![]() ![]() Prospective population-based studies provide strong evidence that the risk of late-life cognitive impairment and dementia is modified by medical comorbidities, lifestyle choices, and other environmental factors. The public health impact of AD and other forms of dementia cannot be overstated, with an estimated cost of $277 billion in the United States in 2018. 8 In otherwise healthy individuals, survival can extend to 15 to 20 years. 2,7 Average survival after diagnosis varies between 4 and 8 years across studies and is impacted by multiple factors, including age at diagnosis, sex, psychotic features, motor system involvement, and medical comorbidities. 6 The overall lifetime risk for AD at age 65 is 21.1% for women and 11.6% for men. 5 Compared to non-Hispanic whites, the incidence of AD is higher in African Americans/blacks and Hispanics/Latinos and lower in Asian Americans. ![]() 5 Nearly two-thirds of patients with AD are women, likely reflecting both increased life duration and biological factors. 2,4,5 The number of patients with AD in the United States is projected to nearly triple by 2050, with the majority of growth attributed to the 85 and older age group. Approximately 80% of patients with AD are older than age 75, with disease incidence increasing from at ages 65 to 74 to at age 85 and older. 2,3 The incidence and prevalence of AD increase dramatically with age. Current approaches to clinical diagnosis and treatment are discussed, and a growing armamentarium of biomarkers that are already transforming AD research and are likely to have an increasing future role in clinical care are introduced.Īn estimated 5.7 million Americans are living with AD dementia, and an additional 11.6 million Americans have mild cognitive impairment (MCI). This article focuses on late-onset AD, defined as symptom onset at age 65 or older, reviewing the epidemiology of the disease and known environmental and genetic risk factors. In subsequent decades, it has become clear that AD is very common, with a prevalence that rivals the most common age-related diseases and continues to grow in the setting of an aging population. In the 1970s, it became apparent that the “neurofibrils” (neurofibrillary tangles) and “miliary foci” (senile plaques) described by Alzheimer were present in the majority of people who developed dementia in late life. ![]() A comprehensive treatment plan for AD includes use of symptomatic medications, optimal treatment of comorbid conditions and neuropsychiatric symptoms, counseling about safety and future planning, and referrals to community resources.īeginning with Alois Alzheimer’s seminal report “On an Unusual Illness of the Cerebral Cortex” in a 51-year-old woman 1 and for most of the 20th century, Alzheimer disease (AD) was considered a rare cause of presenile dementia. Emerging CSF and imaging biomarkers can now detect the key neuropathologic features of the disease (amyloid plaques, neurofibrillary tangles, and neurodegeneration) in living people, allowing for characterization of patients based on biological measures. AD typically presents with early and prominent episodic memory loss, although this clinical syndrome is neither sensitive nor specific for underlying AD neuropathology. The primary genetic risk factor for late-onset AD is the apolipoprotein E ( APOE) ε4 allele. Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease. An estimated 5.7 million Americans are living with AD dementia, with the number of affected individuals growing rapidly because of an aging population. ![]()
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