Epidemiology of Alzheimer disease

Abstract

The global prevalence of dementia is estimated to be as high as 24 million, and is predicted to double every 20 years through to 2040, leading to a costly burden of disease. Alzheimer disease (AD) is the leading cause of dementia and is characterized by a progressive decline in cognitive function, which typically begins with deterioration in memory. Before death, individuals with this disorder have usually become dependent on caregivers. The neuropathological hallmarks of the AD brain are diffuse and neuritic extracellular amyloid plaques—which are frequently surrounded by dystrophic neurites—and intracellular neurofibrillary tangles. These hallmark pathologies are often accompanied by the presence of reactive microgliosis and the loss of neurons, white matter and synapses. The etiological mechanisms underlying the neuropathological changes in AD remain unclear, but are probably affected by both environmental and genetic factors. Here, we provide an overview of the criteria used in the diagnosis of AD, highlighting how this disease is related to, but distinct from, normal aging. We also summarize current information relating to AD prevalence, incidence and risk factors, and review the biomarkers that may be used for risk assessment and in diagnosis.

Brain-Penetrant Tetrahydronaphthalene Thromboxane A2-Prostanoid (TP) Receptor Antagonists as Prototype Therapeutics for Alzheimer’s Disease

“…(E)-Ethyl-3-(6-oxo-5,6,7,8-tetrahydronaphthalen-1-yl)acrylate (2). A solution of 5-bromo-3,4-dihydronaphthalen-2(1H)-one (476.9 mg, 2.12 mmol), ethyl acrylate (0.28 mL, 2.58 mmol), palladium(II) acetate (4.8 mg, 0.02 mmol), and trio-tolylphosphine (33.1 mg, 0.11 mmol) in triethylamine (2 mL) was heated at 100°C in a sealed tube for 4 h. The reaction mixture was cooled to rt, diluted with dichloromethane (15 mL), and washed with hydrochloric acid (1 M, 10 mL).…”

Collaboration of geldanamycin-activated P70S6K and Hsp70 against beta-amyloid-induced hippocampal apoptosis: an approach to long-term memory and learning

“…Reflecting an aging population, Alzheimer's disease (AD) is among the first ten leading causes of death and the first most prevalent form of dementia occurring after age 65 (Reitz et al 2011). Insoluble fibrillar plaques of amyloid β-proteins (Aβ) and neurofibrillary deposits of hyperphosphorylated tau proteins accumulate over the course of decades in the brains of patients with AD (Querfurth and LaFerla 2010).…”

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

“…The pathogenesis of sporadic AD is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors [3]. Among those factors, elevated levels of circulating LDL cholesterol, independent of APOE genotypes, is strongly linked to the pathogenesis of sporadic AD [6][7][8][9][10].…”

“…Although mutations in specific genes, including AβPP, PSEN1, and PSEN2, lead to rare early-onset familial forms of AD, the vast majority of AD cases are late in onset and sporadic in nature. The pathogenesis of sporadic AD is much more complex than that of familial AD and sporadic AD is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors [3]. Of those factors, altered cholesterol homeostasis may have the strongest links to the pathogenesis of late-onset sporadic AD.…”