The common feature in neurodegeneration with dementia is neuronal dysfunction which is mainly and primarily expressed as synaptic dysfunction. The consequence of this dysfunction is neuronal disconnection and dementia if the corresponding hippocampal, basal forebrain and cortical structures are damaged. Neuronal loss is not necessarily a prerequisite for dementia, although it may be observed in some neurodegenerative diseases. If neuronal loss is not the major cause of the symptoms, in principle non-invasive treatment with the aim of cure should be possible, provided intervention occurs early enough. In dementias in which neuronal loss is a major event implantation of nerve cells may become an important aspect in treatment. The latter may apply to vascular dementia (VaD). In contrast neuronal dysfunction may apply for the most common form of dementia, Alzheimer's disease (AD). AD shares some of the characteristic clinical features of VaD, the second most prominent cause of dementia, in which mental deterioration affecting normal brain leads to a loss or impairment of intellectual functions of memory, power of reason and intelligence with interference with patient's conduct of the customary affairs of life. As we begin to understand some of the underlying pathogenetic mechanisms and causes of AD, this most frequent dementing condition is well suited to serve as model system to study the common principles of neurodegenerative diseases. Much of the present knowledge on the molecular and genetic processes that occur in AD came directly or indirectly from the identification of the beta A4 (A beta, beta) amyloid protein and its precursor which is termed amyloid precursor protein, and abbreviated as APP.(ABSTRACT TRUNCATED AT 250 WORDS)