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Targeting Tau-induced cognitive decline with antisense oligonucleotides to synaptogyrin-3

Project description

Antisense oligonucleotides as a novel intervention against neurodegeneration

The tau protein plays a key role in neurotransmission by binding to the cytoskeleton of neurons and assisting the trafficking of neurotransmitter vesicles to the synapse. The accumulation of pathogenic forms of tau reduces vesicle mobility and neurotransmitter release, impairing neural communication and leading to various neurodegenerative conditions including Alzheimer's disease. The EU-funded TARGET_SYNAPTIC_TAU project is focusing on the interaction of tau with the synaptic vesicle-associated protein Synaptogyrin-3. The rationale is to employ antisense oligonucleotides to reduce the levels of Synaptogyrin-3 and thus block the binding of pathogenic tau to synaptic vesicles. Scientists will test this approach as an intervention against tauopathies.

Objective

Tauopathies (that include Alzheimer’s disease) are characterized by hyperphosphorylation or mutations in the microtubuleassociated protein Tau. This reduces the affinity of Tau to bind microtubules and increases the levels of soluble detached Tau in neurons. Previous ERC-supported work from my lab showed that pathogenic Tau accumulates at pre-synaptic terminals and clusters synaptic vesicles in mouse and fly Tauopathy models and in Alzheimer patient brain samples. This pre-synaptic Tau reduces vesicle mobility and neurotransmitter release (Zhou et al., 2017). The interaction of Tau with synaptic vesicles occurs via the synaptic vesicle-associated protein Synaptogyrin-3. Lowering the levels of Synaptogyrin-3 blocks the ability of Tau to efficiently bind to synaptic vesicles (McInnes et al., 2018). Hence, Synaptogyrin-3 is a promising therapeutic target to tackle tauopathies. In this project I propose to use antisense oligonucleotides (ASOs) to reduce the levels of Synaptogyrin-3 in the brain of Tauopathy mouse models to rescue tau-induced pre-synaptic defects, including cognitive decline. ASO-technology has vastly improved over the past years and was recently approved to treat other degenerative disorders. My goal is to provide in vivo proof-of-concept that targeting Synaptogyrin-3 with an ASO in a therapeutic setting suppresses Tau-induced defects, including cognitive decline.

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ERC-POC - Proof of Concept Grant

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Call for proposal

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(opens in new window) ERC-2020-PoC

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Host institution

VIB VZW
Net EU contribution

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€ 150 000,00
Address
SUZANNE TASSIERSTRAAT 1
9052 ZWIJNAARDE - GENT
Belgium

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Region
Vlaams Gewest Prov. Oost-Vlaanderen Arr. Gent
Activity type
Research Organisations
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Total cost

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Beneficiaries (1)

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