Alzheimer's Disease Support Group

As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language (aphasia), skilled movements (apraxia), recognition (agnosia) and those functions (such as decision-making and planning) closely related to the frontal and temporal lobes of the brain as they become disconnected from the limbic system, reflecting extension of the underlying pathological process. This consists principally of neuronal (cell) loss (or atrophy), together with an inflammatory response to the deposition of amyloid plaques and neurofibrillary tangles. Genetic factors are known to be important, and autosomal dominant mutations (variations) in three different genes - Presenilin 1, Presenilin 2, and Amyloid Precursor Protein - have been identified that account for a small number of cases of familial, early-onset AD. For late onset AD (LOAD), only one susceptibility gene has so far been identified - the epsilon 4 allele of the Apolipoprotein E gene. Age of onset itself has a heritability of around 50%.