategies for the treatment of PD such as anti-inflammatories, neurotrophic factors, neurosurgical procedures (DBS), cell based therapies and gene therapies.

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