parkinson's disease

Dementia is an umbrella term describing different types of diseases that lead to cognitive impairment and memory dysfunction, predominantly affecting older adults. The most common forms include Alzheimer's disease (AD), vascular dementia (VaD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). Despite extensive research, there is no definitive cure for dementia, primarily due to its complex and multifactorial nature, particularly the role of genetic abnormalities. Gene therapy, a novel therapeutic approach, aims to correct defective genes or introduce functional gene products by delivering specific DNA sequences to patients, and is often considered for individuals unresponsive to conventional treatments, such as those with dementia. Over the past decade, significant research has explored the potential of gene therapy in dementia, offering new hope for more effective treatments. However, several challenges remain in its practical application. One key challenge is developing safe and efficient gene delivery methods, as the brain's intricate structure and protective barriers present significant obstacles. Furthermore, ensuring the long-term expression and stability of therapeutic genes is crucial for sustained benefit. Future studies should focus on identifying genes implicated in different types of dementia, optimizing gene delivery systems, improving gene-targeting specificity, and conducting comprehensive clinical trials to assess the safety and efficacy of these therapies. Addressing these challenges could pave the way for novel treatment strategies, ultimately improving the quality of life for individuals with dementia.

As the global population continues to age, the prevalence of Parkinson's Disease (PD) is increasing. PD is the second most common neurodegenerative disorder, particularly among the elderly. Its key symptoms include tremors, shaking, movement difficulties, and challenges with balance and coordination. The disease is characterized by the loss of dopaminergic neurons in a specific part of the brain, the substantia nigra pars compacta, and the aggregation of the α-synuclein protein within cells. In recent years, research has highlighted the significant role of inflammatory processes in PD pathology. However, it remains unknown If neuroinflammation is a cause or consequence of PD. Strong evidence suggests that microglia, the resident immune cells in the central nervous system, play a crucial role in protecting neurons and that dysfunctional and overly activated microglia are present in the brains of individuals with PD. Under normal conditions, microglia are in a "homeostatic" state, but in response to disease-related triggers, they transition to a "reactive state." The transition of microglial phenotypes can result in either pro-inflammatory (M1) or anti-inflammatory (M2) states, each characterized by distinct markers and released substances. Prolonged activation of the M1 phenotype is associated with a range of inflammatory conditions, including neurodegenerative diseases such as Parkinson's disease. Consequently, further investigation into the role of microglia is essential for enhancing our understanding of and therapeutic approaches to PD. This review will delve into the involvement of microglia in the neurodegenerative process of PD and explore the impact of microglia-mediated inflammation on the disease.

Parkinson's disease (PD) represents a neurodegenerative condition where oxidative stress significantly contributes to its underlying pathology. Antioxidant agents may reduce neuronal degeneration.

This research explores the impact of hesperidin (HES) on the hippocampus's antioxidant capacity and cholinergic function as well as its effects on memory enhancement and offer neuroprotective benefits in a rat PD model elicited by reserpine (RES).

Forty male Wistar rats were assigned to five experimental groups: The control group, a group receiving HES vehicle (normal saline, NS) combined with RES vehicle (VR + NS), a group treated with RES (0.2 mg/kg for 13 days, intraperitoneally) along with NS (RES + NS), a group administered HES (100 mg/kg for 14 days, orally) plus RES vehicle (HES + VR), and finally the group receiving both RES and HES. Following treatment, assessments for catalepsy and memory were performed. The enzymatic activity within the hippocampus, specifically for catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), was measured employing the ELISA method. Simultaneously, the malondialdehyde (MDA) level was quantified employing the thiobarbituric acid assay, while we evaluated the activity of acetylcholinesterase (AChE) using the Ellman method in the hippocampus. Neuronal density in the hippocampal CA1 and CA3 regions was assessed using stereological techniques.

The results indicated a significant decrease in cataleptic behavior, AChE activity, and MDA levels, along with an increase in CAT, SOD, GPx, and neuronal density in both CA1 and CA3 regions, alongside enhancements in working and avoidance memory in the RES + HES group in relation to the RES + NS group. Also, HES inhibited the RES-elicited rise in AChE levels within the hippocampus.

Hesperidin enhances the hippocampus's antioxidant function, regulates cholinergic activity, and offers neuroprotection against RES-elicited motor-cognitive impairments.

Parkinson's disease (PD) is a chronic, progressive neurological disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra, a region of the brain responsible for motor control. Following Alzheimer's disease, Parkinson's is the second most prevalent neurodegenerative disorder. Despite the availability of various pharmacological treatments, these medications often exhibit side effects and may have varying efficacy and duration of action. To address the limitations of conventional therapies, this review aims to identify the most promising medicinal plants traditionally employed in the management of Parkinson's disease.

This review employed a comprehensive search strategy to identify relevant literature on the use of medicinal plants for Parkinson's disease. Authoritative scientific databases, including Web of Science, PubMed, Scopus, and Google Scholar, were systematically searched using the following keywords: 'medicinal plants,' 'traditional medicine,' 'Parkinson's,' and 'neurology.' Irrelevant articles were excluded from the review process.

Traditional Iranian medicine incorporates a diverse array of medicinal plants for the management of Parkinson's disease. Notable examples include Nigella sativa (black cumin), Boswellia serrata (frankincense), Thymus vulgaris (thyme), Hypericum perforatum (St. John's wort), Zingiber officinale (ginger), Heracleum persicum (Persian hogweed), Curcuma longa (turmeric), Cinnamomum verum (cinnamon), Olea europaea (olive), Camellia sinensis (tea), Prunus domestica (plum), Ficus carica (fig), Echium amoenum (Iranian borage), Prunus dulcis (almond), Lavandula angustifolia (lavender), and various Scutellaria species.

While medicinal plants may offer potential benefits as adjunctive therapies for Parkinson's disease, further research is warranted to establish their efficacy and safety. Current studies on these plants are limited in scope, and additional evidence is required to draw definitive conclusions regarding their role in the management of Parkinson's.

Context: 

Pesticides are widely used in agriculture and household settings and have been associated with various adverse health effects, including a potential link to neurodegenerative diseases (NDs). Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most common disorders in this category, characterized by progressive neuronal cell loss and severe impairments in human functioning. Epidemiological studies have shown significant associations between pesticide exposure—specifically organochlorines, organophosphates (OP), carbamates, DDT, and paraquat—and AD and PD; however, little is known about the underlying biological mechanisms.

Evidence Acquisition: 

A mini-review was conducted in the scientific literature on the biological mechanisms linking pesticide exposure to NDs using scientific databases (PubMed, Scopus, Web of Science, and Google Scholar).

In AD, the connection may involve several biological mechanisms, including hyperphosphorylation of tau protein, which disrupts normal cellular function and contributes to neurofibrillary tangles. Genetic polymorphisms in microtubule-associated protein tau (MAPT) can also influence an individual's susceptibility to AD by affecting tau protein interactions with microtubules. Moreover, exposure to pesticides has been linked to elevated pro-inflammatory markers that exacerbate neuroinflammation, further contributing to neuronal damage. In PD, oxidative stress plays a crucial role by generating reactive oxygen species that damage cellular components. Mitochondrial dysfunction resulting from pesticide exposure impairs energy production in neurons, leading to cell death. Additionally, exacerbation of α-synuclein aggregation is a critical factor in PD pathology, as aggregated forms of this protein are toxic to neurons.

Given the rapid increase of pesticides in the air, water, and food, it is essential to clarify the biological mechanisms linking pesticide exposure to NDs.

Parkinson's disease (PD) is one of the most common diseases of the central nervous system, primarily affecting the elderly. Its symptoms include tremors, slow movement, muscle stiffness (rigidity), and postural instability.This study aimed to investigate the effect of eight weeks of rebound therapy on balance and quality of life in people with PD. This was a quasi-experimental research study with pre-test and post-test. Among patients with PD, 24 individuals with severity levels 2 to 3 according to the Unified Parkinson Disease Rating Scale (UPDRS)  were selected using convenience and judgmental sampling and randomly divided into two groups: a rebound therapy group (n=12) and a control group (n=12). The Parkinson's Disease Quality of Life Questionnaire (PDQL) was used to evaluate quality of life levels. The Single Leg Stance (SLS) and Y-Balance Test (YBT-LQ) were used to evaluate static and dynamic balance, respectively. Theintervention group performed eight week exercises (two one-hour weekly sessions Data were analyzed using repeated measures ANOVA at a significance level of 0.05. The post-test quality of life scores in the rebound therapy group significantly higher than the pre-test scores, indicating an increase in quality of life (QoL) for patients (P ≤ 0.05). Additionally, patients' static and dynamic balance in the rebound therapy group significantly improved from the pre-test to the post-test (P ≤ 0.05). The results indicate that eight weeks of rebound therapy can effectively improve balance and quality of life in patients with PD. There fore rebound therapy can be recommended as a complementary rehabilitation method in medical centers to enhance the health of PD patients.

Parkinson's disease (PD) is the second most common cause of death among neurodegenerative diseases. The aim of the present study was to investigate and compare the effect of eight weeks of interval swimming training (IST) and motor enriched environment activity (MEEA) along with Artemisia (Ar) extract on serotonin and dopamine levels in the brain tissue of rats with PD.  In this experimental study, 42 male Sprague-Dawley rats (250–270 grams, 14–16 months old) were used, with PD induced using 2 mg/kg reserpine. They were divided into six groups: (1) Parkinson's disease control (Res), (2) IST, (3) MEEA, (4) Ar extract only, (5) IST+Ar, and (6) MEEA+Ar. In addition, in order to investigate the effect of Parkinson's disease induction on research variables, 7 healthy rats were selected as a healthy control group (HC).  The serotonin and dopamine levels were significantly higher in the IST, MEEA, Ar, IST+Ar, and MEEA+Ar groups compared to the Res group (P=0.001). Additionally, serotonin and dopamine levels were higher in the IST, MEEA, IST+Ar, and MEEA+Ar groups compared to the Ar alone group (P=0.001). In the IST+Ar and MEEA+Ar groups, dopamine levels were also significantly higher compared to the IST and MEEA groups (P=0.001).  IST, MEEA, and Ar extract, individually and in combination, appear to improve neurotransmitter levels. However, the combination of training and Ar, particularly with overload training principles, may exert more favorable effects on neurotransmitter levels under neurodegenerative conditions.

Parkinson's disease (PD) is a rapidly progressive neurodegenerative disease characterized by the gradual loss of dopaminergic (DA) neurons in the substantia nigra (SNpc) and reduced DA innervation in the striatum.

This study aimed to investigate the impact of rilmenidine on DA neurons in the SNpc using a rat model of PD induced by 6-hydroxydopamine.

A total of thirty Wistar rats were randomly assigned to three groups: Sham, lesion, and treatment. In each group, a behavioral evaluation utilizing apomorphine was conducted one week prior to surgery and repeated four weeks after the procedure. In the treatment group, 10 mg/kg rilmenidine was injected intraperitoneally four times a week after surgery. Microscopic examination of the SNpc was performed after the preparation of brain tissue blocks, Nissl staining, photography of slides, and counting of neurons. The number of rotations and neurons in the SNpc were analyzed after surgery using ANOVA and Tukey’s test. The number of rotations before and after surgery and the number of cells in the right and left hemisphere were compared using the paired t -test. The significance level was set at P ≤ 0.05.

The number of rotations significantly decreased, and the number of neurons in the SNpc significantly increased in the treatment group compared to the lesion group (P ≤ 0.001).

Rilmenidine can reduce the neuronal damage induced by 6-hydroxydopamine in the SNpc.

Parkinson's disease dementia (PDD) and Dementia with Lewy bodies (DLB) are two syndromes categorized under synucleinopathy, sharing comparable symptoms. The identification of biomarkers would offer an accurate approach for improved diagnosis, treatment, and monitoring of treatment efficacy for these distinct forms of dementia.

This study utilized spectral analysis and nonlinear dynamic analysis to compare electroencephalogram (EEG) characteristics between PDD and DLB patients. EEG data was collected from 30 PDD patients, 36 DLB patients, and 36 healthy subjects at rest. Following a conditioning phase to minimize noise and eliminate artifacts, we derived spectral and complexity features using Welch's method and sample entropy. Analysis of variance with repeated measures was performed to compare spectral features and nonlinear dynamics of brain activity between the groups.

Post hoc comparison showed that in the control group, the power of delta and theta bands was lower and the power of alpha and beta bands was higher than in patients with PDD and DLB. (P < 0.05). In the theta and alpha bands, the PDD group showed greater power than the DLB group (P < 0.05). Furthermore, there was a significant main effect of diagnosis (F = 4.67, P = 0.007), and also the diagnosis by region interaction for complexity values (F = 4.58, P = 0.009). Post hoc analysis showed that the EEG complexity of the control group was significantly higher than that of the PDD and DLB groups in the frontal, central, temporal and parietal regions (P < 0.05). Moreover, the EEG complexity of the PDD group was significantly higher than that of the DLB group in the central, temporal and parietal regions (P < 0.05).

Although both PDD and DLB had almost similar patterns compared to the control group, they showed differences in the EEG power spectrum and its nonlinear dynamics. Our findings indicated marked diffuse slowing and lower cortical complexity or activity in DLB patients compared to PDD in all regions, especially in the central, temporal and parietal areas.

Parkinson's disease (PD) poses a significant social burden. Zhengan Xifeng Decoction has been widely used in the treatment of PD.

The aim of this study was to evaluate the clinical efficacy and safety of Zhengan Xifeng Decoction combined with Western medicine in the treatment of PD.

Five independent databases were searched for clinical randomized controlled trials on Zhengan Xifeng Decoction combined with Western medicine for the treatment of PD. The risk of bias and quality of the included studies were assessed, followed by a meta-analysis.

A total of 21 studies, including 1678 patients, were included in the meta-analysis. The results suggested that the combination of Zhengan Xifeng Decoction and Western medicine demonstrated clinical efficacy in the treatment of PD [OR = 6.36, 95% confidence interval [CI] (4.70, 8.60), Z = 11.99 (P < 0.00001)] and reduced Unified Parkinson's Disease Rating Scale (UPDRS) scores [mean difference (MD) = -5.50, 95% CI (-6.93, -4.08)]; UPDRS I, II, III scores [MD = -4.87, 95% CI (-7.27, -2.47)]; UPDRS II, III scores [MD = -7.18, 95% CI (-15.71, -1.35)]; UPDRS I scores [MD = -0.15, 95% CI (-0.27, -0.03)]; UPDRS II scores [MD = -1.62, 95% CI (-2.42, -0.82)]; UPDRS III scores [MD = -2.14, 95% CI (-3.91, 0.38)]; and UPDRS IV scores [MD = -0.40, 95% CI (-0.79, -0.01)]. The differences between the groups were statistically significant (P < 0.05).

Zhengan Xifeng Decoction combined with Western medicine demonstrates improved clinical efficacy in the treatment of PD, and patients tolerate adverse events well.

The physical and psychological symptoms of Parkinson's disease can disrupt patients' social lives, leading them to withdraw from social situations.

The objective of the present study is to identify the social needs and priorities of patients with Parkinson's disease from the perspectives of patients, family caregivers, and health care providers.

The present study employed a qualitative content analysis method to collect data to identify the needs of patients with Parkinson's disease. Semi-structured interviews were conducted with 28 participants using a purposive sampling strategy with maximum diversity in Tehran in 2023. Data analysis was performed using the conventional content analysis approach based on Granheim and Lundman's model. A two-stage Delphi technique was used to identify patients' priorities with 53 participants.

The 28 participants included 11 patients (7 male, 4 female, mean age = 66.27), 11 family caregivers (7 daughters, 3 spouses, 1 son, mean age = 43.81), 4 nurses, and 2 physicians. Three main categories and 12 subcategories were extracted. In the category of "Interactionism by leaving unwanted isolation," the subcategories identified were maintaining and promoting social interactions, maintaining aspects of the job and continuing some professional skills, voluntary membership in groups and institutional participation, and participation in social activities. The category "Continuity of healthcare services delivery" included four subcategories: Continued access to movement disorder specialists, access to coordinated multidisciplinary services, access to supporting organizations and associations, and appropriate insurance coverage. The category "Individual-oriented and community-oriented advocacy programs" included four subcategories: Financial support, social belonging and effective communication, self-care, and comprehensive education programs with multiple target groups. The prioritization was completed after two Delphi steps with a high agreement of 86.90% from 16 patients, 14 family caregivers, and 23 health care providers from eight disciplines.

The results of the study show that patients with Parkinson's disease experience various social needs. Since the nature of Parkinson's disease affects social interactions, patients and their caregivers view social interactions as the missing link to addressing their social needs. Meanwhile, health care providers prioritize educating patients and families and holding specialized Parkinson's disease courses. Policymakers should consider necessary social support programs for these patients and focus on the specialized training of healthcare providers in the field of Parkinson's disease, in addition to providing appropriate care, support, and social services.

In Parkinson's disease (PD), mitochondrial defects and oxidative stress cause an increase in free radicalsand the death of dopaminergic neurons in the substantia nigra. By preventing lipid peroxidation and protecting againstperoxide radicals, vitamin E is the most important antioxidant of biological membranes that can neutralize free radicals.Also, the improvement of the functional status of mitochondria can be influenced by exercise, which can be partially theresult of changes in the mitochondrial mitophagy and dynamics system. This study aimed to investigate the interactiveeffects of six weeks of vitamin E (VE) consumption and training on the mitochondrial function [Cytochrome C (Cyt-C),Adenosine triphosphate (Atp) synthase, optical atrophy1 mitochondrial dynamics like guanosine triphosphatase(GTPase), 8-Oxodequanosin and Pten induced kinase 1 (Pink1) is a protein coding gene] in the hippocampus tissueof PD rats. In this experimental study, 4-6-month-old Sprague-Dawley rats (mean weight 250 ± 30 g)were given parkinsonism with reserpine (2 mg/kg) and were categorized into different groups, including healthy (H),PD, VE solvent+PD (Sham), aerobic exercise+PD (AE+PD), VE+PD, AE+VE+PD. The aerobic training program wascarried out for six weeks and 5 sessions per week and each session lasted 15-22 minutes. VE was also taken orallyat 30 mg/kg daily. A six-week regimen of VE supplement along with the AE significantly reduced the Cyt-C gene expression level,also we observed a significant increase in gene expression level of the Pink1, Atp synthase and Opa1 (P<0.05). There is nosignificant difference was found in the level of 8-Oxog detected in hippocampal tissue samples (P>0.05). The consumption of VE along with AE may provide therapeutic effects on mitochondrial damage in PD rats.

Parkinson’s disease (PD) is a widely prevalent neurodegenerative disorder in the central nervous system, predominantly affecting older adults and frequently coexisting with other health conditions. The heightened vulnerability of individuals with chronic diseases and advanced age to adverse outcomes during the COVID-19 pandemic suggests an increased risk of COVID-19 infection in PD patients.

This cross-sectional study, conducted from July to September 2021, aimed to evaluate the impact of COVID-19 on PD patients by examining infection rates, associated complications, and outcomes.

We utilized hospital records to reach out to 567 PD patients during the designated timeframe. If a patient had passed away, their families were contacted to ascertain whether COVID-19 was a contributing factor.

Among the 558 PD patients who participated, 25.4% were tested for COVID-19, with 42.2% of those tested returning positive results. Significantly, 34.4% of the positive cases required oxygen therapy, 32.8% were admitted to the hospital, and 9.8% needed intensive care unit (ICU) admission. The prevalence of COVID-19 among the families of the patients was 29.8%, with 13.7% requiring hospitalization and 4.2% resulting in death. Common complications included worsening of movement issues (21.3%), weight loss (19.7%), and urinary problems (14.8%). Early-onset Parkinson’s was associated with a decreased risk of COVID-19 (OR: 0.976, 95% CI: 0.953 - 0.999, P = 0.037), whereas the use of Levodopa was linked to an increased risk of infection (OR: 3.672, 95% CI: 1.095 - 12.31, P = 0.037).

This study underscores the changing clinical manifestations of PD during the COVID-19 pandemic. Further research is crucial to clarify the complex interaction between COVID-19 and Parkinson’s disease.