Back

The loss of Tau in the adult brain triggers neuroplastic, epigenetic and behavioral deficits

Silva, J. M.; Lahiri, S. M.; Monteiro-Fernandes, D.; Soares-Cunha, C.; Solis-Mezarino, V.; Volker-Alber, M.; Gomes, P.; Campos-Marques, C.; Coimbra, B.; Campos, I. C.; Samiotaki, M.; Panayotou, G.; Kokras, N.; Dalla, C.; Wolozin, B.; Oliveira, J.; Abisambra, J.; Imhof, A.; Rodrigues, A. J.; Sousa, N.; Sotiropoulos, I.

2026-01-23 neuroscience
10.64898/2026.01.21.700784 bioRxiv
Show abstract

INTRODUCTIONAccumulation of pathological Tau precipitates neuronal malfunction in Alzheimers disease (AD). However, the impact of loss of normal Tau function in the adult brain, independently of Tau aggregates, remains unclarified. METHODSWe used a mouse model with conditional mapt knocking-down in forebrain of 5-7 months old animals (cTau-KO), a virus-driven selective Tau knockdown in wild-types (WT) and Tau re-expression approaches, accompanied by neurostructural, epigenetic, proteomic, electrophysiological, neurochemical and behavioral analyses. RESULTSLoss of Tau in the adult brain of cTau-KOs triggers neuronal atrophy and malfunction, epigenetic as well cognitive and mood deficits. Importantly, these perturbations were confirmed by selective Tau loss in WT adult brain and reverted by Tau re-expression or pharmacologically-induced epigenetic correction in cTau-KOs. DISCUSSIONOur findings highlight the contribution of loss of normal Tau function in the adult brain malfunction that could be relevant in diverse brain pathologies beyond AD, associated to Tau and its dysfunction.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.