Genetics and Genomics of Alzheimer’s Disease

Dear Colleagues,

Alzheimer’s disease (AD) is an age-related neurological disorder, the most common cause form of dementia, and a top 10 cause of death. On average, affected individuals live seven years after diagnosis. In most cases, the primary caretakers are immediate family members, frequently an unaffected, elderly, spouse. In the past 20 years, the number of AD deaths has more than doubled, and the incidence of AD is expected to continue its rapid increase. Despite significant efforts, there are currently no disease-altering treatments, and relatively few clinical trials underway.

AD begins many years before the onset of symptoms. A hallmark pathology of AD is the accumulation of Aβ fragments in the brain, one of which leads to neuronal death. Amyloid precursor protein (APP) is cleaved by α- and β-secretases to create different Aβ fragments, one of which, Aβ₄₂, self-aggregates creating toxic plaques in the brain.

In the past 10 years, significant progress has been made towards solving the genetic architecture of AD. More than 20 different genes have been implicated in genome-wide association studies (GWAS), the majority of which are not functional and have relatively small effects on risk for disease. More recently, numerous rare genomic variants have been reported that influence risk for AD. These rare variants have a large effect on risk for disease and are more likely to be functional.

In this Special Issue of Genes, we extend an invitation for reviews on the current state of genetics and genomics in Alzheimer’s Disease, as well as original research articles. We are especially interested in contributions that utilize novel methods, describe protective variants, consider alternative hypotheses to AD, or contribute to our ability to diagnose AD early. However, we will consider any manuscript describing the genomics of AD.

Dr. Perry G. Ridge
Guest Editor

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