Dear All

it is my pleasure to inform you that this Thursday, April 8th, at 3pm, Prof. Alexej Verkhratsky from the University of Manchester will be our next guest speaker at the Nencki Institute seminar series.

Professor Verkhratsky, one of the leaders in cell glial biology, his work has shaped this field and allowed us to understand better the processes leading to neurodegeneration. He has also contributed immensely towards our understanding of the role of calcium as a messenger in the cell. Prof Verkhratsky will give a lecture entitled "Principles of astrogliopathology"

Abstract

Astroglia represent a main element in the maintenance of homeostasis and providing defense to the brain. Dysfunction of astrocytes underlies many, if not all, neurological disorders. General astrogliopathy is evident in diametrically opposing morpho-functional changes in astrocytes, i.e. their reactive hypertrophy or atrophy with asthenia. These complex plastic changes underlie pathophysiology of all neurological disorders including neuropsychiatric and neurodegenerative diseases. In particular, astrocytes regulate glutamatergic transmission through the removal of glutamate from the extracellular space and by supplying neurones with glutamine. Glutamatergic transmission is generally believed to be significantly impaired in the contexts of all major neuropsychiatric diseases. In most of these neuropsychiatric diseases astrocytes show signs of degeneration and atrophy, which is likely to be translated into reduced homeostatic capabilities. Astroglial glutamate uptake/release and glutamate homeostasis are affected in all forms of psychiatric and neurodegenerative disorders and represent a common mechanism underlying neurotransmission dysbalance, aberrant synaptic connectivity and overall failure on information processing by neuronal networks, thus leading to cognitive and behavioural deficits. In Alzheimer’s disease (AD) astrocytes undergo complex and multifaceted metamorphoses ranging from atrophy with loss of function to reactive astrogliosis with hypertrophy. Astroglial asthenia underlies reduced homeostatic support and neuroprotection that may account for impaired synaptic transmission and neuronal demise. Reactive astrogliosis which mainly develops in astrocytes associated with senile plaques is prominent at the early to moderate stages of AD manifested by mild cognitive impairment; down-regulation of astrogliosis (reflecting astroglial paralysis) is associated with late stages of the disease characterised by severe dementia. Cell-specific therapies aimed at boosting astroglial supportive and defensive capabilities and preventing astroglial paralysis may offer new directions in preventing, arresting or even curing AD-linked neurodegeneration.

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Best regards,
Aleksandra Pękowska