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Pathological hyperphosphorylated forms of the microtubule-associated binding protein Tau (pTau) are commonly found in people with neurodegenerative diseases, including Alzheimer’s disease, Corticobasal degeneration, and Progressive supranuclear palsy.

Graphical abstract of the published paper by Viney et al showing the main observationsTim Viney and colleagues observed in a transgenic mouse model that pTau accumulated in hippocampal pyramidal neurons from an early age, and that these neurons eventually degenerated in aged mice. DPhil student Barbara Sarkany could demonstrate that pTau spread from the axons of the pyramidal neurons to oligodendrocytes. This specialised type of glial cell produces the myelin that insulates the pyramidal neuron axons.

To investigate the consequences of such neurodegeneration and spread of pTau, in collaboration with Professor David Bannerman from the Department of Experimental Psychology, they found that transgenic mice were impaired in recognizing novelty. However, performance in spatial working memory and reference memory tasks was similar to littermates that lacked Tau pathology.

Cortical pyramidal neurons, representing memories, exhibit a wide range of firing rates, and in aged transgenic mice there were significantly fewer high-firing rate pyramidal neurons. Despite the loss of neurons, network oscillations and the activity of pTau-free neurons within pTau hotspots were surprisingly normal. The results support the hypothesis that unaffected subcortical inputs to the hippocampus maintain the network, largely counteracting the high levels of pTau and neurodegeneration.

“Spread of pathological human Tau from neurons to oligodendrocytes and loss of high-firing pyramidal neurons in ageing mice” by Tim J. Viney, Barbara Sarkany, A. Tugrul Ozdemir, Katja Hartwich, Judith Schweimer, David Bannerman, and Peter Somogyi. Published in Cell Reports on 15/11/2022.

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