The proportion of adults aged 60 years and over is expected to increase over the coming decades. This ageing of the population represents an important health issue, given that marked reductions to cerebral macro- and microstructural integrity are apparent with increasing age. Reduced cerebral structural integrity in older adults appears to predict poorer cognitive performance, even in the absence of clinical disorders such as dementia. As such, it is becoming increasingly important to identify those factors predicting cerebral structural integrity, especially factors that are modifiable. One such factor is nutritional intake. While the literature is limited, data from available cross-sectional studies indicate that increased intake of nutrients such as B vitamins (for example, B6, B12 and folate), choline, n-3 fatty acids and vitamin D, or increased adherence to prudent whole diets (for example, the Mediterranean diet) predicts greater cerebral structural integrity in older adults. There is even greater scarcity of randomised clinical trials investigating the effects of nutritional supplementation on cerebral structure, though it appears that supplementation with B vitamins (B6, B12 and folic acid) or n-3 fatty acids (DHA or EPA) may be beneficial. The current review presents an overview of available research examining the relationship between key nutrients or adherence to select diets and cerebral structural integrity in dementia-free older adults.

Background: The risk of developing dementia by elderly patients with only subjective memory complaints (SMC) is unclear. Our objective was to assess the prognosis of such patients regarding subsequent development of dementia.

Methods: From 1992 to 1996, 211 consecutive patients (age 67.4±9.4 years, mean±SD) were diagnosed as having SMC. These patients were followed for 3 years or to the time they were diagnosed with dementia, whichever came first. A survival analysis was performed for occurrence of dementia within 3 years.

Results: The duration of memory decline was shorter among patients who developed dementia than among those who did not (32.6 vs. 49.9 months, F=3.3, p=0.07). Patients who developed dementia tended to be older at the reported onset of memory decline (71 vs. 66.2 years, F=3.2, p=0.07). Lower risk of dementia was associated with higher cognitive performance at entry [odds ratio (OR)=0.74 (0.59–0.92)] and longer time from onset of memory decline to referral [OR=0.91 (0.85–0.98)].

Conclusion: Subjects with SMC have an increased risk of developing dementia, particularly those with lower cognitive status at entry and with older age at onset of memory complaints, and shorter duration of their memory complaints.

Cerebrovascular small vessel disease is now believed to be the major source of vascular burden of the brain. Cerebrovascular small vessel disease and Alzheimer's disease appear to represent pathophysiologic and clinical continua, rather than dichotomous entities. It appears that common etiopathologic mechanisms underlie the clinical presentation of both of these conditions. Therefore, the staging procedures that have been developed for the clinical continuum of age-associated memory impairment, mild cognitive impairment, and the progressive dementia of Alzheimer's disease appear to be applicable for the same continua in cerebrovascular small vessel disease. Although temporal and prognostic aspects have been studied for the Alzheimer's-related portions of this clinical staging continuum, they remain to be elucidated for cerebrovascular small vessel disease.

The provisional criteria for age-associated memory impairment (AAMI) attempt to define a potentially treatable decline in mental function found in people over 50 years of age. It is suggested here that the present criteria are likely to apply to a large proportion of those over age 50 in the population. From a psychometric viewpoint the criteria have several short-comings that are detailed. Finally, the social and ethical problems of the wider use of such a diagnosis are adumbrated.

Recent research aimed at discovering and developing new drugs for diseases of cognition focuses heavily on Alzheimer’s disease and emphasizes mechanistic/biochemical approaches. Originally, research was based on a pragmatic search for compounds that would protect animals front disruptors of learning and memory. A series of compounds called nootropics do protect animals against these disruptions and offer hope that cognitive deficits may be amenable to pharmacological treatment. However, clinical development of these compounds is complicated by a number of factors. Among these is the poor correlation between animal models of cognitive loss and clinical disease states, a notable exception being the amnesic effects of benzodiazepines. Moreover, the inverted U-shaped dose-response function obtained in animal models and the lack of standard clinical outcome measures further complicate the development process. Tests that are beginning to gain acceptance as “standards” need to be characterized in terms of their validity, variability, and stability. There is a dearth of normative, especially longitudinal, data on cognitive decline. However, the great efforts being made in basic and applied research warrant cautious optimism.