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タイトル Neuroglial morphological and metabolical alterations during the progression of Alzheimer´s disease and ageing
講演者 José Julio Rodríguez Arellano, Ph.D.
所属 IKERBASQUE, Basque Foundation for Science, Department of Neuroscience Faculty of Medicine and Odontology, University of the Basque Country
開催日 2014-02-07 17:30
終了日 2014-02-07 18:30
内容

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演者 José Julio Rodríguez Arellano, Ph.D.

 

所属 IKERBASQUE, Basque Foundation for Science, Department of Neuroscience Faculty of Medicine and Odontology, University of the Basque Country

 

講演タイトル:Neuroglial morphological and metabolical alterations during the progression of Alzheimer´s disease and ageing

 

日時 平成26年2月7日(金)17:30-18:30

 

場所 九州大学 医系キャンパス コラボステーションI 1階セミナー室A

 

抄録

Neuroglial cells are fundamental for brain homeostasis and therefore represent the intrinsic brain defence system. Thus, all forms of neuropathological processes inevitably involve glial cells. Neurodegenerative diseases, including Alzheimer´s disease (AD) disrupt brain connectivity affecting neuronal-neuronal, neuronal-glial and glial-glial interaction. Furthermore, neurodegenerative processes trigger universal and conserved glial reactions classically represented by astrogliosis and microglial activation. The recently acquired knowledge allows us to regard the neurodegenerative diseases as primarily gliodegenerative processes, in which glial cells determine the progression and outcome of neuropathological processes such as AD and ageing. We have recently probed this active pathological role, by showing: (i) an astroglial generalised atrophy with a concomitant astrogliosis just restricted to Ab plaques presence, ii) alterations in glutamate glial metabolism, iii) changes in S-100b trophic factor and (iv) an early resting microglial recruitment in the affected areas, even before the presence of activated/macrophagic microglial cells. These glial alterations, which are complex and region dependent are fundamental for the disruption of neural networks connectivity as well as with the neurotransmitters imbalance that underlie the mnesic deficits associated with AD. However, we have recently demonstrated that psychostimulative processes, such as exposure to enriched environment and voluntary running, can not only revert this generalized astrocytic hippocampal and cortical atrophy but also potentiate their hypertrophy which could trigger new insights into the search for a potential therapeutic treatment of AD and pathological ageing.

 

世話人

野田 百美(のだ まみ)

九州大学大学院・薬学研究院・病態生理学分野