Dementia prevention

An epidemic of dementia is occurring in Australia and around the world. Professor Craig Anderson explores the socioeconomic impact of dementia, and the link between vascular risk factors and dementia.

Transcript

Hello, I’m Professor Craig Anderson, professor of stroke medicine and clinical neuroscience at the George Institute for International Health at the University of Sydney and at Royal Prince Alfred Hospital in Sydney, Australia.

I joined the editorial advisory board of Virtual Neurocenter three years ago and today would like to share with you my insights into the prevention of dementia.

An epidemic of dementia is occurring in Australia and other developed countries around the world. Currently there are approximately two hundred thousand people living with dementia in Australia and at least another several hundred thousand people with milder degrees of impairment in memory and thinking that are related to brain disease.

Dementia costs our society many millions of dollars in direct health costs but the socio-economic effect on families and carers are enormous. With an aging population the burden of dementia is likely to rise even more.

So can anything be done to prevent the onset of dementia?

Well, probably. A substantial and ever increasing amount of evidence is mounting to indicate that stroke and cardiovascular disease and its risk factors more broadly, are important in the etiology or may trigger the onset of not just Alzheimer’s disease but other forms of dementia such as over vascular dementia or mixed forms of dementia.

A large number of vascular risk factors have been identified as being associated with dementia. These include a prior history of stroke, high blood pressure, coronary artery disease, diabetes, peripheral arteriosclerosis, smoking and hyperlipidemia.

The association appears greatest when these risk factors are clustered together and hold true whether we examine markers of dementia, such as cerebral atrophy or white matter disease, as well as harder in points such as memory impairment, cognition, and diagnostically classified forms of dementia.

Most of these data are derived from non-experimental observation and clinical studies and of course the most robust evidence of association comes from randomized controlled trials. But to date these have produced mixed results. For example the trials of cholesterol lowering amongst people with high risk of cardiovascular disease have not shown an effect on cognition or dementia.

Things are a little bit more promising in trials of blood pressure lowering where there have been data derived from five large randomized control trials to date. These have produced results that trend towards a significance in showing a positive benefit in the prevention of dementia and cognition.

In particular the Perindopril Protection Against Recurrent Stroke study or Progress showed that active treatment resulted in an overall but not significant twelve percent reduction in the risk of dementia. But amongst those who received a combination of blood pressure lowering treatment and therefore were a greater reduction in blood pressure, there was a borderline significant twenty three percent reduction in the risk of dementia.

The benefit of blood pressure lowering appeared to be mainly as a result of preventing dementia as a consequence of recurrent stroke. These data indicate that blood pressure reduction not only protects patients from recurrent stroke but can also have benefits in terms of preventing dementia and of cognitive decline.

The exact mechanism by which vascular risk factors might increase the risk of dementia are not clear. The most obvious example is a large stroke causing major brain damage; however, dementia appears to arise from the effects of small strokes or other direct / indirect manifestations of cerebral vascular disease.

The possibility of an additive or synergistic effect on the combination of cerebral vascular disease on preexisting, early Alzheimer’s disease, appears the most compelling scientific rationale. Autopsy studies suggest that the presence of even a small amount of infected brain tissue can substantially amplify the effect of Alzheimer’s neuropathology on cognition and particularly when the changes are extensive.

To summarize then, current evidence indicates that blood pressure in particular but all other vascular risk factors can have a pernicious effect on brain structure and  function that may begin in middle adult life. Current evidence is string that aggrieve management of vascular risk factors may not only translate into immediate health benefits including the prevention of heart disease and stroke, but could also translate into substantially increasing the likelihood of better brain health in later life.

Thank you very much for watching and have a great day.