In conclusion, statin users had lower risk of breast cancer death compared to non-users in a nationwide cohort of Finnish breast cancer patients. Combined with previous evidence from in vitro, epidemiological and clinical studies our study suggests that, apart from cardiovascular benefits, statins may have beneficial effect against breast cancer progression. However, because uncertainty remains due to biases related to differing likelihood for statin use in different patient groups our results need to be confirmed in a randomized clinical trial before statins can be recommended for breast cancer treatment. The human brain changes structurally, functionally, and metabolically throughout the lifespan. Programmed dendritic growth followed by pruning, neuronal loss, shifts in energy metabolism from ketone body to glucose consumption, and rapid myelination occur during development. Many of these changes are completed within the first two decades of life, although myelination can continue into the fourth decade. In middle age, the brain reaches a level of homeostatic stability, but neuronal and synaptic loss associated with cognitive changes can appear later on. Aging also is a risk factor for progressive brain disorders in which neuroinflammation plays a prominent role. Neuroinflammation involves activation of resident brain microglia and astrocytes, and can be produced by different internal or external stresses. Downstream activation of IL-1 receptors and TNFa receptors on astrocytes and other cell types alters levels of transcription factors such as nuclear factorkappa B and activator protein -2, which can increase expression of a number of inflammatory genes. The term “inflamm-aging” has been proposed to describe the progressive increase in Remdesivir proinflammatory status in the brain with senescence. Inflamm-aging may prime brain microglia and astrocytes to respond excessively to different stressors, including neurodegenerative, traumatic or infectious insults. Increased inflammatory response markers with late-state brain aging have been documented in rodents, nonhuman primates, and humans. Increases have been noted in proinflammatory cytokines IL-1a, IL-1b, IL-18 and IFNc, major histocompatibility complex class II, CD11b, scavenger receptors CD68, CD86 and CD40, and TLRs 1, 2, 4, 5, 7, and 9. In the human brain, increased TNFa and interferon gammainducible protein 16 were reported, as were increased mRNA and protein levels of CD11b, glial fibrillary associated protein, IL-1b, iNOS, NF-kB p50, cytosolic phospholipase A2 Type IVA and cyclooxygenase -2, while levels of brain derived neurotropic factor protein and synaptophysin were reduced. Cytokines, chemokines, growth and other microglial and astrocytic factors.