Positioning ethnicity in dementia awareness research: does the use of senility risk ascribing racialised knowledge deficits to minority groups?

To provide updated estimates of Alzheimer disease (AD) dementia prevalence in the United States from 2010 through 2050. Probabilities of AD dementia incidence were calculated from a longitudinal, population-based study including substantial numbers of both black and white participants. Incidence probabilities for single year of age, race, and level of education were calculated using weighted logistic regression and AD dementia diagnosis from 2,577 detailed clinical evaluations of 1,913 people obtained from stratified random samples of previously disease-free individuals in a population of 10,800. These were combined with US mortality, education, and new US Census Bureau estimates of current and future population to estimate current and future numbers of people with AD dementia in the United States. We estimated that in 2010, there were 4.7 million individuals aged 65 years or older with AD dementia (95% confidence interval [CI] = 4.0-5.5). Of these, 0.7 million (95% CI = 0.4-0.9) were between 65 and 74 years, 2.3 million were between 75 and 84 years (95% CI = 1.7-2.9), and 1.8 million were 85 years or older (95% CI = 1.4-2.2). The total number of people with AD dementia in 2050 is projected to be 13.8 million, with 7.0 million aged 85 years or older. The number of people in the United States with AD dementia will increase dramatically in the next 40 years unless preventive measures are developed.

Nelson et al. describe a recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: Limbic-predominant Age-related TDP-43 Encephalopathy (LATE). They review the literature and present consensus-based recommendations of an international, multidisciplinary working group, providing guidelines for diagnosis and staging of LATE neuropathological changes.

Alzheimer's disease is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. The humanized monoclonal antibody solanezumab was designed to increase the clearance from the brain of soluble Aβ, peptides that may lead to toxic effects in the synapses and precede the deposition of fibrillary amyloid.