In general, two main groups of dementia can be distinguished, requiring different types of treatment:
In primary forms of dementia (about 90%), the condition is due to neurodegenerative and/or vascular intracerebral changes which are treated primarily using antidementia treatment strategies.
Non-cerebro-organic forms of dementia (10%) are due to another underlying disease (e.g. cardiovascular disease, alcohol abuse, metabolic disturbance or encephalitis) in which causal treatment is the top priority and thus produces a positive effect on the reversible cognitive disturbances.

Neurodegenerative dementia
In the group of primary forms of dementia about every second case of dementia belongs to the neurodegenerative dementia syndrome. The commonest representative of these is Alzheimer´s Disease. Characteristic morphological features are atrophy of the hippocampal and cortical regions, pathological protein deposits known as amyloid plaques and neurofibrillary tangles. In a large epidemiological study (the so-called Rotterdam study), AD was diagnosed in 72% of cases [Ott et al., 1995].
Characteristics of Alzheimer´s Disease
The characteristic clinical feature of AD is a gradual onset which usually becomes noticeable from the age of 65 (AD of late onset), although it also appears in younger people (AD of earlier onset, < 65 years), particularly in the form of cognitive disturbances. The course of AD is uniform and progresses with increasingly manifest symptoms of amnesia, apraxia, agnosia and aphasia. Ultimately, patients not only suffer from further impairment of cognitive function but above all lose the ability to cope with everyday life and their independence [Füsgen, 2001; Förstl, 2001]. Patients with early onset of AD are generally observed to have rapid loss of cognitive and functional skills, plus lesions of the temporal and parietal lobes, with dysphasia and dyspraxia [Henderson and Jorm, 2000].
Vascular dementia
Vascular dementias (VaD) with an estimated proportion of about 20% are often called "multi-infarct dementias". VaDs can be divided into groups of subcortical arteriosclerotic encephalopathies, territorial and border-zone infarcts, cerebral amyloid angiopathies and small, multiple cortical and subcortical infarcts [Diehl and Kurz, 2002].
Depending on the ischemically damaged regions of the brain, the VaD can manifest itself clinically either suddenly or gradually over a particular period. Patients with VaD often have a history of transient ischemic attacks, apoplectic shock or ischemic cerebral infarcts with considerable physical disability. In the course of VaD, other, non-cognitive impairments usually appear, such as unilateral spasticity of the extremities and/or unilaterally increased tendon reflexes [Henderson and Jorm, 2000].
Mixed forms
With increasing age mixed types often occur, the clinical picture of which includes symptoms of vascular and neurodegenerative (e.g. AD) dementia [MRC CFAS, 2001].