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Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by the degeneration of dopamine neurons in the substantia nigra pars compacta, leading to motor and non-motor symptoms. While motor symptoms such as rigidity, tremor, bradykinesia/akinesia, and postural instability are well-recognized, non-motor symptoms including cognitive decline, depression, and anxiety also significantly impact patients' quality of life. Preclinical research utilizing animal models has been instrumental in understanding PD pathophysiology and exploring therapeutic interventions. Various approaches, including genetic manipulations and toxin-induced insults, aim to recapitulate both motor and non-motor aspects of PD in animal models. However, no single model fully replicates the complex spectrum of PD symptoms. Behavioral assessments play a crucial role in evaluating motor impairments in PD animal models, focusing on the manifestation of Parkinsonian motor phenotype. These assessments encompass locomotor activities, motor behavior abnormalities, and induced rotational behavior. Similarly, non-motor features are assessed through tests evaluating behavioral alterations such as depression, anxiety, and cognitive impairment. Although numerous animal models of PD have been developed, including non-human primates and both mammalian and non-mammalian species, this review focuses on motor and non-motor testing methodologies in rodent models, which are the most commonly used. Emphasizing genetic and toxin-induced PD models in mice and rats, we highlight key testing strategies and the significance of each method in addressing specific research questions and interpreting experimental data. By providing a comprehensive overview of these testing approaches, this review aims to advance understanding and foster progress in PD research. [ABSTRACT FROM AUTHOR]

• PDGFRβ-CreERT2 mice enable Cre-mediated recombination specifically in pericytes. • Pericyte ablation can be titrated based on tamoxifen dose. • Pericyte ablation causes hypoactivity and impairs motor function. • Pericyte ablation increases brain vessel lumen area and induces mild blood–brain barrier leakage. • Pericyte ablation leads to elevated astrocyte and microglia reactivity throughout the brain. Capillary pericytes are important regulators of cerebral blood flow, blood–brain barrier integrity and neuroinflammation, but can become lost or dysfunctional in disease. The consequences of pericyte loss or dysfunction is extremely difficult to discern when it forms one component of a complex disease process. To evaluate this directly, we examined the effect of adult pericyte loss on mouse voluntary movement and motor function, and physiological responses such as hypoxia, blood–brain barrier (BBB) integrity and glial reactivity. Tamoxifen delivery to Pdgfrβ-CreERT2:: Rosa26-DTA transgenic mice was titrated to produce a dose-dependent ablation of pericytes in vivo. 100mg/kg of tamoxifen ablated approximately half of all brain pericytes, while two consecutive daily doses of 300mg/kg tamoxifen ablated >80% of brain pericytes. In the open field test, mice with ∼50% pericyte loss spent more time immobile and travelled half the distance of control mice. Mice with >80% pericyte ablation also slipped more frequently while performing the beam walk task. Our histopathological analyses of the brain revealed that blood vessel density was unchanged, but vessel lumen width was increased. Pericyte-ablated mice also exhibited: mild BBB disruption; increased neuronal hypoxia; astrogliosis and increased IBA1+ immunoreactivity, suggestive of microgliosis and/or macrophage infiltration. Our results highlight the importance of pericytes in the brain, as pericyte loss can directly compromise brain health and induce behavioural alterations in mice. [ABSTRACT FROM AUTHOR]

Background: While it is evident that stroke impairs motor control, it remains unclear whether stroke impacts motor adaptation-the ability to flexibly modify movements in response to changes in the body and the environment. The mixed results in the literature may be due to differences in participants' brain lesions, sensorimotor tasks, or a combination of both., Objective: We first sought to better understand the overall impact of stroke on motor adaptation and then to delineate the impact of lesion hemisphere and sensorimotor task on adaptation poststroke., Methods: Following the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines, we conducted a systematic review and meta-analysis of 18 studies comparing individuals poststroke to neurotypical controls, with each group consisting of over 200 participants., Results: We found that stroke impairs motor adaptation ( d  = -0.63; 95% confidence interval [-1.02, -0.24]), and that the extent of this impairment did not differ across sensorimotor tasks but may vary with the lesioned hemisphere. Specifically, we observed greater evidence for impaired adaptation in individuals with left hemisphere lesions compared to those with right hemisphere lesions., Conclusions: This review not only clarifies the detrimental effect of stroke on motor adaptation but also underscores the need for finer-grained studies to determine precisely how various sensorimotor learning mechanisms are impacted. The current findings may guide future mechanistic and applied research at the intersection of motor learning and neurorehabilitation., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.