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Basal Ganglion

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Anita S. Halper – One of the best experts on this subject based on the ideXlab platform.

  • Oropharyngeal swallowing after stroke in the left Basal Ganglion/internal capsule
    Dysphagia, 2016
    Co-Authors: Jeri A. Logemann, Therese K. Shanahan, Alfred W. Rademaker, Peter J. Kahrilas, Richard Lazar, Anita S. Halper

    Abstract:

    One of the foci of Martin Donner’s work was the neural control of swallowing. This present investigation continues that work by examining oropharyngeal swallowing in 8 patients identified with a single, small, left-Basal Ganglion/internal capsule infarction and 8 age-matched normal subjects. Stroke patients were assessed with a bedside clinical and radiographic swallowing assessment, and normal subjects received only the radiographic study. Results revealed disagreement between the bedside and radiographic assessments in one of the 8 stroke patients. Stroke and normal subjects differed significantly on some swallow measures on various bolus viscosities, but behaved the same as normal subjects on a number of measures. Differences in swallowing in the stroke subjects were not enough to prevent them from eating orally. The significant differences seen in the Basal ganglia/intemal capsule stroke subjects may result from damage to the sensorimotor pathways between the cortex and brainstem. These differences emphasize the importance of cortical input to the brainstem swallowing center in maintaining the systematic modulations characteristic of normal swallowing physiology.

  • oropharyngeal swallowing after stroke in the left Basal Ganglion internal capsule
    Dysphagia, 1993
    Co-Authors: Jeri A. Logemann, Therese K. Shanahan, Alfred W. Rademaker, Peter J. Kahrilas, Richard Lazar, Anita S. Halper

    Abstract:

    One of the foci of Martin Donner’s work was the neural control of swallowing. This present investigation continues that work by examining oropharyngeal swallowing in 8 patients identified with a single, small, left-Basal Ganglion/internal capsule infarction and 8 age-matched normal subjects. Stroke patients were assessed with a bedside clinical and radiographic swallowing assessment, and normal subjects received only the radiographic study. Results revealed disagreement between the bedside and radiographic assessments in one of the 8 stroke patients. Stroke and normal subjects differed significantly on some swallow measures on various bolus viscosities, but behaved the same as normal subjects on a number of measures. Differences in swallowing in the stroke subjects were not enough to prevent them from eating orally. The significant differences seen in the Basal ganglia/intemal capsule stroke subjects may result from damage to the sensorimotor pathways between the cortex and brainstem. These differences emphasize the importance of cortical input to the brainstem swallowing center in maintaining the systematic modulations characteristic of normal swallowing physiology.

Dali Li – One of the best experts on this subject based on the ideXlab platform.

  • wdr45 contributes to neurodegeneration through regulation of er homeostasis and neuronal death
    Autophagy, 2020
    Co-Authors: Qi Wang, Xiuting Chen, Qiufang Zeng, Yanjiao Shao, Houqin Fang, Xun Liao, Husong Li, Tianle Xu, Miaomiao Diao, Dali Li

    Abstract:

    ABSTRACTMutations in the macroautophagy/autophagy gene WDR45 cause β-propeller protein-associated neurodegeneration (BPAN); however the molecular and cellular mechanism of the disease process is largely unknown. Here we generated constitutive wdr45 knockout (KO) mice that displayed cognitive impairments, abnormal synaptic transmission and lesions in several brain regions. Immunohistochemistry analysis showed loss of neurons in prefrontal cortex and Basal Ganglion in aged mice, and increased apoptosis in prefrontal cortex, recapitulating a hallmark of neurodegeneration. Quantitative proteomic analysis showed accumulation of endoplasmic reticulum (ER) proteins in KO mouse. At the cellular level, accumulation of ER proteins due to WDR45 deficiency resulted in increased ER stress and impaired ER quality control. The unfolded protein response (UPR) was elevated through ERN1/IRE1 or EIF2AK3/PERK pathway, and eventually led to neuronal apoptosis. Suppression of ER stress or activation of autophagy through MTOR i…

  • wdr45 contributes to neurodegeneration through regulation of er homeostasis and neuronal death
    bioRxiv, 2018
    Co-Authors: Qi Wang, Dali Li, Xiuting Chen, Qiufang Zeng, Yanjiao Shao, Houqin Fang, Xun Liao, Husong Li, Tianle Xu, Bo Meng

    Abstract:

    Mutations in the autophagy gene WDR45 cause β-propeller protein-associated neurodegeneration (BPAN); however the molecular and cellular mechanism of the disease process is largely unknown. Here we generated constitutive Wdr45 knockout (KO) mice that displayed cognitive impairments, abnormal synaptic transmission and lesions in hippocampus and Basal ganglia. Immunohistochemistry analysis shows loss of neurons in prefrontal cortex and Basal Ganglion in aged mice, and increased apoptosis in these regions, recapitulating a hallmark of neurodegeneration. Quantitative proteomic analysis shows accumulation of endoplasmic reticulum (ER) proteins in KO mouse. Furthermore, we show that a defect in autophagy results in impaired ER turnover and ER stress. The unfolded protein response (UPR) is elevated through IRE1α and possibly other kinase signaling pathways, and eventually leads to neuronal apoptosis. Suppression of ER stress, or activation of autophagy through inhibition of mTOR pathway rescues neuronal death. Thus, our study not only provides mechanistic insights for BPAN, but also suggests that a defect in macroautophagy machinery leads to impairment in selective organelle autophagy.

Jeri A. Logemann – One of the best experts on this subject based on the ideXlab platform.

  • Oropharyngeal swallowing after stroke in the left Basal Ganglion/internal capsule
    Dysphagia, 2016
    Co-Authors: Jeri A. Logemann, Therese K. Shanahan, Alfred W. Rademaker, Peter J. Kahrilas, Richard Lazar, Anita S. Halper

    Abstract:

    One of the foci of Martin Donner’s work was the neural control of swallowing. This present investigation continues that work by examining oropharyngeal swallowing in 8 patients identified with a single, small, left-Basal Ganglion/internal capsule infarction and 8 age-matched normal subjects. Stroke patients were assessed with a bedside clinical and radiographic swallowing assessment, and normal subjects received only the radiographic study. Results revealed disagreement between the bedside and radiographic assessments in one of the 8 stroke patients. Stroke and normal subjects differed significantly on some swallow measures on various bolus viscosities, but behaved the same as normal subjects on a number of measures. Differences in swallowing in the stroke subjects were not enough to prevent them from eating orally. The significant differences seen in the Basal ganglia/intemal capsule stroke subjects may result from damage to the sensorimotor pathways between the cortex and brainstem. These differences emphasize the importance of cortical input to the brainstem swallowing center in maintaining the systematic modulations characteristic of normal swallowing physiology.

  • oropharyngeal swallowing after stroke in the left Basal Ganglion internal capsule
    Dysphagia, 1993
    Co-Authors: Jeri A. Logemann, Therese K. Shanahan, Alfred W. Rademaker, Peter J. Kahrilas, Richard Lazar, Anita S. Halper

    Abstract:

    One of the foci of Martin Donner’s work was the neural control of swallowing. This present investigation continues that work by examining oropharyngeal swallowing in 8 patients identified with a single, small, left-Basal Ganglion/internal capsule infarction and 8 age-matched normal subjects. Stroke patients were assessed with a bedside clinical and radiographic swallowing assessment, and normal subjects received only the radiographic study. Results revealed disagreement between the bedside and radiographic assessments in one of the 8 stroke patients. Stroke and normal subjects differed significantly on some swallow measures on various bolus viscosities, but behaved the same as normal subjects on a number of measures. Differences in swallowing in the stroke subjects were not enough to prevent them from eating orally. The significant differences seen in the Basal ganglia/intemal capsule stroke subjects may result from damage to the sensorimotor pathways between the cortex and brainstem. These differences emphasize the importance of cortical input to the brainstem swallowing center in maintaining the systematic modulations characteristic of normal swallowing physiology.