Neuroscience letters
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Neuroscience letters · Jan 2019
ReviewWhy do so many genetic insults lead to Purkinje Cell degeneration and spinocerebellar ataxia?
The genetically heterozygous spinocerebellar ataxias are all characterized by cerebellar atrophy and pervasive Purkinje Cell degeneration. Up to date, more than 35 functionally diverse spinocerebellar ataxia genes have been identified. ⋯ In this review, we discuss the current consensus on shared mechanisms underlying the pervasive Purkinje Cell loss in spinocerebellar ataxia. Additionally, using recently published cell type specific expression data, we identified several Purkinje Cell-specific genes and discuss how the corresponding pathways might underlie the vulnerability of Purkinje Cells in response to the diverse genetic insults causing spinocerebellar ataxia.
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Neuroscience letters · Nov 2018
Gait bradykinesia and hypometria decrease as arm swing frequency and amplitude increase.
People with Parkinson's disease (PD) have decreased arm swing movements during walking, which can be related to PD motor signs and symptoms. In this context, the aim of this study was to determine the effects of an increased arm swing frequency or amplitude on the gait parameters in people with PD and healthy older adults. Seventeen individuals with PD and 19 older people were invited to walk on a 10 m pathway under three experimental conditions: (i) usual walking (no arm swing instructions); (ii) an increased arm swing amplitude; and (iii) an increased arm swing frequency. ⋯ People with PD were able to modulate the gait parameters according to the experimental conditions, but at a smaller magnitude than the older individuals. These results indicate that bradykinesia and hypometria of gait can be positively overcome by increasing the amplitude and frequency of arm swing. Arm movements should be included in gait rehabilitation protocols for PD.
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Neuroscience letters · Nov 2018
A new central post-stroke pain rat model: autologous blood injected thalamic hemorrhage involved increased expression of P2X4 receptor.
Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. ⋯ A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a significant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
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Neuroscience letters · Oct 2018
Meta AnalysisCerebrospinal fluid NFL in the differential diagnosis of parkinsonian disorders: A meta-analysis.
Neurofilament light chain (NFL) in cerebrospinal fluid (CSF) is a promising biomarker candidate which may discriminate atypical parkinsonian disorders (APD), mainly including multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD), from Parkinson's disease (PD). We aim to evaluate the diagnostic accuracy of CSF NFL level as a differentiating biomarker between APD and PD. Databases of PubMed, OVID and Web of Science were searched for studies (published until May 31, 2017) that reported on CSF NFL as a diagnostic biomarker between APD and PD. ⋯ The results of Deeks' test revealed a low risk of publication bias. The CSF NFL level may be used as a biomarker in discriminating APD from PD with high diagnostic accuracy at an early stage of disease. Large and longitudinal studies are still needed on individuals who are suspected to have APD.
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Neuroscience letters · Sep 2018
The left central nucleus of the amygdala contributes to mechanical allodynia and hyperalgesia following right-sided peripheral nerve injury.
The left and right central nucleus of the amygdala (CeA) exert asymmetric pronociceptive functions. In the setting of a transient noxious stimulus or persistent inflammatory pain, neuronal activity increases in the right but not left CeA, regardless of side of injury. Much less is known regarding this lateralization with respect to the behavioral manifestations of persistent neuropathic pain. ⋯ Following right-sided SNI, we observed a modality-dependent effect: mechanical allodynia was attenuated by inactivation of the left but neither the right nor bilateral CeA, mechanical hyperalgesia was attenuated by left, right and bilateral intra-CeA lidocaine, and cold allodynia was unaffected. These data suggest that CeA-mediated control of neuropathic pain is not strictly limited to the right CeA as previously assumed. We conclude that functional lateralization depends on the type of pain, side of injury and the sensory modality, and that the left CeA contributes to mechanical allodynia and hyperalgesia after peripheral nerve injury to the right side of the body.