Parkinson’s disease: pathogenesis, aetiology, symptoms, diagnostics, and its course

Baat, C. de; Stiphout, M.A.E. van; Lobbezoo, Frank; Dijk, Karin D. van; Berendse, H W

doi:10.5177/ntvt.2018.10.18176

Cited by 10 publications

(3 citation statements)

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“…Neurodegenerative diseases involve mitochondrial dysfunction caused by various factors, which ultimately leads to progressive degeneration, apoptosis, or necrosis of neurons (Srivastava and Yadav, 2016). Degeneration can be selective for specific neuron types, such as in Parkinson’s disease (PD), where selective degeneration of substantia nigra (SN) dopaminergic neurons occurs; in contrast, Alzheimer’s disease (AD) and Huntington’s disease (HD) neuropathology shows extensive neuronal degeneration (Mavroudis et al, 2010; Dexter and Jenner, 2013; Saudou and Humbert, 2016; de Baat et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

SIRT3 Regulation of Mitochondrial Quality Control in Neurodegenerative Diseases

Meng

Yan

Lei

et al. 2019

Front. Aging Neurosci.

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Neurodegenerative diseases are disorders that are characterized by a progressive decline of motor and/or cognitive functions caused by the selective degeneration and loss of neurons within the central nervous system. The most common neurodegenerative diseases are Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD). Neurons have high energy demands, and dysregulation of mitochondrial quality and function is an important cause of neuronal degeneration. Mitochondrial quality control plays an important role in maintaining mitochondrial integrity and ensuring normal mitochondrial function; thus, defects in mitochondrial quality control are also significant causes of neurodegenerative diseases. The mitochondrial deacetylase SIRT3 has been found to have a large effect on mitochondrial function. Recent studies have also shown that SIRT3 has a role in mitochondrial quality control, including in the refolding or degradation of misfolded/unfolded proteins, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis, all of which are affected in neurodegenerative diseases.

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Section: Introductionmentioning

confidence: 99%

SIRT3 Regulation of Mitochondrial Quality Control in Neurodegenerative Diseases

Meng

Yan

Lei

et al. 2019

Front. Aging Neurosci.

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“…As a result of the examination of more PARK genes [ 5 ], more PARK gene variations were discovered in people with early-onset Parkinson’s disease (EOPD), which also demonstrated that certain symptoms are connected to unusual PARK gene variants [ 6 ]. According to research, homocysteine, immunoinflammatory processes, excitatory neurotoxicity, oxidative stress damage, apoptosis, and autophagy all have a role in the etiology of Parkinson’s disease [ 7 ]. Experimental research has demonstrated that Hcy can be neurotoxic and excitatory to the substantia nigra among them.…”

Section: Introductionmentioning

confidence: 99%

Effects of rasagiline combined with levodopa and benserazide hydrochloride on motor function and homocysteine and IGF-1 levels in elderly patients with Parkinson’s disease

Yang,

Gao,

Gao

et al. 2023

BMC Neurol

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Background During the course of their illness, people with Parkinson’s disease may see changes in their insulin-like growth factor (IGF-1) and serum homocysteine (Hcy) indices. In this study, patients with intermediate to severe Parkinson’s disease were examined for how Resagiline and levodopa and benserazide hydrochloride affected their motor performance, serum levels of homocysteine (Hcy), and insulin-like growth factor (IGF-1). Methods From June 2020 to December 2021, a total of 100+ cases of Parkinson’s patients over 60 years old in the middle and late stages of Parkinson’s were seen in the outpatient and inpatient departments of the Third People’s Hospital of Chengdu City and had a detailed observation record, and according to the inclusion criteria, the patients who met the criteria were randomly grouped into a clinical observation group and a control group. The subjects in the control group received only levodopa and benserazide hydrochloride treatment, while the observation group was treated with Resagiline in combination with the clinical control group. The total treatment observation period was 1 year for both groups, and the motor function and serum Hcy and IGF-1 indexes of both groups were compared after the end of treatment. Results We randomly and evenly grouped 64 patients who met the requirements of the inclusion criteria into a clinical observation group and a control group, each with 32 patients, from among 168 patients over 60 years of age with detailed observation records in the middle and late stages of Parkinson’s. After the 1-year observation period, we found that the total effective rate after treatment in the clinical observation group (93.75%) and significantly higher than that in the control group (68.75%) (P < 0.05); after 1 year of treatment, the UPDRS score decreased in both groups, and the observation group was significantly lower than the control group (P < 0.05); after treatment, serum Hcy decreased and IGF-1 increased in both groups, and the observation group was higher than the control group mean values (P < 0.05). Conclusions In patients with Parkinson’s disease who are in the middle and late stages of the disease, the administration of Resagiline combined with levodopa and benserazide hydrochloride can significantly lower the body’s serum Hcy level, significantly raise IGF-1 levels, and significantly improve motor function in patients with Parkinson’s disease. It can also have significant therapeutic effects.

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“…The basic pathological changes of PD are the chronic progressive degeneration of dopamine neurons in the substantia nigra and the acidification of the microenvironment around dopamine neurons. PD patients were found with neuronal apoptosis and massive proliferation of glial cells (7).…”

Section: Introductionmentioning

confidence: 99%

Association between BDNF G196A (Val66Met) polymorphism and cognitive impairment in patients with Parkinson's disease: a meta-analysis

Wang

Liu

Guo

et al. 2019

Braz J Med Biol Res

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Brain-derived neurotrophic factor (BDNF) is widely expressed in the central nervous system and prolongs the survival of dopaminergic neurons in the substantia nigra. Several studies have recently investigated the association between BDNF G196A (Val66Met), a single nucleotide polymorphism influencing cognitive processes, and cognitive impairment in Parkinson's disease (PD), but with contradictory findings. Thus, this meta-analysis was performed to clarify the possible association. Relevant studies were identified by a systematic search of PubMed, Embase, and China National Knowledge Infrastructure (CNKI) databases. The strength of the association was evaluated using crude odds ratios and 95% confidence interval. Finally, six studies involving 532 cases and 802 controls were included. Our analyses suggested the G196A (Val66Met) polymorphism was significantly associated with cognitive impairment in PD, especially in Caucasian populations. In conclusion, BDNF G196A (Val66Met) is confirmed to be a risk factor for cognitive impairment in PD.

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Parkinson’s disease: pathogenesis, aetiology, symptoms, diagnostics, and its course

Cited by 10 publications

References 0 publications

SIRT3 Regulation of Mitochondrial Quality Control in Neurodegenerative Diseases

SIRT3 Regulation of Mitochondrial Quality Control in Neurodegenerative Diseases

Effects of rasagiline combined with levodopa and benserazide hydrochloride on motor function and homocysteine and IGF-1 levels in elderly patients with Parkinson’s disease

Association between BDNF G196A (Val66Met) polymorphism and cognitive impairment in patients with Parkinson's disease: a meta-analysis

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