Garcia-Alloza M, Subramanian M, Thyssen D, Borrelli LA, Fauq A, Das P, Golde TE, Hyman BT, Bacskai BJ. Existing plaques and neuritic abnormalities in APP:PS1 mice are not affected by administration of the gamma-secretase inhibitor LY-411575. Mol Neurodegener. 2009;4:19. PubMed.

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  1. A similar result has been previously published with lithium treatment and tau protein, showing that pre-formed neurofibrillary tangles do not revert.

    We used a transgenic model that overexpresses tau protein with three FTDP-17 mutations and GSK-3β to address two issues: first, whether chronic lithium treatment was able to prevent the formation of aberrant tau aggregates that result from the overexpression of FTDP-17 tau and GSK-3β; second, whether lithium is able to change back already formed NFTs in aged animals. Our data suggest that progression of the tauopathy can be prevented by administration of lithium when the first signs of neuropathology appear. Furthermore, it is still possible to partially reverse tau pathology in advanced stages of the disease, although NFT-like structures cannot be changed. The same results were obtained after shutdown of GSK-3β overexpression, supporting the possibility that GSK-3 inhibition is insufficient to reverse NFT-like aggregates.

    References:

    Engel T, Goñi-Oliver P, Lucas JJ, Avila J, Hernández F. Chronic lithium administration to FTDP-17 tau and GSK-3beta overexpressing mice prevents tau hyperphosphorylation and neurofibrillary tangle formation, but pre-formed neurofibrillary tangles do not revert. J Neurochem. 2006 Dec;99(6):1445-55. PubMed.

    View all comments by Felix Hernandez

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