Cognitive and social cognitive functioning in spinocerebellar ataxia

Garrard, Peter; Martin, Naomi; Giunti, Paola; Cipolotti, Lisa

doi:10.1007/s00415-008-0680-6

Cited by 94 publications

(121 citation statements)

References 48 publications

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“…A previous study showed that a p38 inhibitor protects immature, vulnerable Purkinje neurons from neurotoxic stress [63]. Mice with Purkinje neuron degeneration have shown a spatial learning deficit in the water maze test [61,64,65]. These studies along with our current findings suggest that aberrant p38 activation/accumulation perturbs the movement-controlling function of Purkinje neurons.…”

Section: Discussionsupporting

confidence: 78%

Purkinje-neuron-specific down-regulation of p38 protects motoric function from the repeated use of benzodiazepine

Jung¹,

Metzger²

2013

ABB

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Benzodiazepine (BZD) is the most prescribed CNS depressant in America to treat hyper-excitatory disorders such as anxiety and insomnia. However, the chronic use of BZD often creates adverse effects including psychomotor deficit. In this study, we investigated a novel mechanism by which chronic BZD impedes motoric function in female mice. We used female mice because BZD use is much more prevalent in female than male populations. We tested the hypothesis that the accumulation of p38 (stress-activated protein) in cerebellar Purkinje neurons mediates motoric deficit induced by chronic BZD. To test this hypothesis, we generated transgenic mice that lack p38 in cerebellar Purkinje neurons by crossing Pcp2 (Purkinje cell protein 2)-Cre mice with p38 loxP/loxP mice. p38-knockdown mice and wild-type mice received BZD (lorazepam, 0.5 mg/kg) for 14 days. During this period, they were tested for motoric performance using Rotarod assay in which a quicker fall from rotating rod indicates poorer motoric performance. Cerebellum was then collected to detect p38 in Purkinje neurons and to measure mitochondrial respiration using immunohistochemistry and real-time XF respirometry, respectively. Compared to vehicletreated mice, BZD-treated mice showed poorer motoric performance, a higher number of Purkinje neurons containing p38, and lower mitochondrial respiration. These effects of BZD were much smaller in p38-knockdown mice. These results suggest that the excessive accumulation of p38 in cerebellar Purkinje neurons contributes to motoric deficit associated with chronic BZD. They also suggest that Purkinje neuronal p38 mediates BZD-induced mitochondrial respiratory inhibition in cerebellum. Our findings may provide a new mechanistic insight into chronic BZD-induced motoric deficit.

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Section: Discussionsupporting

confidence: 78%

Purkinje-neuron-specific down-regulation of p38 protects motoric function from the repeated use of benzodiazepine

Jung¹,

Metzger²

2013

ABB

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“…Alternatively, autistic action models may be tuned to both atypical (autistic) and typical movements. (Caillies, Hody, & Calmus, 2012;Eddy & Cavanna, 2015;Eddy & Rickards, 2015;Garrard, Martin, Giunti, & Cipolotti, 2008). Furthermore, our results may help to explain why children with Attention Deficit Hyperactivity Disorder (ADHD) and motor dysfunctions are rated as having more social interaction difficulties than children with ADHD only (Tervo, Azuma, Fogas, & Fiechtner, 2007).…”

Section: Discussionmentioning

confidence: 80%

Interaction takes two: Typical adults exhibit mind-blindness towards those with autism spectrum disorder.

Edey¹,

Cook²,

Brewer³

et al. 2016

Journal of Abnormal Psychology

153

147

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Recent work suggests that we are better at interpreting the movements of others who move like us, and that individuals with Autism Spectrum Disorder (ASD) move in a quantifiably different way from typical individuals. Therefore, 'social impairments' exhibited by individuals with ASD may, at least in part, represent a failure by typical individuals to infer the correct mental states from the movements of those with ASD. To examine this possibility, individuals with ASD and typical adults manually directed two triangles to generate animations depicting mental state interactions. Kinematic analysis of the generated animations demonstrated that the participants with ASD moved atypically, specifically with increased jerk compared to the typical participants. In confirmation of our primary hypothesis, typical individuals were better able to identify the mental state portrayed in the animations produced by typical, relative to autistic individuals. The participants with ASD did not show this 'same group' advantage, demonstrating comparable performance for the two sets of animations. These findings have significant implications for clinical assessment and intervention in ASD, and potentially other populations with atypical movement.

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“…A patient with cerebellar atrophy exhibited deficient RMET performance (Parente et al, 2013). Absence of deficits in mental state attribution but altered attribution of emotions to a character of a short story were reported in eight patients with SCA types 1, 2, and 7 (Sokolovsky et al, 2010), with the opposite picture in 15 patients with SCA 3 and 6 (Garrard et al, 2008). This dissociation could reflect distinct pathophysiology in SCA subtypes.…”

Section: Evidence From Cerebellar Degenerationmentioning

confidence: 90%

The Cerebellum in Social Cognition

Sokolov

2018

Front. Cell. Neurosci.

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Cognitive and social cognitive functioning in spinocerebellar ataxia

Cited by 94 publications

References 48 publications

Purkinje-neuron-specific down-regulation of p38 protects motoric function from the repeated use of benzodiazepine

Purkinje-neuron-specific down-regulation of p38 protects motoric function from the repeated use of benzodiazepine

Interaction takes two: Typical adults exhibit mind-blindness towards those with autism spectrum disorder.

The Cerebellum in Social Cognition

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