Could an old brain be made young again?

Quick Response Code: As we age, so do our brains. Brain aging, like aging of the rest of the body, is accompanied by complex forms of stochastic damage that occurs to all our classes of macromolecules. Damage occurs to DNA in various forms including base pair mutations, causing loss of information content. DNA damage alone can drive many other features of aging. Damage also accumulates in lipids, including those associated with myelin in the brain, as well as myelin itself, which is very long-lived. And perhaps most damningly, age-associated damage to the extracellular matrix (ECM) alone, like DNA damage, drives many or most of the features of aging.[7] e ECM is largely made of proteins and carbohydrates, some of which once made, do not turnover for life. Extracellular carbohydrates remain poorly studied (we still have not come close to cataloguing all their species) and the damage they accumulate is largely understudied due to a lack of tools, but this damage is nevertheless likely to be daunting in its complexity. e types of age-associated damage found in extracellular scaffolding proteins are somewhat better studied. ese include forms of glycation, carbamylation, carbonylation, lipoxidation, mineralization, deamidation, racemization, fragmentation, denaturation, and aggregation. Most of these stochastic nonenzymatic forms of damage are problematic because there exists no repair machinery to reverse them, and in many cases, proteins that accumulate damage, such as collagens, become resistant to extracellular proteases.