Determinants of hippocampal atrophy with arterial disease

Dementia is a growing problem in industrialized countries. With the prolonged life expectancy the size of the older population will grow considerably. With rising age, the prevalence and incidence of dementia will increase exponentially. It is estimated that the prevalence of dementia doubles every five years after the age of 60 and that the overall incidence rate of dementia in people over 90 years of age is as high as 18% per year. Dementia is characterized by progressive cognitive impairment as well as non-cognitive symptoms such as mood and personality changes. One of the first structures to be affected in dementia is the hippocampus. The hippocampus, consisting of the ammon’s horn, the dentate gyrus and subiculum, is part of the medial temporal lobe. It belongs to the limbic systems and is involved in episodic memory. Several studies have shown that the hippocampal volume loss is associated with cognitive decline in nondemented populations. The last past decades there have been considerable advances in the understanding of Alzheimer’s disease and other dementias, however, to date no fully effective treatments and preventive strategies have been found. Early identification and institution of preventive measures for risk factors predisposing to cognitive decline are of high priority. It is important to further unravel the etiology of Alzheimer’s disease and other dementias to gain insight into mechanisms that cause the disease enabling development of preventive and curative strategies. In this thesis we investigated the age-related changes in hippocampal volumes in non- demented elderly. Furthermore, we investigated the effect of ischemia, hypoxia and high levels of glucocorticoids as risk factors that have been suggested to be particular detrimental for the hippocampus. Data were used from the Second Manifestation of ARTerial disease Memory, depression and aging (SMART-Medea) study.