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Adrian Ivanoiu - UCL: GABAergic neurotransmission in Alzheimer’s disease


2016 - Alzheimer's disease (AD) is traditionally regarded as a clinico-pathological entity, in which cognitive and behavioral impairments are associated with the presence of typical brain lesions (amyloid deposits and abnormal tau protein structures). Unfortunately, the extensive research focusing on these lesions did not alter the course of cognitive and behavioral dysfunction, i.e. the evolution towards dementia. Synaptic function, presumably the root cause of cognitive impairment in AD, has only received little attention so far. Synapses are structures that allow communication between neurons and their function depends on fine tuning between substances (neurotransmitters) that provide excitatory and inhibitory transmission. In adults, gamma-amino-butyric acid (GABA) is the main neurotransmitter inhibitor. These excitatory or inhibitory effects depend on the expression of certain proteins, in particular KCC2, which controls the concentration of chlorine in the cell. Professor Octave's (UCL) team recently observed a sharp decrease in KCC2 expression in the brains of AD patients and in vitro in neurons in culture overexpressing the APP protein that produces the amyloid peptide. We postulate that an overexpression of APP may lead to a downregulation of KCC2, resulting in a dysfunction of GABAergic neurotransmission, itself responsible for the cognitive impairment, in particular, the impairment of memory. With mouse models and patients in the early stages of the disease we will evaluate this hypothesis at the cellular level and the cerebral electrical activity.

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