Alzheimer's disease: amyloid beta-peptide antibody vaccine as plaque remover.

Abstract

Alzheimer’s disease (AD) is a major cause of dementia. It is believed to affect 11% of all humans over 65 years of age and 50% over the age of 85 in caucasian populations. It is a chronic brain disorder with a lengthy preclinical phase followed by a malignant stage associated with neuronal degeneration, loss of specific synaptic connections and progressive erosion of cognitive ability. AD begins with a subtle failure of memory, slowly becoming more severe and eventually incapacitating the patient. Neuronal degeneration in AD is highly selective for certain brain regions and types of neurons and can lead to a profound atrophy of the cerebral cortex. The amygdala, hippocampus and parahippocampus show a high degree of neurodegeneration, whereas the striatum and cerebellum are less affected. Subcortical pathways involving catecholaminergic, seritonergic and cholinergic transmissions are affected, whereas neocortical interneurons such as GABAergic and inhibitory are relatively unaffected. A subset of pyramidal cells in layers II, III and V that use excitatory amino acids as transmitters are highly vulnerable in AD. The loss of neurons has a variable time course between individuals and it could take months to years for a neuron to degenerate. Neuronal degeneration in AD starts rapidly from the medial temporal lobe and gradually spreads to other neocortical areas (Vickers et al 2000).