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TAU-NOW

Financiado

Tau Pathology in Alzheimer s disease Spreading and Resilience

Alzheimer’s disease (AD) poses a major challenge, as 40 million people worldwide are diagnosed with AD and there is currently no cure. AD is characterized by Aβ plaques and tau neurofibrillary tangles. Recently, several phase III... ver más

30/11/2026

LUNDS UNIVERSITET

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

LUNDS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 3 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-03-16

ERC-2020-STG: ERC STARTING GRANTS

I+D

Cerrada hace 5 años

0% 100% 100%

3 Participantes

LUNDS UNIVERSITET

860.19K€ | Lider

OVIARAGON

514.44K€ | Participante

STICHTING AMSTERDAM UMC

639.81K€ | Participante

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Duración del proyecto: 68 meses Fecha Inicio: 2021-03-16
Fecha Fin: 2026-11-30

Líder del proyecto

LUNDS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Alzheimer’s disease (AD) poses a major challenge, as 40 million people worldwide are diagnosed with AD and there is currently no cure. AD is characterized by Aβ plaques and tau neurofibrillary tangles. Recently, several phase III clinical trials targeting the Aβ pathway have failed to reach their primary endpoints. This stresses the need for diversification of the drug portfolio. Tau pathology is a promising drug target due to its strong associations with synaptic density, atrophy and cognition. I envision two treatment options to be potentially effective in halting or slowing AD: 1) preventing the spreading of pathological tau, and 2) boosting resilience against tau pathology. Both processes are currently insufficiently understood, especially in living humans. Since a few years, AD-specific tau pathology can be measured in vivo using PET. TAU-NOW uniquely utilizes longitudinal tau PET in conjunction with functional and structural MRI, biofluid and cognitive data, to investigate mechanisms of tau spread and resilience in humans. In WP1, I will test the hypothesis that tau predominantly spreads through functionally connected regions, by relating tau PET changes over time to the functional architecture of the brain. Next, molecular (CSF) and genetic (GWAS) drivers of tau spread will be identified. On top of that, I will assess whether functional disconnection in subjects who underwent epileptic surgery (i.e. unilateral medial temporal lobe resection or corpus callosotomy) leads to an asymmetric tau PET pattern decades later. In WP2, I will investigate the functional (fMRI), molecular and genetic modifiers that render individuals resilient to tau pathology. In WP3, I will examine the consequences of tau spreading and resilience for important clinical trial outcomes like cognitive and volumetric changes over time. Altogether, TAU-NOW will enhance our understanding of tau spreading and resilience and may ultimately identify novel leads for drug discovery against AD.

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