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RNA-seq of frontal cortex in a novel mouse model of Alzheimer's disease.

ABSTRACT: There is accumulating evidence that amyloid beta and tau proteins may act synergistically to cause synapse and neural circuit degeneration in Alzheimer’s disease. In order to study this, we designed a new mouse model which lacks endogenous mouse tau, but expresses both the APP/PS1 transgene, which causes well-characterised plaque-associated synapse loss, and also reversibly expresses wild-type human tau (which can be suppressed with doxycycline). We examined the transcriptional changes in the frontal cortex of this mouse model, along with behaviour, pathology, synaptic plasticity, synapse degeneration and accumulation of amyloid beta and tau at synapses, and compared with littermate control genotypes: those lacking endogenous mouse tau, those lacking endogenous mouse tau but expressing the APP/PS1 transgene only, and those lacking endogenous mouse tau but reversibly expressing wild-type human tau only.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Owen Robert Dando

PROVIDER: E-MTAB-7856 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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