[Neuroimmunology of Alzheimer's disease]

Alzheimer's disease (AD) is the most frequent cause of premature, irreversible cognitive decline in man, the consequence of which is complete psycho-social incompetence. 60% of all dementias are of the AD type, with its prevalence increasing logarithmically with age. Statistics from countries where average life expectancy is around 70 years show that 1% of the total population suffers from AD. If current demographic trends do not change, 40% of the population will be over 60 in 20 to 25 years and the number of AD sufferers will increase 5 times. AD is the fourth commonest cause of death in humans, after heart attack, cancer and stroke. We do not have any cure or efficient preventive measures against AD. The duration of the disease varies from 4-12 years and it is always fatal. Pathological characteristics of AD are neurofibrillatory tangles and senile plaques. Despite the identification and molecular characterization of the pathological forms of tau and beta-amyloid found in these pathological features, little is known of the etiology and the pathogenesis for AD. The main goal of current research is the identification of interactions between the nervous and immune systems which may be involved in the neuropathology and pathogenesis of AD. Namely, the identification of those sequences of molecular, cellular and systemic mechanisms which lead to the fatal neuronal degeneration which ultimately results in dementia. Understanding AD pathogenesis may lead to early AD diagnostic assay and new potentials for therapy.