The hippocampus undergoes changes with aging that impact neuronal function, such as synapse loss and altered neurotransmitter release. Nearly half of the aged population also develops deficits in spatial learning and memory. To identify age-related hippocampal changes that may contribute to cognitive decline, transcriptomic analysis of synaptosome preparations from adult (12 months) and aged (28 months) Fischer 344-Brown Norway rats assessed for spatial learning and memory was performed. Bioinformatic analysis identified the MHCI pathway as significantly upregulated with aging. Age-related increases in mRNAs encoding the MHCI genes RT1-A1, RT1-A2, and RT1-A3 was confirmed by qPCR in synaptosomes and in CA1 and CA3 dissections. Elevated levels of the MHCI cofactor (B2m), antigen-loading components (Tap1, Tap2, Tapbp), and two known MHCI receptors (PirB, Klra2) were also confirmed. Protein expression of MHCI was elevated with aging in synaptosomes, CA1, and DG, while PirB protein expression was induced in both CA1 and DG. MHCI expression was localized to microglia and neuronal excitatory postsynaptic densities, and PirB localized to neuronal somata, axons and dendrites. Induction of the MHCI antigen processing and presentation pathway in hippocampal neurons and glia may contribute to age-related hippocampal dysfunction by increasing neuroimmune signaling or altering synaptic homeostasis.

Ion channels have been shown to be involved in oncogenesis and efforts are being poured in to target the ion channels. There are many clinically approved drugs with ion channels as "off" targets. The question is, can these drugs be repurposed to inhibit ion channels for cancer treatment? Repurposing of drugs will not only save investors' money but also result in safer drugs for cancer patients. Advanced bioinformatics techniques and availability of a plethora of open access data on FDA approved drugs for various indications and omics data of large number of cancer types give a ray of hope to look for possibility of repurposing those drugs for cancer treatment. This article is part of a Special Issue entitled: Membrane channels and transporters in cancers.

Fasting-induced changes in clinical pathology results were consistent with hemoconcentration and altered nutrition and metabolic function. Most changes occurred at 16 hours, with minimal subsequent changes. Hence, a 16-hour fasting duration may be recommended for preclinical studies involving clinical pathology measurements.

No abstract