New Genes that May Contribute to Alzheimer’s Identified

Summary: Studying the exomes of 6,000 Alzheimer’s patients and 5,000 without the disease, researchers have identified new rare variations in genes that may contribute to dementia.

Source: Boston University School of Medicine.

Researchers from Boston University School of Medicine, working with scientists across the nation on the Alzheimer’s Disease Sequencing Project (ADSP), have discovered new genes that will further current understanding of the genetic risk factors that predispose people to the development of Alzheimer’s disease (AD). The ADSP was developed by the National Institutes of Health (NIH) in response to the National Alzheimer’s Project Act milestones to fight AD.

The incidence of AD is increasing each year and is the most common cause of dementia. Also, it is the fifth leading cause of death in those 65-years and older, according to the CDC. AD is characterized by the formation of senile plaques (extracellular deposits of β-amyloid protein) and neurofibrillary tangles (aggregates of hyper-phosphorylated tau protein) in the brain, leading to neurodegeneration and decline in memory, and eventually death. Despite the growing prevalence of AD and cost to society, the genetic and environmental factors that make some more susceptible to the development of AD is still not well understood.

“This large and deep gene sequencing study is an important part of identifying which variations may play a part in risk of getting Alzheimer’s or protection against it,” said Eliezer Masliah, MD, director of the Division of Neuroscience at the National Institute on Aging, part of NIH. “Big data efforts like the ADSP are really helping research move forward. Identifying rare variants could enhance our ability to find novel therapeutic targets and advance precision medicine approaches for Alzheimer’s disease.”

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By comparing the exomes (gene-coding portions of entire genetic sequences) of nearly 6,000 individuals with AD and 5,000 cognitively healthy older adults, the researchers were able to find rare variations in genes that they believe may contribute to the development of common AD. NeuroscienceNews.com image is in the public domain.

By comparing the exomes (gene-coding portions of entire genetic sequences) of nearly 6,000 individuals with AD and 5,000 cognitively healthy older adults, the researchers were able to find rare variations in genes that they believe may contribute to the development of common AD. These newly discovered genes may suggest an inflammatory response and changes in the protein production. These combined changes are thought to contribute to the overall neurodegeneration witnessed in AD.

The researchers hope their work will help bridge the knowledge gaps of the genetic architecture related to AD, which is a necessary step toward a better understanding of mechanisms leading to AD and eventual therapeutic treatments. “Many of our findings will provide insight into disease mechanisms and targets for biological experiments to gain further understanding about the role of these genes in AD pathogenesis,” explained corresponding author Lindsay A. Farrer, PhD, Chief of Biomedical Genetics and a professor of Medicine, Neurology, Ophthalmology, Epidemiology and Biostatistics at Boston University Schools of Medicine and Public Health.

The research team emphasizes that further research will need to be done to find other genes hidden throughout the genome, as the current paradigm is that many genes contribute to the development of AD.

About this neuroscience research article

Funding: Funding for the study was provided by the National Institutes of Health including grants U01AG032984, R01AG033193, UF1AG047133, U01AG049505, U01AG049506, U01AG049507, U01AG049508, U01AG052411, U01AG052410, U01AG052409, HL105756, RC2HL102419, AG033193, U01 2U01HL096812, 2U01HL096814, 2U01HL096899, 2U01HL096902, 2U01HL096917, R01HL70825, U01HL080295, U01HL130114, R01AG023629, R01AG15928, R01AG20098, AG054076, AG049607, AG033040, R01NS017950, U54HG003273, U54HG003067, U01AG057659, U54HG003079, U24AG021886, U01AG016976, and U24AG041689.

Source: Gina DiGravio – Boston University School of Medicine
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Molecular Psychiatry.

Cite This NeuroscienceNews.com Article

[cbtabs][cbtab title=”MLA”]Boston University School of Medicine”New Genes that May Contribute to Alzheimer’s Identified.” NeuroscienceNews. NeuroscienceNews, 14 August 2018.
<https://neurosciencenews.com/alzheimers-new-genes-9699/>.[/cbtab][cbtab title=”APA”]Boston University School of Medicine(2018, August 14). New Genes that May Contribute to Alzheimer’s Identified. NeuroscienceNews. Retrieved August 14, 2018 from https://neurosciencenews.com/alzheimers-new-genes-9699/[/cbtab][cbtab title=”Chicago”]Boston University School of Medicine”New Genes that May Contribute to Alzheimer’s Identified.” https://neurosciencenews.com/alzheimers-new-genes-9699/ (accessed August 14, 2018).[/cbtab][/cbtabs]

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  1. I think medicine is looking too deep into the causes of Alzheimer’s disease. Always thinking that the answer can be found in our genes or the magic white pill…

    I watched Alzheimer’s disease from close by. A family member had this disease for eight years. I knew his lifestyle and habits.

    Yesterday I watched a TV documentary about sleep. Beta-amyloid, the protein that helps cause the plack, is removed from the brain with good sleep. My family member did not have good sleep. He probably had sleep apnea. He slso had more belly fat than he needed. He smoked for decades but not the last 30 years. He exercised but not enough and probably had a diet that was lacking in vitamins and minerals.

    If you can start with improving these factors, I expect fewer cases of Alzheimer’s disease. The answer is lifestyle changes. Preventive medicine.

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