Whoever would have thought that bone health could impact the development of dementia? Until I learned about new research in this regard, I wouldn’t have connected the two. The operant word here is “health” and that is a function of exercise. Now, if you’ve read these newsletters in the past you’re probably thinking; Oh boy, here comes another sermon on the value of exercise. And guess what? You’re right!
The research connecting the two is from the fields of neuroscience and endocrinology. It turns out that our bones are an endocrine organ that produces a hormone called osteocalcin. Osteocalcin acts on many organs in the body including the brain but also on gene expression (the functionality of genes). Regular exercise promotes bone mass (helping prevent fracture) and the increased mass leads to higher output of osteocalcin.
At a brain level osteocalcin improves the production of serotonin, dopamine, GABA and other neurotransmitters. These chemicals are vital to establishing new memories and maintaining previous memories.
At a genetic level osteocalcin ramps up gene expression (function) of RbAp48. This gene is critical for protein formation that allows the brain to convert short term memory to long term memory. Research in mice demonstrated that a normal part of aging is reduced osteocalcin production which is also true in humans hence the usual “benign senescent forgetfulness” which is not dementia. But in mice, experiments knocking out the RbAp48 gene led to very early and rapid onset of dementia. Injecting RbAp48 into these young, demented mice allowed recovery of memory function. The next step will be to extend these findings to humans