Mechanisms underlying Alzheimer’s disease

Alzheimer’s disease (AD) is the most common kind of dementia in the elderly. It progresses over the years and leads to severe deficits in cognitive functions. The deficits are caused by parahippocampal atrophy that is thought to be an effect of amyloid beta deposition. The disease is pathologically defined by severe neuron loss, amyloid beta aggregation and formation of neurofibrillary tangles consisting of hyperphosphorylated tau protein.

There are several hypotheses regarding mechanisms and causes of the disease, but the etiology of Alzheimer’s disease is not yet fully understood. Two kinds of AD are recognized: early-onset AD (EOAD), of which many cases are genetically inherited familial AD (FAD), and late-onset AD (LOAD), which is not necessarily inherited. Although FAD is a very uncommon form of dementia, its etiology is very well recognized. The more common LOAD is much more difficult to explain, since it seems to be very differentiated.

The diagnosis is based on a large range of tools that detect both early changes and their progression in the later phases of the disease. Using both biomarkers and cognitive markers allows one to diagnose physiological, structural and cognitive changes.

Research ongoing for the past years brought us a few hypotheses about the formation of impairments in AD, and the methods of diagnosis. Therefore the aim of this article is to present the newest ones as well as those that are well established.