One of more remarkable epidemiological changes witnessed over the 20^th century is the aging of the population. This change has led to a marked alteration of disease profiles, characterized by a drastic increase in aging-related disorders affecting almost all organ systems. Some, such as the blood have an excellent compensatory capacity, while in other systems, this capacity is quite limited. The brain is probably the most vulnerable to this aging process. Cumulative damage to this organ eventually outpaces the considerable innate redundancy present and the limited capacity for reorganization and compensation.
It is well established that atherosclerosis starts quite early in life, probably in early adulthood, although its clinical manifestation only becomes evident several decades later. These clinical manifestations include strokes of various kinds, although many strokes are clinically silent. In other cases, the vascular changes are not evident as separate strokes but rather as white matter changes leading to extrapyramidal manifestations, which are referred to as vascular parkinsonism or cognitive decline. Such changes are not always clinically identifiable, but are easily seen on imaging as lacunes or leucoaraiosis.
In the context of cognitive impairment, it has become clear over the past few years that cases of multi-infarct dementia are outnumbered by cases where the vascular damage is insidious. Even more common are those cases in which one considers the vascular damage to the brain under the backdrop of Alzheimer changes. Like atherosclerosis, these changes also begin during early adulthood and their insidious progression could go unnoticed, if not for the cumulative effect of vascular changes on the brain. In older cohorts, autopsy very frequently shows evidence of dual pathology.
The present volume provides important information on several of these topics, ranging from anatomical, functional and imaging aspects to the neuropsychological manifestations, and includes therapeutic approaches for the treatment of vascular dementia.
Recent years have witnessed an impressive accumulation of knowledge with regard to the epidemiology and pathogenesis of dementia. The most common cause of dementia is thought to be Alzheimer’s disease (AD), followed by vascular dementia (VaD). Conceptually these are two unrelated disorders. AD is attributed to a primary neurodegenerative process while VaD is secondary to a host of different processes, which include not only frank strokes but also lacunes and white matter ischemic damage. However, the distinction between VaD and AD is not well defined and “mixed dementia” is quite common. Therefore it is logical to examine drugs which are effective in AD for their efficacy in VaD.
Therapy for VaD remains a challenge. Obviously, primary prevention should be the main goal. Almost by definition, treatment aimed at risk factors should work, but very little evidence exists to support this. Aggressive therapy for hypertension can reduce the incidence of VaD but since there are many factors contributing to strokes, elimination of  all potential causes of stroke is required. Although proof of the efficacy of such treatments for strokes is available, the endpoints of dementia are frequently not targeted - these require a larger population size and longer follow-up period. Moreover, there may be other yet unidentified factors which contribute to the occurrence of vascular brain disease including VaD. Some of these may be genetic. For example, CADASIL and Fab ry’s disease may result in dementia, but the effects of conventional therapies to delay strokes probably are ineffective in these disorders.
At present in most countries, there is no drug approved for the treatment of VaD. Several factors contribute to this unfortunate situation. Firstly, the definition of VaD is problematic. VaD is neither a disease nor a syndrome. It is caused by several factors, and has heterogeneous clinical and imaging phenotypes. Thus, a significant obstacle to the development of drugs for VaD is the heterogeneity of the pathogenic processes leading to cognitive impairment. The four main pathogenic processes involved are:

1. Strokes leading to damage in areas in the cortex or thalamus strategic to cognitive function.
2. Subcortical damage affecting the white matter The ensuing leucoencephalopathy will impair connectivity between brain regions.
3. Damage to specific tracts, e.g., cholinergic pathways of the nucleus basalis of Meynert to the cortex.
4. Hypoperfusion of brain areas such as the hippocampus, which may not result in acute strokes, yet nonetheless causes cumulative damage to areas important to certain cognitive tasks.

There is no reason to assume that a given drug will be effective against recurrent cardiogenic strokes and progressive subcortical leucoencephalopathy, which are assumed to be caused by cerebral microangiopathy and frequently lead to cognitive deterioration.
The editor and authors of this volume are to be congratulated on producing this important publication that will hopefully be a useful resource for the many professionals who are involved in various aspects of investigation and care of patients with dementia.