A.I. Virtanen Institute for Molecular Sciences/ University of Eastern Finland
Faculty of Health Sciences
Polina Abushik (b. 1987 Sankt-Petersburg) is a neurobiologist and doctor of philosophy who works as a postdoctoral researcher in Neurophysiology at the University of Eastern Finland. She is responsible for the patch-clamp unit in the neuroinflammation research group at the University of Eastern Finland's A.I. at the Virtanen Institute. The research group is investigating ways to regulate the brain's inflammatory response in neurodegenerative diseases such as Alzheimer's disease. Abushik graduated from the Sankt-Petersburg Polytechnical University with a master's degree in philosophy (applied physical-chemical biology, 2011) and the University of Eastern Finland with a doctorate in philosophy (neurobiology, 2016). Her dissertation in English (2016) dealt with excitotoxicity mechanisms related to neurodegenerative pathologies. The research work was titled The Mechanisms of Neurotoxicity Induced by the Activation of Glutamate Receptors in Rat Central and Peripheral Neurons. Since 2022, Abushik take part in the HUMANE project supported by the European Research Council (ERC) Consolidator Grant that focusing on the assess neuron-glia network activities and functions indicative of early AD pathology in humans.

Presenter of 1 Presentation

SYNAPTIC ACTIVITY AND MORPHOLOGY OF HUMAN NEURONS IN ACUTE SLICES OF FRONTAL CORTEX BIOPSIES OF PATIENTS WITH ALZHEIMER’S DISEASE PATHOLOGY

Session Type
SYMPOSIUM
Date
Thu, 07.03.2024
Session Time
16:20 - 18:20
Room
Auditorium II
Lecture Time
17:05 - 17:20

Abstract

Aims

Most electrophysiological studies on Alzheimer's Disease (AD) have been performed using AD mouse models. The electrophysiological properties of neurons in the human AD brain have not been described due to the lack of suitable material for such investigations.

Methods

Here we describe, using the whole-cell patch-clamp technique in acute slices, the electrophysiological properties of human neurons in cortical biopsies obtained from idiopathic normal pressure hydrocephalus patients undergoing shunt surgery. Due to the beta-amyloid and tau pathology present in the subpopulation of these biopsies, they offer a tissue model for investigation on how AD-related pathology affects neuronal operational properties in the human brain.

Results

We recorded several neuronal parameters including sodium and potassium currents, the shape and action potential firing pattern, and spontaneous post-synaptic activity of both pyramidal cells and fast-firing parvalbumin interneurons in these biopsies. We found alterations in the excitation and inhibition balance in neurons in biopsies with AD-related pathology. Morphological reconstruction of the recorded neurons filled with biocytin revealed alterations in the spine density in neurons recorded in biopsies with AD-related pathology.

Conclusions

This is the first study to report the impact of AD-related pathology on single-neuron operational properties and morphology. Our integrative analysis of human neuronal electrophysiology and subsequent cell morphology reconstruction allows us to register primary pathological changes in neuronal functions in correlation with spine distribution impacted by AD pathology.

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