Non-motor Symptoms Research Articles

Parkinson’s Disease: Biomarkers for Diagnosis and Disease Progression

Parkinson’s disease (PD) is a progressive neurological disease that causes both motor and nonmotor symptoms. While our understanding of putative mechanisms has advanced significantly, it remains challenging to verify biomarkers with sufficient evidence for regular clinical use. Clinical symptoms are the primary basis for diagnosing the disease, which can be mild in the early stages and overlap with other neurological disorders. As a result, clinical testing and medical records are mostly relied upon for diagnosis, posing substantial challenges during both the initial diagnosis and the continuous disease monitoring. Recent biochemical, neuroimaging, and genetic biomarkers have helped us understand the pathophysiology of Parkinson’s disease. This comprehensive study focuses on these biomarkers, which were chosen based on their relevance, methodological excellence, and contribution to the field. Biochemical biomarkers, including α-synuclein and glial fibrillary acidic protein (GFAP), can predict disease severity and progression. The dopaminergic system is widely used as a neuroimaging biomarker to diagnose PD. Numerous genes and genome wide association study (GWAS) sites have been related to the development of PD. Recent research on the SNCA gene and leucine-rich repeat protein kinase 2 (LRRK2) has shown promising results. By evaluating current studies, this review intends to uncover gaps in biomarker validation and use, while also highlighting promising improvements. It emphasizes the need for dependable and reproducible indicators in improving PD diagnosis and prognosis. These biomarkers may open up new avenues for early diagnosis, disease progression tracking, and the development of personalized treatment programs.

Correlation between blepharospasm and psychological diseases: the anxiety, depression and sleep disorder study

AIM: To investigate the relationship between benign essential blepharospasm (BEB) symptoms and depression/anxiety/sleep disorder in a prospective manner and to determine whether treatment the BEB with botulinum toxin type A (BoNT/A) can impact psychological symptoms. METHODS: This prospective interventional case series recruited 61 adults with evidence of BEB. Patients were administered the Jankovic Rating Scale (JRS), the Blepharospasm Disability Index (BSDI), Personal Health Questionnaire Depression Scale (PHQ-8), Generalized Anxiety Disorder 7-item scale (GAD-7) and the Athens insomnia scale (AIS) to evaluate the severity of BEB symptoms, depression, anxiety and sleep disorder before and 1wk, 1, 3mo after the BoNTA treatment. Statistical analysis was performed to assess the relationships between changes in the survey scores. RESULTS: The mean score for JRS, BSDI, PHQ-8, and GAD-7 improved significantly (P<0.0001), respectively, compared to the initial visit at follow-up. At baseline, worse BSDI scores were correlated with worse GAD-7 and PHQ-8, but not with worse AIS. At 1mo follow-up visit, there was no correlation between change in BSDI and PHQ-8/AIS, the change in GAD-7 showed a mild association with change in BSDI. The change in BSDI was correlated with the change in both PHQ-8 and GAD-7 in the subgroup of patients without a prior diagnosis of depression or anxiety. Patient satisfaction with BoNT/A treatment reached the highest at 1mo of follow-up (83.6%, 51/61). CONCLUSION: BEB may lead to psychological diseases. BoNT/A can significantly improve motor and non-motor symptoms of BEB, which emphasize the effectiveness of BoNT/A and therefore pave the way for its use in the field of psychiatry. However, further research is needed to confirm these findings and understand the underlying mechanisms.

Opposite effects of low and high frequency deep brain stimulation of lateral hypothalamus on arousal and temperature in a monkey pilot study.

Deep brain stimulation is a well-established treatment for improving motor symptoms in Parkinson's disease. However, persistent non-motor symptoms, such as excessive daytime sleepiness, remain a significant challenge and necessitate further investigation. In this study, we conducted repeated measurements of daytime sleepiness using a modified multiple sleep latency test in a healthy monkey (macaca fascicularis), which was later rendered parkinsonian through MPTP administration. Deep brain stimulation targeting the lateral hypothalamic area revealed frequency-dependent modulation of both sleepiness level and core body temperature. High-frequency stimulation (80Hz) increased sleepiness in the healthy state, while low-frequency stimulation (20Hz) promoted wakefulness in the parkinsonian state. These findings suggest a promising therapeutic approach for addressing sleep/wake disturbances, not only in Parkinson's disease but also in other severe sleep disorders.

The microbiota-gut-brain axis: a potential target in the small-molecule compounds and gene therapeutic strategies for Parkinson's disease.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by motor symptoms and non-motor symptoms. It has been found that intestinal issues usually precede motor symptoms. Microorganisms in the gastrointestinal tract can affect central nervous system through the microbiota-gut-brain axis. Accumulating evidence has shown that disturbances in the microbiota-gut-brain axis are linked with PD. Thus, this pathway appears to be a promising therapeutic target for treatment of PD. In this review, we mainly described gut dysbiosis in PD and their underlying mechanisms for mediating neuroinflammation and peripheral immune response in PD pathology and futher discussed the potential small-molecule compounds and genic therapeutic strategies targeting the microbiota-gut-brain axis and their applications in PD. Studies have found that some small molecule compounds and alterations of inflammation-related genes can improve the motor and non-motor symptoms of PD by improving the microbiota-gut-brain axis, which may provide potentially beneficial drugs and molecular targets for the therapies of PD.

Exploring the Impact of Parkinson's Disease on Driving: A Population-Based Survey.

Persons with Parkinson's disease (PD) experience progressive motor and non-motor symptoms which may influence their ability to drive a car. This is experienced as a massive challenge by many affected individuals, for whom being able to drive a car is vital to maintain functional independence. We assessed how the diagnosis of PD affected the possession of a driving license, how people with PD had adapted their driving style, and to what extent they had communicated about their driving ability with their healthcare professionals. We also evaluated their knowledge on insurance- and Driver and Vehicle Licensing Agency (DVLA)-related implications. A cross-sectional 10-item survey was completed by 540 participants of a population-based cohort of persons with PD in the Netherlands (PRIME-NL study). Participants had a mean age of 70 years and disease duration of 7.3 years. 84% possessed a valid driving license. Of those who gave up their license, this was done mostly (78%) on a voluntarily basis. Forty percent of those with a driving license adjusted their driving style. Over 50% of respondents had not discussed the impact of PD on their driving ability with their healthcare professionals. Although not compulsory by Dutch law, 52% of the respondents had informed the DVLA about their diagnosis. This study highlights the need for information and support from healthcare professionals to proactively address driving in their clinical practice. This will help persons with PD in their efforts to maintain their driving license for as long as possible.

The effects of free dance versus hatha yoga on quality of life and motor and non-motor symptoms in people with Parkinson's disease: protocol study for a randomized clinical trial

Objective: To describe a protocol comparing the effects of free dance, hatha yoga, and a control group on quality of life, motor and non-motor symptoms in people with Parkinson's disease (PwP). Methods: This is a randomized three-arm study. Inclusion criteria will be people with clinically diagnosed Parkinson's disease (PD), ≥ 45 years old, and in stages I to IV of the Hoehn and Yahr Disability Scale (HY). Who do not reach the cut-off point of the Montreal Cognitive Assessment (MoCA) and classified in stage V of the HY will be excluded. The interventions will last 60 minutes, twice a week, progressing from light to vigorous intensity. The primary outcome will be quality of life assessed by the Parkinson's Disease Questionnaire (PDQ39). Secondary outcomes will include the Unified Parkinson's Disease Rating Scale (UPDRS), the evaluation of motor and physical function such as shoulder and hip range of motion (goniometer), cardiorespiratory fitness (six-minute walk test), balance (MiniBESTest), as well as non-motor aspects such as anxiety (Beck Anxiety Inventory), self-esteem (Rosenberg Self-Esteem Scale), cognition (MoCA), hope (Herth Hope Scale), fecal incontinence (Fecal Incontinence Quality of life), urinary incontinence (International Consultation on Incontinence Questionnaire - Short Form), and depressive symptoms (Beck Depression Inventory). Data will be collected at baseline and post-intervention. Discussion: If study interventions are deemed effective compared to standard of care (i.e. control group), the present study will advance current knowledge on non-pharmacological therapeutic strategies for People with Parkinson. Study registered RBR-54s92mh on 02/29/24.

Anxiety, memory, and social impairments in the YAC128 mouse model of Huntington’s disease

Background Huntington’s disease (HD) is an autosomal dominant hereditary disorder, caused by an expansion of polyglutamine in the huntingtin protein. HD is characterized by a progressive decline in motor functions. This decline includes involuntary movements (chorea) and the worsening of controlled motions caused mainly by neuronal dysfunction in the striatum. In addition to the deterioration of motor symptoms, HD patients also suffer from cognitive changes, mood swings, apathy, depression, outbursts of anger, psychosis, and social withdrawal. Objective A comprehensive examination of cognitive, affective, and social changes in the HD mouse model is required for the development of combined therapy for both motor and non-motor deficits in HD. Methods The behavioral tests for anxiety, memory, and social traits were used in this study. Results YAC128 HD transgenic mice exhibited anxiolytic behavior in the novel brightly illuminated environment of the open field and light-dark place preference tests. Moreover, YAC128 HD mice also suffered from a decline in their recognition memory during the novel object recognition test. YAC128 HD mice demonstrated reduced exploration interest during the open field with a non-social target as well as during the first day of the three-chamber social test. Social interaction was also impaired in YAC128 HD mice as it was shown in the social interaction with resident intruder test. Conclusions YAC128 HD mouse model may be used as a model system to test the possible treatments for both motor and non-motor symptoms including memory loss, agitation and social withdrawal.

The Present Difficulties and Potential Benefits of Dopaminergic Agents in Parkinson's Disease Treatment

Parkinson's disease (PD) is a progressive neurological condition characterized by bradykinesia, rigidity, tremors, and impaired balance, among other motor impairments. The issue arises from dopaminergic neurons located in the spinal column of the brain. This research report examines the therapeutic potential of dopaminergic medications in the management of Parkinson's disease. The central concept of Parkinson's disease (PD) revolves around the notion that dopaminergic pathways exert significant influence over the regulation of movement. The book examines various dopaminergic medications, elucidating their mechanisms of action and the impact they exert on dopamine signaling. Examples of these medications include levodopa, dopamine agonists, and monoamine oxidase-B (MAO-B) inhibitors. Although dopaminergic medicines initially aid in the treatment of Parkinson's disease (PD), prolonged usage of these medications gives rise to several complications. Experiencing dyskinesias and motor fluctuations, characterized by episodes of involuntary movements and behaviors that are undesired, is a significant challenge. This study investigates the underlying causes of these difficulties and explores potential treatment options, including the use of controlled-release formulations and further therapy. The book discusses the non-motor symptoms of Parkinson's disease (PD), as well as the use of dopaminergic medications to treat mood disorders, autonomic dysfunction, and cognitive loss. Dopaminergic medications remain crucial in reducing motor symptoms and enhancing the quality of life for those with Parkinson's disease. Parkinson's disease (PD) is a complex condition with multiple distinct variations. In order to address its existing challenges and explore its potential implications for future Parkinson's disease medications, a comprehensive and effectively coordinated strategy is required.

Clinical features and progression of Parkinson's disease with LRRK2 variants: A prospective study.

We established a prospective cohort study to investigate the differences in motor and non-motor symptoms between idiopathic Parkinson's disease (IPD) and Parkinson's disease in carriers of leucine-rich repeat kinase 2 (LRRK2) gene risk variants (LRRK2-PD). The study included 1407 individuals with IPD and 649 individuals with LRRK2-PD (comprising 304 with LRRK2-G2385R, 220 with LRRK2-R1628P, and 105 with LRRK2-A419V). Differences in symptoms between LRRK2-PD and IPD were analyzed using LCMM modeling and Cox regression analysis. The LRRK2-G2385R variant showed slower progression in tremor symptoms and excessive daytime sleepiness compared with IPD. In contrast, symptoms associated with LRRK2-R1628P and LRRK2-A419V were more similar to those of IPD. Survival analysis revealed that LRRK2-PD does not affect life expectancy compared with IPD. Our extended longitudinal follow-up of LRRK2-PD in the Chinese population provided valuable insights, further confirming the clinical characteristics of the three LRRK2 variants.

Novelty Seeking in Parkinson’s Disease: A Candidate Biomarker for Cognitive Changes

Background: Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by motor impairments, cognitive decline, and affective changes. Beyond the well-described motor symptoms, neuropsychiatric symptoms play a crucial role in PD disability burden. Novelty seeking, a trait extensively studied within various models of personality, may influence the manifestation of these non-motor symptoms. Methods: A narrative review of articles determined relevant by the author(s) was undertaken. Results: The literature indicates that PD patients typically exhibit low novelty seeking initially. However, dopaminergic therapies can increase novelty-seeking behaviors, sometimes leading to impulse control disorders (ICD). Studies using the Temperament and Character Inventory (TCI) suggest a complex interplay between disease state, medication, and baseline personality, which is not fully elucidated. High novelty seeking scores predict a higher risk of ICDs, yet they also correlate with a more benign clinical phenotype and improved quality of life post-DBS surgery. Conclusions: Novelty seeking is a significant trait in PD, influencing non-motor symptoms and treatment responses. Understanding its neurobiological basis and clinical implications could lead to better diagnostic and therapeutic strategies through the use of objective, practical tools for disease monitoring, individualized therapy, and pharmacological development.

Changes in brain functional connectivity between on and off states and their relationship with cognitive impairment in Parkinson’s disease

Parkinson’s disease (PD) is characterized by motor and non-motor symptoms. Cognitive decline is crucial in disease progression and affect quality of life; however, their underlying mechanisms in PD remain unclear. We explored the relationship between cognitive impairment and functional connectivity (FC) using resting-state functional magnetic resonance imaging in 26 patients with sporadic PD, focusing on the changes in FC between on and off states. Cognitive function was assessed using the Mini-Mental State Examination (MMSE) score. The correlation between MMSE scores and changes in FC values during on and off states was assessed using Pearson’s correlation coefficient. The correlation between changes in FC during the on and off periods and cognitive function differed for each cognitive function item. MMSE memory scores were positively correlated with FC between the brainstem and the left cerebral hemisphere. MMSE attention scores were positively correlated with FC between the bilateral thalamus and frontal lobes and negatively correlated with FC between the left cerebral hemispheres. These findings may facilitate our understanding of the neural correlates underlying cognitive impairment in PD and help develop treatment strategies to preserve cognitive function.

Intersection of Sleep Disorders and Parkinson Disease: Unveiling the Bidirectional Relationship.

Patients with Parkinson's Disease (PD) frequently exhibit non-motor symptoms, particularly sleep disturbances. Sleep disorders in PD patients are intricately linked to the pathogenesis and progression of PD itself, exacerbating neurodegenerative processes and worsening patient quality of life. This review underscores the significance of sleep disorders in PD, highlighting their prevalence, impact on disease progression, and the bidirectional relationship between sleep disruption and neurodegeneration. It aims to enhance clinician awareness for better diagnosis and management of sleep-related comorbidities in PD. A comprehensive literature search was conducted in PubMed and Scopus using key terms such as "sleep disorders", "Parkinson's disease", "REM sleep behavior disorder", "restless legs syndrome", "insomnia", "obstructive sleep apnea", "excessive daytime sleepiness", "circadian rhythm disorders", "sleep and neurodegeneration". Sleep disorders are prevalent in PD affecting up to 90% of patients. Conditions such as insomnia, REM sleep behavior disorder, restless legs syndrome, obstructive sleep apnea, excessive daytime sleepiness, and circadian rhythm disorders are commonly reported. These disorders are linked to multifactorial biological mechanisms and are associated with more severe disease phenotypes. Of note, several evidence shows that sleep abnormalities may contribute to neuroinflammation and neurodegeneration, further accelerating the disease course. Sleep disturbances are critical non-motor symptoms in PD. Early diagnosis and tailored management of sleep disorders are essential for improving clinical outcomes and potentially offering neuroprotective benefits.

Clinical and cognitive features associated with psychosis in Parkinson's disease: a longitudinal study

BackgroundParkinson's disease psychosis (PDPsy) is associated with increased nursing home placement and mortality and is closely linked with cognitive dysfunction.ObjectiveAssess the clinical and cognitive features associated with PDPsy in patients without dementia.MethodsWe prospectively recruited people with Parkinson's disease (PwP) without dementia for a 3-year, longitudinal study at an outpatient movement disorders clinic. Participants completed annual visits involving assessment of motor and non-motor symptoms including neuropsychological testing. PDPsy was defined as the recurring presence of visual illusions, sense of presence, hallucinations, or delusions for at least 1 month. Using generalized estimating equations, we conducted two sets of analyses to separately assess the clinical and the cognitive predictors of PDPsy.ResultsWe enrolled 105 participants. At baseline, mean age was 67.8 (SD = 8.0), median disease duration was 4.9 years (IQR: 3.4–7.7), and mean MoCA was 24.8 (SD = 2.3). Prevalence of PDPsy increased over 3 years from 31% (n = 32) to 39% (n = 26). Forty-five participants (43%) experienced PDPsy. Visual illusions were most common (70%, n = 84), followed by hallucinations (58.3%, n = 70). In multivariate analysis, of the clinical variables, only depressive symptoms [OR 1.09, 95% CI: (1.03, 1.16), p = 0.004] increased the odds of PDPsy; of the cognitive variables, only Trail Making Test B-A scores [OR 1.43, 95% CI: (1.06, 1.93), p = 0.018] significantly increased the odds of PDPsy.ConclusionsIn PwP without dementia, depressive symptoms were associated with increased risk of PDPsy. Executive/attentional dysfunction was also associated with PDPsy and may mark the transition from isolated minor hallucinations to more complex psychotic symptoms.

Parkinson's Disease: Unravelling the Medicinal Perspectives and Recent Developments of Heterocyclic Monoamine Oxidase-B Inhibitors.

Parkinson's disease is a neurodegenerative condition characterized by slow movement (bradykinesia), tremors, and muscle stiffness. These symptoms occur due to the degeneration of dopamine- producing neurons in the substantia nigra region of the brain, leading to reduced dopamine levels. The development of Parkinson's Disease (PD) involves a combination of genetic and environmental factors. PD is associated with abnormal regulation of the monoamine oxidase (MAO) enzyme. Monoamine oxidase inhibitors (MAOIs) are an important class of drugs used to treat PD and other neurological disorders. In the early stages of PD, monotherapy with MAO-B inhibitors has been shown to be both safe and effective. These inhibitors are also commonly used as adjuncts in long-term disease management, as they can improve both motor and non-motor symptoms, reduce "OFF" periods, and potentially slow disease progression. However, current MAO-B inhibitors come with side effects like dizziness, nausea, vomiting, light-headedness, and fainting. Therefore, accelerating the development of new MAO-B inhibitors with fewer side effects is crucial. This review explores natural compounds that may inhibit monoamine oxidase B (MAO-B), focusing on key findings from the past seven years. It highlights the most effective heterocyclic compounds against MAO-B, including thiazolyl hydrazone, pyridoxine-resveratrol, pyridazine, isoxazole, oxadiazole, benzothiazole, benzoxazole, coumarin, caffeine, pyrazoline, piperazine, piperidine, pyrrolidine, and morpholine derivatives. The review covers in vitro, in silico, and in vivo data, along with the structure- activity relationship of these compounds. These findings offer valuable insights for the development of more effective MAO-B inhibitors and advancements in Parkinson's disease research.

Botulinum Toxin Effects on Freezing of Gait in Parkinson’s Disease: A Systematic Review

Freezing of gait is a frequent phenomenon and can be one of the most debilitating motor impairments in Parkinson’s disease, especially in the advanced stages. It is currently defined as a brief episodic absence or any marked reduction in the forward progression of the feet, despite the intention to walk. Greater severity of freezing of gait has been associated with more frequent falls, postural instability, and executive dysfunction. However, botulinum neurotoxin is one of the most widely administered therapies for motor and non-motor symptoms, including freezing of gait, in parkinsonism. To date, the literature has had conflicting results on the use of botulinum toxin in the treatment of freezing of gait in Parkinson’s disease patients. In light of this, we reviewed the findings of past studies that specifically investigated the effects of botulinum toxin on freezing of gait in Parkinson’s disease in order to better understand this issue.

The Parkinson's disease DJ-1/PARK7 gene controls peripheral neuronal excitability and painful neuropathy.

Parkinson's disease is a progressive neurodegenerative disease with well-documented motor symptoms as well as less recognised, but significant, non-motor symptoms. These non-motor symptoms include prodromal pain and peripheral neuropathy, the causes of which are unknown. We investigated the role of DJ-1/PARK7, a Parkinson's disease-associated gene, in prodromal pain and peripheral neuropathy. Using DJ-1 deficient mice, we conducted comprehensive sensory tests, cutaneous staining, molecular analyses and electrophysiological studies on mouse and human primary sensory neurons from dorsal root ganglia. We found that these mice exhibited cold hypersensitivity, oxidative stress, and neuropathy of the cutaneous fibres of primary sensory neurones before any motor impairments were observed. Mechanistically, DJ-1 in primary sensory neurones regulated this hypersensitivity and neuropathy via TRPA1 signalling. Interestingly, we discovered that DJ-1 also plays a role in the progression of chemotherapy-induced peripheral neuropathies. Pain and mechanisms associated with these neuropathies were exacerbated in DJ-1 deficient mice but were significantly reduced by the pharmacological activation of DJ-1. Importantly, we also confirmed the expression of DJ-1 and its therapeutic potential in human primary sensory neurons. Thus, we uncover a peripheral mechanism of DJ-1 and propose that it may serve as a new target for developing therapeutic approaches for Parkinson's disease-linked and other painful neuropathies.

High correlation of quantitative susceptibility mapping and echo intensity measurements of nigral iron overload in Parkinson's disease.

Quantitative susceptibility mapping (QSM) and transcranial sonography (TCS) offer proximal evaluations of iron load in the substantia nigra. Our prospective study aimed to investigate the relationship between QSM and TCS measurements of nigral iron content in patients with Parkinson's disease (PD). In secondary analyses, we wanted to explore the correlation of substantia nigra imaging data with clinical and laboratory findings. Eighteen magnetic resonance imaging and TCS examinations were performed in 15 PD patients at various disease stages. Susceptibility measures of substantia nigra were calculated from referenced QSM maps. Echogenicity of substantia nigra on TCS was measured planimetrically (echogenic area) and by digitized analysis (echo-intensity). Iron-related blood serum parameters were measured. Clinical assessments included the Unified PD Rating Scale and non-motor symptom scales. Substantia nigra susceptibility correlated with echogenic area (Pearson correlation, r = 0.53, p = 0.001) and echo-intensity (r = 0.78, p < 0.001). Individual asymmetry indices correlated between susceptibility and echogenic area measurements (r = 0.50, p = 0.042) and, more clearly, between susceptibility and echo-intensity measurements (r = 0.85, p < 0.001). Substantia nigra susceptibility (individual mean of bilateral measurements) correlated with serum transferrin saturation (Spearman test, r = 0.78, p < 0.001) and, by trend, with serum iron (r = 0.69, p = 0.004). Nigral echogenicity was not clearly related to serum values associated with iron metabolism. Susceptibility and echogenicity measurements were unrelated to PD duration, motor subtype, and severity of motor and non-motor symptoms. The present results support the assumption that iron accumulation is involved in the increase of nigral echogenicity in PD. Nigral echo-intensity probably reflects ferritin-bound iron, e.g. stored in microglia.

New insights on the link between Epstein‑Barr virus infection and cognitive decline in neurodegenerative diseases (Review).

Cognitive decline is a frequent complaint in healthy controls and neurological patients, regardless of the underlying pathology. Whilst cognitive impairment can be easily diagnosed in the more advanced stages of neurodegenerative diseases, early detection can be challenging. This is mainly the consequence of the incomplete understanding of the underlying pathophysiological mechanisms. In addition, currently available neurological treatments do not specifically target cognitive decline, since other motor and non-motor symptoms, such as bradykinesia, tremor, autonomic disturbances and depression, are of greater relevance from a therapeutic perspective. In this context, prospective studies must address a number of issues, including the risk factors associated with cognitive deficits in neurodegenerative diseases. The present review aims to offer a novel perspective on the association between Epstein-Barr virus infection and cognitive decline found in patients with neurodegenerative disorders. Specifically, relevant epidemiological studies and clinical trials explaining this connection were reviewed, focusing on the most frequent neurodegenerative disorders. They are namely Alzheimer's disease, Parkinson's disease and multiple sclerosis. Despite their limitations, possible underlying pathophysiological mechanisms that explain the impact of Epstein-Barr virus infection on cognitive decline are expected to offer novel study directions on this clinically relevant topic.

Advancements in Autologous Stem Cell Transplantation for Parkinson's Disease.

Parkinson's disease (PD) is a progressive neurodegenerative disease marked by comparatively focal dopaminergic neuron degeneration in the substantia nigra of the midbrain and dopamine loss in the striatum, which causes motor and non-motor symptoms. Currently, pharmacological therapy and deep brain stimulation (DBS) are the primary treatment modalities for PD in clinical practice. While these approaches offer temporary symptom control, they do not address the underlying neurodegenerative process, and complications often arise. Stem cell replacement therapy is anticipated to prevent further progression of the disease due to its regenerative capacity, and considering the cost of immunosuppression and the potential immune dysfunctions, autologous stem cell transplantation holds promise as a significant method against allogeneic one to treat Parkinson's disease. In this review, the safety concerns surrounding tumorigenicity and complications associated with transplantation are discussed, along with methods utilized to evaluate the efficacy of such procedures. Subsequently, we summarize the preclinical and clinical studies involving autologous stem cell transplantation for PD, and finally talk about the benefits of autologous stem cell transplantation against allogeneic transplants.

Choroidal thickness in the eyes of Parkinson's disease patients measured using optical coherence tomography: A systematic review and meta-analysis

BackgroundParkinson's disease (PD) presents a complex etiology involving genetics and environmental factors. Non-motor symptoms often precede motor manifestations. Dopaminergic neuron degeneration, oxidative stress, and vascular changes characterize PD. Retinal changes are studied as potential biomarkers, yet choroidal involvement remains unclear. This review aims to clarify choroidal thickness's role in PD progression for diagnostic advancements. MethodsWe examined PubMed, Scopus, and Embase databases. Depending on the heterogeneity, an appropriate model was used for the meta-analysis. Additionally, meta-regression, publication bias, subgroup analyses, and quality evaluation were carried out. ResultsWe evaluated twelve studies involving 442 PD patients and 608 healthy controls. This study found insignificant differences in choroidal thickness between PD patients and healthy controls. ConclusionChoroidal thickness is influenced by age, axial length, and intraocular pressure, with PD potentially impacting thickness through neurodegenerative mechanisms. However, inconsistencies exist in the findings, warranting further investigation. Future studies should explore the impact of disease severity, medication effects, and other confounding variables on choroidal thickness in PD patients. Additionally, advanced imaging modalities like optical coherence tomography angiography (OCTA) may provide more comprehensive evaluations of choroidal vascular changes in PD.