Progressive Neurological Disorder Research Articles

Psilocybin-assisted psychotherapy for Parkinson's disease without depression: A case-report

Background Psychedelic assisted psychotherapy (PAP) can improve treatment-resistant depression. Its usefulness in Parkinson's disease (PD) is unknown. PD patients may have problems adjusting to their chronic progressive neurological disease. A change from emotional avoidance to acceptance has been reported following psilocybin administration in patients with treatment-resistant depression. Objective To report for the first time the effect of psilocybin in a PD patient. Methods A non-depressed 43-year-old female with a 2-year history of PD presented with difficulty adjusting to PD, anxious ruminations and pessimism. The patient declined an increase in dopaminergic medication or the introduction of an anxiolytic. Therapeutic patient education was not beneficial. The patient received four sessions of high-dose PAP within one year. Neurological and psychiatric assessments were performed before and at one year follow-up using qualitative interviews and quantitative assessment of motor status, dispositional optimism, depression, anxiety, apathy, and well-being. Results PAP was well tolerated. It significantly improved the patient's overall pessimistic outlook on her future and decreased her anxious ruminations and worries about potential handicap due to PD. Her general well-being improved, as well as all psychometric scores except for the apathy scale. Motor status remained unchanged. Better acceptance of PD allowed her to accept pharmacological treatment adjustment. Conclusions PAP could be a safe and useful treatment for PD patients with dispositional pessimism and difficulties accepting their disease by promoting profound decentration from habitual thoughts and emotions, improving mood and PD acceptance. Randomized, controlled studies are needed to confirm this result.

Time of the Day of Traumatic Brain Injury has Minimal Effects on Behavioral and Histological Outcomes in Mice of Both Sexes.

Transcription of > 50% of the mammalian coding genes follows circadian rhythm in an organ-specific manner. Recent findings highlighted the influence of time of the day in the progression of various neurological diseases and therapies. In the present study, we evaluated the effect of time of occurrence of traumatic brain injury (TBI) on behavioral and neuropathological outcomes in mice of both sexes. Following a controlled cortical impact injury induced between Zeitgeber time (ZT)1-4 or ZT13-16, behavioral deficits and brain damage were evaluated. There were no significant differences in post-TBI motor function between groups ZT1-4 and ZT13-16 in either male or female mice compared with the sex-matched naïve control. TBI-induced anxiety-like behavior was significantly higher in the female ZT13-16 cohort compared to the naïve cohort; but, no difference was observed between injured groups in both sexes. Similarly, spatial learning and memory were not significantly different between the ZT1-4 and ZT13-16 groups in both sexes. Post-TBI cortical lesion volume was also not significantly different between ZT1-4 and ZT-13-16 groups in both sexes. The present study observed no significant effects of occurrence time on TBI-induced brain damage or behavioral deficits in male and female mice.

Remote neurodegeneration in the lumbosacral cord one month after spinal cord injury: a cross-sectional MRI study.

To characterize structural integrity of the lumbosacral enlargement and conus medullaris within one month after spinal cord injury (SCI). Lumbosacral cord MRI data were acquired in patients with sudden onset (<7 days) SCI at the cervical or thoracic level approximately one month after injury and in healthy controls. Tissue integrity and loss were evaluated through diffusion tensor (DTI) and T2*-weighted imaging (cross-sectional area [CSA] measurements). Associations with the degree of neurological impairment were assessed using linear mixed-effects models. Twenty-one patients with SCI showed lower white matter (WM) fractional anisotropy (FA) (≤-13.3%) and higher WM radial diffusivity (≤14.6%) compared to 27 healthy controls. Differences were most pronounced in the lateral columns of WM. CSA measurements revealed no group differences. For the lateral columns, lower FA values were associated with lower motor scores and lower amplitudes of motor evoked potentials. For the dorsal columns, lower FA values were associated with lower amplitudes of somatosensory evoked potentials from the lower extremities. One month after SCI, first signs of WM degeneration were apparent, without indication of tissue loss. The more pronounced differences observed in the lateral column could be attributed to anterograde degeneration of the motor tracts. The variability among DTI measurements remote from the lesion site can be partially explained by the degree of the SCI-induced neurological impairment. Together with previous studies, our findings indicate that impaired tissue integrity precedes tissue loss. The presented techniques have potential applications in monitoring the progression of various neurological diseases.

Friedreich ataxia: what can we learn from non-GAA repeat mutations?

Friedreich ataxia (FRDA) is a slowly progressive neurological disease resulting from decreased levels of the protein frataxin, a small mitochondrial protein that facilitates the synthesis of iron-sulfur clusters in the mitochondrion. It is caused by GAA (guanine-adenine-adenine) repeat expansions in the FXN gene in 96% of patients, with 4% of patients carrying other mutations (missense, nonsense, deletion) in the FXN gene. Compound heterozygote patients with one expanded GAA allele and a non-GAA repeat mutation can have subtle differences in phenotype from typical FRDA, including, in patients with selected missense mutations, both more severe features and less severe features in the same patient. In this review, we propose explanations for such phenotypes based on the potential for activities of frataxin other than enhancement of iron-sulfur cluster synthesis, as well as crucial future experiments for fully understanding the role of frataxin in cells.

The effect of interferon beta on quality of life in patients with multiple sclerosis: A systematic review and meta-analysis study

Background: Multiple sclerosis (MS) is one of the most common progressive neurological disorders affecting young adults. This study aimed to perform a meta-analysis on the effect of interferon beta (IFN-β) on the quality of life (QOL) of patients with MS. Methods: Using valid keywords and searching through databases like Medlib, ScienceDirect, PubMed, etc., 10 articles published between 1999 and 2020 were collected. The inclusion criteria were developed based on clinical guidelines, focusing on studies involving adults with MS treated with IFN-β, with outcomes measuring QOL. The exclusion criteria included studies not in English, those involving pediatric populations, or those lacking a control group. In the reviewed studies, 14 scales of QOL were measured at the beginning and the end of treatment with IFN-β. Stata software. Publication bias was not significant. Heterogeneity was evaluated using the Q test and the I2 index. In heterogeneous studies, subgroup analysis and meta-regression were used for meta-analysis. The random-effect model was used for analyses with I2 of more than 50%. Results: A total number of 1320 people with an average age of 32.40 ± 8.77 years were included in this study. On average, there was a slight decline in energy and satisfaction with sexual function scales (SSF), while a slight improvement was seen in the other 12 scales, following the treatment with IFN-β. However, no significant changes were observed in any of the QOL scales following treatment, except for health distress (HD) (P &lt; 0.001), role limitation due to physical problems (RLPP) (P &lt; 0.001), and role limitation due to emotional problems (RLEP) (P = 0.037), all of which showed a slight but natable improvement. The physical and mental components, showed significant increases of 0.189 [95% Confidence interval (CI): 0.083, 0.295, I2 = 0%] and 0.221 (95% CI 0.119, 0.324, I2 = 0%) in the scores after using IFN-β, respectively. Conclusion: This study's results showed that treatment with IFN-β does not negatively affect the QOL of patients with MS. Moreover, this treatment can slightly improve most QOL scales associated with the disability observed in MS.

Incidence of HTLV-1-associated myelopathy in the UK from 1991 to 2024: a longitudinal observational cohort study.

Human T-cell lymphotropic virus type 1 (HTLV-1) may cause spinal cord inflammation, leading to HTLV-1-associated myelopathy (HAM). HAM is a chronic and progressive neurological disorder that is associated with increased mortality and impaired quality of life. There are limited data on the incidence of HAM, with higher rates seen in Latin America and the Caribbean compared to Japan. We investigated the incidence of HAM in a cohort of initially asymptomatic people with HTLV-1 in the United Kingdom (UK). This is a longitudinal retrospective observational study of people with confirmed HTLV-1 infection who first attended the National Centre for Human Retrovirology in London, UK, between 1st March 1991 and 31st March 2024. Clinical records were analysed to calculate the incidence rate and cumulative incidence of HAM. A secondary analysis was conducted to assess HAM incidence in people living with HTLV-1 and HIV coinfection. At the first visit, the HTLV-1 proviral load was compared between incident cases and those who remained asymptomatic during follow-up. In a cohort with up to 33 years of follow-up of individuals living with HTLV-1 in the UK, the cumulative incidence of HTLV-1-associated myelopathy (HAM) was found to be 1.35% (4/297), with an incidence rate of 1.98 per 1,000 person-years. All people who developed HAM had a high proviral load at the first clinic visit. No cases of incident HAM were observed among individuals who had HIV-HTLV-1 coinfection during the study period. The incidence of HAM in the UK cohort is comparable to the rates reported in Latin America and the Caribbean and is higher than reported in other high-income countries. High proviral load of HTLV-1 predates the development of HAM.

Living with progressive neurological disease and breathing difficulties

Living with progressive neurological disease and breathing difficulties

Integrating neuroscience and artificial intelligence: EEG analysis using ensemble learning for diagnosis Alzheimer's disease and frontotemporal dementia.

Alzheimer's disease (AD) and frontotemporal dementia (FTD) are both progressive neurological disorders that affect the elderly. Distinguishing between individuals suffering from these two diseases in the early stages can be quite challenging, and due to their different treatments, it has become an important problem. Machine learning (ML) algorithms can be helpful in this matter due to their high ability to manage large data and deliver high-quality diagnostic results. In this research, we integrate multiple ML algorithms into 10 ensemble learning techniques, utilizing 7 distinct features: 3 from the time domain and 4 from the frequency domain. They are used to achieve a higher diagnostic accuracy level in binary and multiclass classification of samples from electroencephalography (EEG) signals of elderly patients with AD, FTD, and healthy age-matching controls (CN), during the eye resting state. The best results in carrying out binary AD/CN, FTD/CN, and AD/FTD classifications with significant accuracy>95% have been obtained with the help of the light gradient boosting machine (LGBM) method applying the wavelet transform feature. This combination (LGBM&wavelet) also displays the best performance in the AD/FTD/CN multiclass classification process with accuracy>93%.

The Role of Adaptive Coping Strategies in Speech Rehabilitation for Patients with Progressive Neurological Disorders

The Role of Adaptive Coping Strategies in Speech Rehabilitation for Patients with Progressive Neurological Disorders

A Review on Blood Brain Barriers Receptor

The blood–brain barrier is playing a critical role in controlling the influx and efflux of biological substances essential for the brain’s metabolic activity as well as neuronal function. Thus, the functional and structural integrity of the BBB is pivotal to maintain the homeostasis of the brain microenvironment. The different cells and structures contributing to developing this barrier are summarized along with the different functions that BBB plays at the brain–blood interface. We also explained the role of shear stress in maintaining BBB integrity. Furthermore, we elaborated on the clinical aspects that correlate between BBB disruption and different neurological and pathological conditions. Blood vessels are critical to deliver oxygen and nutrients to all of the tissues and organs throughout the body. The blood vessels that vascularize the central nervous system (CNS) possess unique properties, termed the blood–brain barrier, which allow these vessels to tightly regulate the movement of ions, molecules, and cells between the blood and the brain. This precise control of CNS homeostasis allows for proper neuronal function and also protects the neural tissue from toxins and pathogens, and alterations of these barrier properties are an important component of pathology and progression of different neurological diseases. The physiological barrier is coordinated by a series of physical, transport, and metabolic properties possessed by the endothelial cells (ECs) that form the walls of the blood vessels, and these properties are regulated by interactions with different vascular, immune, and neural cells. Understanding how these different cell populations interact to regulate the barrier properties is essential for understanding how the brain functions during health and disease.

Disruption of RNA-binding proteins in neurological disorders.

RNA-binding proteins (RBPs) are multifunctional proteins essential for the regulation of RNA processing and metabolism, contributing to the maintenance of cell homeostasis by modulating the expression of target genes. Many RBPs have been associated with neuron-specific processes vital for neuronal development and survival. RBP dysfunction may result in aberrations in RNA processing, which subsequently initiate a cascade of effects. Notably, RBPs are involved in the onset and progression of neurological disorders via diverse mechanisms. Disruption of RBPs not only affects RNA processing, but also promotes the abnormal aggregation of proteins into toxic inclusion bodies, and contributes to immune responses that drive the progression of neurological diseases. In this review, we summarize recent discoveries relating to the roles of RBPs in neurological diseases, discuss their contributions to such conditions, and highlight the unique functions of these RBPs within the nervous system.

Cellular mechanisms of copper neurotoxicity in human, differentiated neurons

Copper (Cu) is an essential trace element involved in fundamental physiological processes in the human body. Even slight disturbances in the physiological Cu homeostasis are associated with the manifestation of neurodegenerative diseases. While suggesting a crucial role of Cu in the pathogenesis, the exact mechanisms of Cu neurotoxicity involved in the onset and progression of neurological diseases are far from understood. This study focuses on the molecular and cellular mechanisms of Cu-mediated neurotoxicity in human brain cells. First, the cytotoxic potential of Cu was studied in fully differentiated, human neurons (LUHMES cells). Lysosomal integrity was considerably affected following incubation with 420 µM CuSO4 for 48 h. Further mechanistic studies revealed mitochondria and neuronal network as most susceptible target organelles (already at 100 µM CuSO4, 48 h), while the generation of reactive oxygen species turned out to be a rather later consequence of Cu toxicity. Besides Cu, the homeostasis of other elements might be involved and are likely to contribute to the pathology of Cu-mediated neurological disorders. Besides Cu, also effects on the cellular levels of magnesium, calcium, iron, and manganese were observed in the neurons, presumably aggravating the consequences of Cu neurotoxicity. In conclusion, insights in the underlying mode of action will foster the development of treatment strategies against Cu-mediated neurological diseases. Particularly, the interplay of Cu with other elements might provide a powerful diagnostic tool and might be used as therapeutic approach.

Small Molecules in Parkinson's Disease Therapy: From Dopamine Pathways to New Emerging Targets.

Parkinson's disease (PD) is a chronic, progressive neurological disorder affecting approximately 10 million people worldwide, with prevalence expected to rise as the global population ages. It is characterized by the degeneration of dopamine-producing neurons in the substantia nigra pars compacta, leading to motor symptoms such as tremor, rigidity, bradykinesia, postural instability, and gait disturbances, as well as non-motor symptoms including olfactory disturbances, sleep disorders, and depression. Currently, no cure exists for PD, and most available therapies focus on symptom alleviation. This dopamine deficiency impairs motor control, and since dopamine itself cannot cross the blood-brain barrier (BBB), the precursor L-Dopa is commonly used in treatment. L-Dopa is administered with enzyme inhibitors to prevent premature conversion outside the brain, allowing it to cross the BBB and convert to dopamine within the central nervous system. Although these therapies have improved symptom management, recent research has revealed additional molecular factors in PD pathology, such as α-synuclein aggregation, mitochondrial dysfunction, and lysosomal abnormalities, contributing to its complexity. These discoveries open up possibilities for neuroprotective therapies that could slow disease progression. In this review, we categorize PD therapeutic targets into two main groups: currently used therapies and targets under active research. We also introduce promising small-molecule compounds studied between 2019 and 2023, which may represent future treatment options. By examining both established and emerging targets, we aim to highlight effective strategies and potential directions for future drug development in Parkinson's disease therapy.

Integrated approach of scalp electroacupuncture and pharmacotherapy in managing Parkinson's disease: A systematic review, meta-analysis, and trial sequential analysis of randomized clinical trials.

Parkinson disease (PD) is a progressive neurological disorder that may be managed with therapies like scalp electroacupuncture (SEA). The combination of SEA and medication could potentially offer a new approach for managing PD symptoms. The systematic review and meta-analysis aimed to assess the combined impact of SEA and medication on PD through a comprehensive analysis of randomized clinical trials, focusing on outcomes like effective rate and various scores (total Unified Parkinson Disease Rating Scale (UPDRS), UPDRS III, and Webster). It was conducted an unrestricted search from the beginning of each database until April 19, 2024, across 7 databases. These included 4 international databases: PubMed, Web of Science, Scopus, and Cochrane Library, and 3 Chinese databases: CNKI, VIP, and Wanfang. Review Manager, version 5.3 was used to calculate the mean difference (MD) or risk ratio along with a 95% confidence interval (CI). The Comprehensive Meta-Analysis version 3.0 was employed for conducting bias analyses, meta-regression, and sensitivity analyses. From 1422 records identified in the databases, 17 articles were included in both the systematic review and meta-analysis. The pooled risk ratio and its 95%CI in the intervention (SEA + medication) group compared to the control (medication) group for the effective rate is 1.24 [1.17, 1.32] with a P < .00001. The pooled MD and its 95%CI for the Webster score is -0.51 [-6.36, 5.35] with a P = .86. The pooled MD and its 95%CI for total UPDRS is 8.73 [2.88, 14.58] with a P = .003. The pooled MD and its 95%CI for UPDRS III is 4.42 [3.23, 5.61] with a P < .00001. The results for total UPDRS and UPDRS III showed that intervention reduced the severity and progression of PD in patients more than medication. The intervention (SEA + medication) has shown significant effectiveness compared to the control (medication) in terms of the effective rate, total UPDRS, and UPDRS III in PD patients. However, it did not show a significant effect on the Webster score.

Optimized Hybrid Deep Learning Framework for Early Detection of Alzheimer's Disease Using Adaptive Weight Selection.

Alzheimer's disease (AD) is a progressive neurological disorder that significantly affects middle-aged and elderly adults, leading to cognitive deterioration and hindering daily activities. Notwithstanding progress, conventional diagnostic techniques continue to be susceptible to inaccuracies and inefficiencies. Timely and precise diagnosis is essential for early intervention. We present an enhanced hybrid deep learning framework that amalgamates the EfficientNetV2B3 with Inception-ResNetV2 models. The models were integrated using an adaptive weight selection process informed by the Cuckoo Search optimization algorithm. The procedure commences with the pre-processing of neuroimaging data to guarantee quality and uniformity. Features are subsequently retrieved from the neuroimaging data by utilizing the EfficientNetV2B3 and Inception-ResNetV2 models. The Cuckoo Search algorithm allocates weights to various models dynamically, contingent upon their efficacy in particular diagnostic tasks. The framework achieves balanced usage of the distinct characteristics of both models through the iterative optimization of the weight configuration. This method improves classification accuracy, especially for early-stage Alzheimer's disease. A thorough assessment was conducted on extensive neuroimaging datasets to verify the framework's efficacy. The framework attained a Scott's Pi agreement score of 0.9907, indicating exceptional diagnostic accuracy and dependability, especially in identifying the early stages of Alzheimer's disease. The results show its superiority over current state-of-the-art techniques. The results indicate the substantial potential of the proposed framework as a reliable and scalable instrument for the identification of Alzheimer's disease. This method effectively mitigates the shortcomings of conventional diagnostic techniques and current deep learning algorithms by utilizing the complementing capabilities of EfficientNetV2B3 and Inception-ResNetV2 by using an optimized weight selection mechanism. The adaptive characteristics of the Cuckoo Search optimization facilitate its application across many diagnostic circumstances, hence extending its utility to a wider array of neuroimaging datasets. The capacity to accurately identify early-stage Alzheimer's disease is essential for facilitating prompt therapies, which are crucial for decelerating disease development and enhancing patient outcomes.

Neuroprotective effects of GLP-1 class drugs in Parkinson’s disease

Parkinson’s disease (PD) is a chronic, progressive neurological disorder primarily affecting motor control, clinically characterized by resting tremor, bradykinesia, rigidity, and other symptoms that significantly diminish the quality of life. Currently, available treatments only alleviate symptoms without halting or delaying disease progression. There is a significant association between PD and type 2 diabetes mellitus (T2DM), possibly due to shared pathological mechanisms such as insulin resistance, chronic inflammation, and mitochondrial dysfunction. PD is caused by a deficiency of dopamine, a neurotransmitter in the brain that plays a critical role in the control of movement. Glucose metabolism and energy metabolism disorders also play an important role in the pathogenesis of PD. This review investigates the neuroprotective mechanisms of glucagon-like peptide-1 (GLP-1) and its receptor agonists, offering novel insights into potential therapeutic strategies for PD. GLP-1 class drugs, primarily used in diabetes management, show promise in addressing PD’s underlying pathophysiological mechanisms, including energy metabolism and neuroprotection. These drugs can cross the blood–brain barrier, improve insulin resistance, stabilize mitochondrial function, and enhance neuronal survival and function. Additionally, they exhibit significant anti-inflammatory and antioxidative stress effects, which are crucial in neurodegenerative diseases like PD. Research indicates that GLP-1 receptor agonists could improve both motor and cognitive symptoms in PD patients, marking a potential breakthrough in PD treatment and prevention. Further exploration of GLP-1’s molecular mechanisms in PD could provide new preventive and therapeutic approaches, especially for PD patients with concurrent T2DM. By targeting both metabolic and neurodegenerative pathways, GLP-1 receptor agonists represent a multifaceted approach to PD treatment, offering hope for better disease management and improved patient outcomes.

Degenerative Cervical Myelopathy: History, Physical Examination, and Diagnosis.

Background: Degenerative cervical myelopathy is a progressive neurological disorder that is commonly encountered in clinical practice and its incidence is expected to increase alongside the aging population. Given the importance of early and accurate diagnosis in this patient population, this narrative review aims to provide a repository of up-to-date information regarding pertinent patient history, physical exam findings, and potential alternate diagnoses. Methods: The PubMed database was queried for publications from 1 January 2019 to 19 March 2024. The search terms utilized are as follows: cervical myelopathy", "cervical spondylotic myelopathy", "degenerative cervical myelopathy", "epidemiology", "prevalence", "incidence", "etiology", "diagnosis", "differential", "symptoms", "clinical presentation", and "atypical symptoms". The resultant articles were reviewed for relevance and redundancy and are presented within the following categories: Natural History, Epidemiology, Clinical Presentation, Diagnosis, and Management. Results: Myelopathy patients often present with subtle and non-specific symptoms such as sleep disturbances, increased falls, and difficulty driving, which can lead to underdiagnosis and misdiagnosis. Failing to diagnose degenerative cervical myelopathy in a timely manner can result in progressive and irreparable neurological damage. Although many nonoperative treatment modalities are available, surgical decompression is ultimately recommended in most cases to limit further deterioration in neurological function and optimize long-term patient outcomes. Conclusions: A thorough clinical history and physical examination remain the most important diagnostic tools to avoid misdiagnosis and implement early treatment in this patient population.

Hypoxic Human Microglia Promote Angiogenesis Through Extracellular Vesicle Release.

Microglia, the brain-resident immune cells, orchestrate neuroinflammatory responses and are crucial in the progression of neurological diseases, including ischemic stroke (IS), which accounts for approximately 85% of all strokes worldwide. Initially deemed detrimental, microglial activation has been shown to perform protective functions in the ischemic brain. Besides their effects on neurons, microglia play a role in promoting post-ischemic angiogenesis, a pivotal step for restoring oxygen and nutrient supply. However, the molecular mechanisms underlying microglia-endothelial cell interactions remain largely unresolved, particularly in humans. Using both in vitro and in vivo models, we investigated the angiogenic signature and properties of extracellular vesicles (EVs) released by human microglia upon hypoxia-reperfusion stimulation. EVs were isolated and characterized in terms of their size, concentration, and protein content. Their angiogenic potential was evaluated using endothelial cell assays and a zebrafish xenograft model. The in vivo effects were further assessed in a mouse model of ischemic stroke. Our findings identified key proteins orchestrating the pro-angiogenic functions of human microglial EVs under hypoxic conditions. In vitro assays demonstrated that hypoxic EVs (hypEVs) promoted endothelial cell migration and tube formation. In vivo, hypEVs induced vessel sprouting in zebrafish and increased microvessel density in the perilesional area of mice following ischemic stroke.

Parkinson’s disease in the Lebanese population: knowledge and attitude scales’ validation and correlates

BackgroundParkinson’s disease (PD) is a progressive degenerative neurological disorder that negatively affects the quality of life of affected individuals as well as their care givers. There is limited information in both epidemiological data and awareness level on PD in the Middle East. Considering the increasing prevalence of PD, the lack of awareness and negative attitudes toward PD pose a barrier in the provision of appropriate care for individuals with PD.ObjectiveThis study aimed to validate scales to explore the knowledge and attitude towards PD among the general population in Lebanon and identify the associated factors related to the knowledge and attitude assessment. This study’s results would guide awareness strategies in the country including public health strategies, campaigns and education sessions for the general population as well as targeted people.MethodologyAn online cross-sectional study was conducted between July and September 2023 in Lebanon. Snowball sampling was used to recruit 400 Lebanese adults living in Lebanon. The validity and reliability of the knowledge and attitude scales were assessed, followed by a thorough statistical analysis to explore the factors associated with these scales.ResultsThe knowledge and attitude scales generated by this study were valid and reliable; Cronbach’s alpha values for knowledge and attitude scales were 0.697 and 0.901, respectively. Using these scales, 91.8% demonstrated inappropriate knowledge and 93% showed positive attitude towards PD. Higher knowledge scores were significantly associated with female gender (Beta = 1.130), being a healthcare professional (Beta = 2.514), having heard about PD (Beta = 5.338), obtaining the source of information from electronic databases (Beta = 1.283), from pharmacist or physician (Beta = 1.212), from personal readings (Beta = 2.386), and having PD or knowing someone with PD; a friend or a family member (Beta = 1.179). However, being illiterate or having primary or secondary education (Beta = -0.874), having a higher household crowding index (Beta = -1.890), not knowing if contents from sources provide negative images about PD (Beta = − 1.908) and preferring not to say to which social class they belong (Beta = − 1.602) were significantly associated with lower knowledge scores. Believing that contents from sources provide negative images about PD (Beta = 8.246) was significantly associated with a higher attitude score, i.e., a more negative attitude towards PD.ConclusionThis study showed low levels of knowledge and an overall positive attitude towards PD in Lebanon. Factors associated with higher knowledge and attitude scores, including gender, education level, profession, knowing someone with the disease, household crowding index, social class, source of information and contents of such sources, reflect the need to consider those when implementing targeted corrective actions. Future studies can focus on educational campaigns to improve public awareness, reduce misconceptions and limit barriers to the early diagnosis and provision of optimal care to the affected patients.

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.