Is aging normal or abnormal/pathological? No one quite knows the answer to that question. What we do know is that as we age, neurological disorders become increasingly common. These may range from well defined neurodegenerative diseases like Alzheimers dementia, Parkinson disease and amyotophic lateral sclerosis to other less well defined conditions like gait disorders, “balance problems”, “forgetfulness and senior moments” and increased propensity to falls. Strokes become more common in the aged brain vessels.
As life expectancy increases and more and more people live past the eight decade, neurological conditions become common and account for substantial morbidity and mortality in the oldest old (above 85). Earlier when the life expectancy was in the 60s, we did not see so much Alzheimers dementia, Parkinson’s disease or brain tumors. People died of other “natural” and “unnatural” causes before the brain showed clinical manifestations of neurodegeneration.
Is it the norm that as we age, a substantial majority of us are destined to develop dementia? Clinical studies have clearly shown that Alzhemier disease pathology increases with age and the incidence of the disease becomes increasingly common as one goes past 85 (the oldest old). Other studies suggest that though not all the oldest old show clinical dementia, a substantial majority have cognitive difficulties if carefully tested for at the bedside.
Why do neurological conditions become more “common” as we age and can we do anything to alter this? Many theories have been propounded. Increased amyloid deposition in the brain has causal association with Alzheimers dementia, in the same vein deposition of iron in the basal ganglia has been postulated to cause various basal ganglia pathology. There is increased oxidative stress in the “aged” brain which leads to free radical formation and damage to the cellular DNA. Genes get switched off or on triggering the disease process. A lot still needs to be learned about the neurology of aging.
While the mechanisms are still been elucidated, is there anything which we can do to change our “risks”. In the absence of good studies most of the data is open to interpretation. Aspirin prophylaxis, modification of microvascular and macrovascular risk factors like hypertension, diabetes mellitis and dyslipidemia (high “bad” cholesterol) all seem to be reasonable interventions. Obesity and sedentary life styles are bad for the brain too. Regular physical as well as brain exercises (neurobics) keeps the brain healthy and increases neuronal reserve. The role of anti-oxidants like coenzyme Q10 and alpha lipoic acid is still been defined. As they are relatively innocuous and free from side-effects, I would recommend them on a case by case basis. Episodes of major depression “hurt” the brain and aggressive treatment with anti-depressants should be initiated early rather than late.
The neurology of aging remains an uncharted territory but there is hope yet.
Nitin Sethi, MD