Alzheimer’s disease, the 2nd most common neurodegenerative disease world wide. Unfortunately, there are currently no effective treatment methods nor early detection methods. Furthermore, the majority of  disease underlying molecular mechanisms are yet mainly poorly understood. Global bulk gene expression profiling have recently suggested that the disease is mainly governed by diverse transcriptional regulatory networks. I have recently analysed global RNA expression and high confidence as well as alternative splicing differences in single-nuclei cells collected from the brains of two Alzheimer’s disease (AD) post-mortem patients samples in disease stages Break I and II, as well as age- and as compared with two age- and gender-matched controls hippocampal (HIPP) brain samples. My bioinformatic/computational data analysis have so far identified discrete glial, immune, neuronal and vascular cell populations spanning patients and controls. Both astrocytes and microglia cell marker genes displayed the greatest transcriptomic changes and neuronal genes changed as well. Both A-beta and Tau proteins may form brain toxic aggregates which may lead to cellular death in affected cells. Furthermore, microRNAs, 19-25 nucleotide long RNA regulating molecules,  may also be involved in AD, as well as long non-coding RNAs (lncRNAs). Additionally, several RNA binding proteins (RBPs) have been linked to the disease, including the Tau protein. In terms of molecular processes that might be involved in AD, the immune system. Inflammation and  mitochondrial changes might be involved. Insights based on such studies may advance development of novel disease future therapeutics.