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德国慕尼黑工业大学神经科学研究所主任 Technical University Munich, Germany
德国科学院院士及巴伐利亚科学院院士,Brain prize 获得者
Professor Arthur Konnerth is a renowned senior scholar in the field of neuroscience. In the 1980s and 1990s, he developed and applied the whole-cell patch clamp recording technique on fresh brain slices, which became an important tool for quantitative neurophysiological measurements. In recent years, he has devoted himself to the development and application of high-resolution, in vivo physiological functional imaging techniques in animals, particularly two-photon calcium imaging. One of his major achievements was the discovery of specific calcium wave activity in cortical neurons in an Alzheimer's disease animal model. Another significant accomplishment was measuring the sensory input received by individual dendritic spines in multiple sensory cortices. Arthur Konnerth has received dozens of highly influential academic awards, including the Leibniz Prize and the Max Planck Research Prize. In 2001, Konnerth was elected to the German Academy of Sciences Leopoldina. In 2015, he shared the Brain Prize awarded by the Lundbeck Foundation in Denmark, with Winfried Denk, Karel Svoboda and David W. Tank, for invention, refinement and use of two-photon microscopy.
报告题目:
Perturbation of neuronal function in Alzheimer's Disease
报告摘要:
Progressive accumulation of neurotoxic amyloid β (Aβ) in the brain is a defining feature of Alzheimer disease (AD). Pathological Aβ accumulations cause at late stages of AD neurodegeneration and cell death. However, neuronal dysfunction, consisting of an excessively increased activity in a fraction of brain neurons, occurs already at early stages of the disease. We explored the cellular basis of this hyperactivity in mouse models of AD. We demonstrate that Aβ-mediated hyperactivation is due to a defect in synaptic transmission that becomes relevant exclusively in active neurons, with the most active neurons having the highest risk of hyperactivation. Importantly, Aβ-containing brain extracts from human AD patients sustain this vicious cycle and underscore the relevance of this pathological mechanism for AD in humans.
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Professor Arthur Konnerth is a renowned senior scholar in the field of neuroscience. In the 1980s and 1990s, he developed and applied the whole-cell patch clamp recording technique on fresh brain slices, which became an important tool for quantitative neurophysiological measurements. In recent years, he has devoted himself to the development and application of high-resolution, in vivo physiological functional imaging techniques in animals, particularly two-photon calcium imaging. One of his major achievements was the discovery of specific calcium wave activity in cortical neurons in an Alzheimer's disease animal model. Another significant accomplishment was measuring the sensory input received by individual dendritic spines in multiple sensory cortices. Arthur Konnerth has received dozens of highly influential academic awards, including the Leibniz Prize and the Max Planck Research Prize. In 2001, Konnerth was elected to the German Academy of Sciences Leopoldina. In 2015, he shared the Brain Prize awarded by the Lundbeck Foundation in Denmark, with Winfried Denk, Karel Svoboda and David W. Tank, for invention, refinement and use of two-photon microscopy.
报告题目:
Perturbation of neuronal function in Alzheimer's Disease
报告摘要:
Progressive accumulation of neurotoxic amyloid β (Aβ) in the brain is a defining feature of Alzheimer disease (AD). Pathological Aβ accumulations cause at late stages of AD neurodegeneration and cell death. However, neuronal dysfunction, consisting of an excessively increased activity in a fraction of brain neurons, occurs already at early stages of the disease. We explored the cellular basis of this hyperactivity in mouse models of AD. We demonstrate that Aβ-mediated hyperactivation is due to a defect in synaptic transmission that becomes relevant exclusively in active neurons, with the most active neurons having the highest risk of hyperactivation. Importantly, Aβ-containing brain extracts from human AD patients sustain this vicious cycle and underscore the relevance of this pathological mechanism for AD in humans.