Israel et al. Supp Fig1: Experimental design.
Alzheimer’s disease (AD) is a devastating neurodegenerative disease that could become an even more massive public health problem than it already is, if current projections hold. Some predict that by 2050, 1 in 85 individuals will be affected by the disease. Currently, there is no cure, but there are neurotransmitter-enhancement-based strategies to slow down the cognitive deficits [the loss of cholinergic neurons is implicated in some of the memory problems associated with AD so therefore, pharmacological enhancement of brain acetylcholine concentration can partially alleviate some memory-based symptoms.] However, as with many neurodegenerative diseases, these stop-gap treatments only work for so long, until the cells responding to neurotransmitter supplementation treatments die off completely. Therefore, diverse strategies designed to cure or at least slow down AD are imperative.
While a number of AD transgenic mouse models have been created, based on the various mutations identified in patients, the trouble is that these models still utilize the cross-species approach of studying “diseased” mouse neurons expressing mutated human genes. And perhaps an even bigger problem with many mouse models, genetically-inherited forms of AD represent only ~0.1% of cases, with the remainder being “sporadic” (although there are genetic risk factors influencing the emergence of sporadic AD.)