Synergy between depression and Alzheimer's disease: A spectrum model of genomic vulnerability with therapeutic

We have previously postulated that Alzheimer’s disease (AD), mild cognitive impairment (MCI), and accelerated aging progress with similar molecular signaling and are a result of genomic vulnerability. Chronic depression–nothwithstanding comorbidties–may also enter the same pathways due to mutant alleles in the depression associated genes such as neurotransmitter-serotonin transporter proteins, e.g. 5-HTT. When depression, AD, and MCI are predisposed due to genomic vulnerability, molecular cascades for the illnesses may combine. Thus, phenotypes may reinforce each other and present an enhanced pathogenic intensity. We suggest that this model can highlight the genotypic and phenotypic interactions of these two neuropathologies and can be used to create new treatment approaches.