Fear-of-falling (FOF) in Parkinson's disease (PD) reflects both motor and non-motor determinants and is associated with reduced quality of life (QoL). However, its dominant clinical drivers in highly concerned patients remain unclear.

Autonomic dysfunction, particularly orthostatic hypotension (OH), is common and predicts poor outcomes in Parkinson's disease (PD). Brain contributions to autonomic failure in PD are suspected but understudied.

Dipeptidyl peptidase-4 inhibitors (DPP4i) are commonly used oral hypoglycemic agents that enhance the bioavailability of active glucagon-like peptide-1 by inhibiting its degradation. Recent studies suggest possible neuroprotective effects of DPP4i in Parkinson's disease (PD); however, their association with mortality in PD is unclear.

Pure autonomic failure (PAF) is a neurodegenerative disease that leads to widespread autonomic dysfunction. To date, no studies have specifically assessed health-related quality of life (HRQoL) and disability in PAF patients.

Postural abnormalities (PA) and motor complications (MCs, including motor fluctuations - MFs- and levodopa-induced dyskinesia - LIDs) are hallmark of Parkinson's disease (PD) progression, yet their relationship remains poorly understood.

Patients with Parkinson's disease (PD) face heightened risks during hospitalization, including prolonged hospital stay and discharge to higher levels of care. Possible contributing factors include non-adherence to home medication regimens and administration of contraindicated medications.

Parkinson's disease (PD) is a neurodegenerative disease common in older people and clinically manifests as resting tremors, bradykinesia, muscle stiffness, and impaired postural balance. Diabetes mellitus (DM) is a metabolic disease characterized by high blood sugar levels, independent of insulin alterations. With the aging global population, comorbidities of PD and DM have become a major burden on healthcare systems; however, the underlying links between the two diseases remain incompletely understood. Previous work has suggested that PD and DM have several potentially overlapping mechanisms of action. This systematic review addresses a critical need for integrating clinical and preclinical evidence to identify novel therapeutic strategies for co-managing PD and DM. Here, we summarize the findings from recent publications, focusing on the pathogenesis of PD and DM, insulin resistance, treatment of PD by antidiabetic drugs, or on the contrary, treatment of DM by common PD therapeutics.

Clinical success of deep brain stimulation (DBS) depends on accurate electrode placement and stimulation within the brain targets. This study aims to explore the optimal stimulation site in the globus pallidus interna (GPi) to address the existing knowledge gap.

Infection-related movement disorders (IRMD) constitute nearly one-fifth of secondary movement disorders, with higher prevalence in endemic regions. Timely recognition is critical, as many are treatable or preventable yet they often mimic primary movement disorders, leading to diagnostic delays.

In recent years, retinal structural changes have attracted considerable attention as a potential biomarker of neurodegeneration in Parkinson's disease (PD). Several studies have reported a reduced Retinal Nerve Fiber Layer (pRNFL) thickness in patients with PD compared with age-matched controls. However, potential retinal differences between "idiopathic" PD and GBA1-associated PD (GBA-PD) remain largely unexplored.

Blinking abnormalities are among the earliest and most common symptoms in Gilles de la Tourette syndrome (GTS) but have not been studied using precise quantitative methods. Here, we use automated video-based analyses to assess blinking abnormalities in GTS in terms of blink rates as well as alterations in spatiotemporal blink features.

Cervical dystonia (CD) may affect not only head posture but also gait and balance. The relationship between quantitative gait abnormalities and perceived disability, the contribution of head tremor (HT) and the impact of botulinum toxin (BoNT) on these disturbances remain unclear.

Classical clinical assessments of Parkinson's disease (PD) severity are subjective and prone to variability. Wearable sensors, particularly inertial measurement units (IMUs), offer a quantitative approach to assessing gait abnormalities, which are critical markers of disease progression.

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common monogenic cause of Parkinson's disease (PD), with the p.Gly2019Ser (G2019S) variant being particularly prevalent. The LRRK2 gene encodes a large, multi-domain protein (LRRK2) belonging to the Roco family, possessing both kinase and GTPase activities. Because normal LRRK2 function is critical for neuronal development, synaptic plasticity, vesicle trafficking, mitochondrial homeostasis, and neuroinflammatory pathways, pathogenic LRRK2 variants likely impair these functions. This is supported by rodent models and induced pluripotent stem cell (iPSC) studies suggesting that G2019S LRRK2 variants accelerate neuronal differentiation and disrupt synaptic function early in development, while kinase overactivity (phosphorylation of various substrates) is critical during normal embryonic growth. Contrary to the dominant gain-of-toxic-function hypothesis, these observations support an alternative loss-of-function framework, whereby increased kinase activity may be a compensatory cellular strategy to counteract the loss or alteration of the homeostatic and neurodevelopmental functions associated with G2019S LRRK2. If validated by further studies, including ongoing LRRK2 kinase inhibitor trials, future LRRK2-PD therapeutic strategies may shift from broad kinase inhibition toward individualized modulation of specific LRRK2-mediated impairments, such as vesicle trafficking, mitochondrial integrity, or microglial dysfunction. Such an approach would recognize LRRK2-PD not as a single entity but as a biologically heterogeneous group of PD subtypes.