The current literature available on databases in medicine and related areas clearly shows a remarkable growth of knowledge in neuro-degenerative and cerebrovascular diseases. However, it shows an equally remarkable gap between the ‘neurodegenerative field’ and the ‘vascular field’. Research on dementia/cognitive impairment is heavily ‘alzheimerised’, giving vascular pathologies secondary status. Research on stroke/cerebrovascular disorders has a tendency to leave out cognition. This separation has led to two main lines of studies, focused on two extremes: clinical stroke and dementia. Both stroke and dementia are common in older age, so their joint occurrence is not a rare phenomenon. An examination of the literature of related disciplines shows that stroke and dementia actually have more in common than was previously thought.

Outcomes in epidemiological studies, stroke and dementia are difficult to define, as both are heterogeneous and multifactorial conditions with genetic and environmental risk factors. Most epidemiological studies do not have reliable information about stroke/dementia types and the mechanisms involved. Stroke is usually classified as ischaemic or haemorrhagic, but the aetiology is far more heterogeneous: approximately 50% of ischaemic strokes, for example, are caused by large-artery atherosclerosis, 25% by small-vessel disease, 20% by cardiac embolism and 5% by other causes, e.g. arterial dissection.¹ Various subtypes of ischaemic stroke may have different risk factors, e.g. atrial fibrillation and mitral valve disease are related to cardioembolic stroke, but not to atherosclerotic stroke. A history or indication of recent stroke is included in the diagnostic criteria for vascular dementia (VaD), so risk factors for VaD are presumed to be similar to those of cerebrovascular disease. However, to complicate matters, cerebrovascular lesions often co-exist and interact with neurodegenerative changes, playing an important role in dementia of Alzheimer’s disease (AD). The co-existence of AD type and vascular changes seems to be more frequent than would be expected by chance,^2,3 and AD and VaD have a significant overlapping of risk factors, clinical features and pathology. ‘Pure’ AD and VaD can be considered opposite ends of a dementia aetiology continuum, in which most cases have combinations of AD type and vascular changes of different degrees.⁴ Epidemiological studies with stroke or dementia (i.e. clinical extremes) as outcomes merely see the tip of the iceberg. Subclinical vascular disease (e.g. silent infarcts, microhaemorrhages) is more frequent than clinical stroke,⁵ and can lead to subtle cumulative brain damage over time, increasing the risk of clinical stroke and dementia (AD, VaD or mixed). AD has a long pre-clinical phase, with neuropathological changes starting decades before the disease becomes clinically manifest as cognitive impairment/dementia. The concepts of vascular cognitive impairment (VCI) and mild cognitive impairment (MCI) are attempts to refine outcomes and define groups of individuals who may benefit more from interventional strategies. For example, patients with cognitive impairment are often excluded/not identified in stroke clinical trials. In confronting stroke and dementia, the best time for preventative interventions would be the ‘brain at risk’ stage before clinical manifestations appear.⁵

The purpose of this article is to give a brief overview of lifestyle-related factors in stroke and dementia, with an emphasis on integration instead of separation. Both stroke and dementia represent major public health problems. Evidence from epidemiological studies indicates that their risk profiles have many similarities (see Table 1), so integrated intervention strategies will be required for effective prevention.