Most common cause of dementia; 10% of all persons age >70 have significant memory loss, and in more than half the cause is AD. Cost is >$50,000 annually for a pt with advanced AD.
Cognitive changes follow a characteristic pattern beginning with memory impairment and spreading to language and visuospatial deficits, although 20% present with nonmemory complaints such as word-finding, organizational, or navigational difficulty. Memory loss is often not recognized initially, in part due to preservation of social graces until later phases; impaired activities of daily living (keeping track of finances, appointments) draw attention of friends/family. Once the memory loss becomes noticeable to the pt and spouse and falls 1.5 standard deviations below normal on standardized memory tests, the term mild cognitive impairment (MCI) is applied; roughly 50% will progress to AD over 4 years. Increasingly, the MCI construct is being replaced by the notion of “early symptomatic AD” to signify that AD is considered the underlying disease. Recent evidence suggests that partial and sometimes generalized seizures herald AD and can occur even prior to dementia onset, especially in younger pts. Disorientation, poor judgment, poor concentration, aphasia, and apraxia are increasingly evident as the disease progresses. Pts may be frustrated or unaware of deficit. In end-stage AD, pts become rigid, mute, incontinent, and bedridden. Help may be needed with the simplest tasks, such as eating, dressing, and toilet function. Often, death results from malnutrition, secondary infections, pulmonary emboli, heart disease, or, most commonly, aspiration. Typical duration is 8-10 years, but the course can range from 1 to 25 years.
Risk factors for AD: old age, positive family history, and a history of head trauma with concussion. Pathology: neuritic plaques composed in part of Aβ amyloid, derived from amyloid precursor protein (APP); neurofibrillary tangles composed of abnormally phosphorylated tau protein. The apolipoprotein E (apoE) ε4 allele accelerates age of onset of AD and is associated with sporadic and late-onset familial cases. ApoE testing is not indicated as a predictive test. Rare genetic causes of AD are Down syndrome and mutations in APP, presenilin-1, and presenilin-2 genes; all increase production of Aβ amyloid. Genetic testing available for presenilin mutations; likely to be revealing only in early-age-of-onset familial AD. Genome-wide association studies have implicated several genes, including TREM2, a gene involved with inflammation that increases the likelihood of dementia.
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Alzheimer's Disease
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