Transcriptional, Behavioral and Biochemical Profiling in the 3xTg-AD Mouse Model Reveals a Specific Signature of Amyloid Deposition and Functional Decline in Alzheimer's Disease.

Our finding that, in this model, the number of differentially expressed genes follow a decreasing trend in time, as the actual pathology aggravates, also suggests that most gene expression changes measured in post-mortem samples obtained from AD patients could represent a small proportion of the most critical gene expression alterations effectively linked to the initial onset of this condition, a circumstance that could also hold for other neurological conditions (i.e., Parkinson’s disease, schizophrenia, and others).

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Using a complementary approach, gene ontology analysis revealed a highly significant enrichment of learning and memory, associative, memory, and cognitive functions only among down-regulated, but not up-regulated, DEGs.

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