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Alzheimer's, Dementia & Mental Health

Game-Changing Find in Battle Against Alzheimer’s: A Gene Offers Protection

Study links cognitive decline in senior citizens with Alzheimer’s disease; says amyloid-beta plaque is cause of AD

July 12, 2012 - New research by deCODE Genetics is a game-changer in the battle against Alzheimer’s disease. It reveals a gene that protects against Alzheimer’s disease (AD) and even cognitive decline in the elderly. The discovery also finds linkage between age-related cognitive decline and late-onset forms of AD, the most common cause of dementia.

The gene that protects against AD is a variant of the amyloid precursor protein (APP) gene.

“APP was discovered 25 years ago in patients with rare, inherited forms of Alzheimer’s that strike in middle age,” writes Ewen Callaway in a news report in the journal Nature, which reported the research.


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“In the brain, APP is broken down into a smaller molecule called amyloid-β. Visible clumps, or plaques, of amyloid-β found in the autopsied brains of patients are a hallmark of Alzheimer’s, but scientists have long debated whether the plaques are a cause of the neuro­degenerative condition or a consequence of other biochemical changes associated with the disease.

Callaway adds, “The latest finding supports other genetics studies blaming amyloid-β, and it makes the protein ‘the prime therapeutic target’, says Rudolph Tanzi, a neurologist at the Massachusetts General Hospital in Boston and a member of one of the four teams that discovered APP’s role in the 1980s.”

Alzheimer’s disease is a progressive neurodegenerative disease long associated with the production and accumulation of beta-amyloid plaque. While several mutant forms of the APP gene have been linked to early-onset, aggressive forms of AD, there has been limited evidence supporting a role for mutations in the gene in the more common late-onset form of the Alzheimer’s disease.

 “Our results suggest that late-onset Alzheimer‘s disease may represent the extreme of more general age-related decline in cognitive function,” said study lead author Kari Stefansson, M.D., Dr. Med., CEO of deCODE Genetics. “Also important, these data support certain Alzheimer‘s disease drug development programs - some of which are already in human clinical trials.”

In searching for low-frequency variants of the APP gene associated with AD, deCODE scientists, together with their colleagues from the pharmaceutical company Genentech, found a significant association with a mutation in whole genome sequence data from 1,795 people in Iceland.

The research team showed that the mutation is significantly more common in the study‘s elderly control group than in those with AD, suggesting that the mutation protects against the disease. The researchers eventually  studied the variant in nearly 400,000 Scandinavians.

The Genentech team then tested these findings and found a significantly reduced production of amyloid beta in cells.

“Our genetic data indicate that the mutation is protective against Alzheimer‘s disease,” said Stefansson.

“Our findings and the in vitro work done by Genentech also provide a proof of principle for the idea that blocking BACE1 cleavage of APP may protect against Alzheimer‘s, offering greater confidence to pharmaceutical companies with active BACE1 inhibitor drug development programs.”

Gene Mutation Defends Against Alzheimer’s Disease: Key Finding

Rare genetic variant suggests a cause and treatment for cognitive decline; discovery confirms the principal suspect that is responsible for Alzheimer’s

By Ewen Callaway, Nature

July 12, 2012 - Almost 30 million people live with Alzheimer’s disease worldwide, a staggering health-care burden that is expected to quadruple by 2050. Yet doctors can offer no effective treatment, and scientists have not been able definitively to pin down the underlying mechanism of the disease. Read more at Nature...

A study of a rare gene mutation that protects people against Alzheimer’s disease

This study “provides the strongest evidence yet that excessive levels of a normal brain substance, beta amyloid, are a driving force in the disease — bolstering hopes that anti-amyloid drugs already under development might alter the disease’s course or even prevent it,” according to an article in the New York Times by Gina Kolata.

“So far, the drugs have not succeeded. But scientists not connected with the new study said it suggested that the drug companies’ big bets on anti-amyloid treatments could yet pay off.”

Cognitive Decline in the Elderly

To study the association of the protective mutation with general cognitive decline, the research team examined the frequency of the mutation in the original Icelandic control group of those cognitively intact at age 85. The team found an enrichment of the mutation in this group, consistent with its protective effect against AD.

Extending this work further, the team investigated cognitive function using a seven-category test in carriers of the mutation and non-carriers in the age range of 80 to 100 years old. The research team found a statistically significant difference between carriers and non-carriers, with the carriers of the mutation having a score indicative of better-conserved cognition. After removing known AD cases, the team again found that carriers had better cognitive function, suggesting that the mutation extends its protective effect to the elderly in general.

"The implication of these data is that general cognitive decline and late-onset Alzheimer‘s disease share biological pathways,” said Stefansson. “It also suggests that approaches to treating Alzheimer’s may have benefit to those elderly who do not carry the protective mutation, and do not suffer from AD.”

"What Is Alzheimer's Disease"
[2 min 29 sec]

> Click to NIHSeniorHealth Video

Alzheimer’s Disease

Alzheimer’s disease, a progressive neurodegenerative disorder, is the most common form of dementia that affects four to eight percent of the elderly population worldwide. The neuropathological features of AD are the presence of extracellular amyloid plaques and intracellular neurofibrillary tangles in the hippocampus and cortical grey matter of the AD brain.

Age-specific prevalence of AD nearly doubles after age 65, leading to a prevalence of greater than 25 percent in those over the age of 90.

About deCODE

Headquartered in Reykjavik, Iceland, deCODE genetics is a global leader in analyzing and understanding the human genome. Using its unique expertise and population resources, deCODE has discovered genetic risk factors for dozens of common diseases ranging from cardiovascular disease to cancer.

In order to most rapidly realize the value of genetics for human health, deCODE partners with life sciences companies to accelerate their target discovery, validation, and prioritization efforts, yielding improved patient stratification for clinical trials and essential companion diagnostics. In addition, through its CLIA- and CAP-certified laboratory, deCODE offers DNA-based tests for gauging risk and empowering prevention of common diseases. deCODE also licenses its tests, intellectual property, and analytical tools to partner organizations. deCODE’s corporate information can be found at with information about our genetic testing services at and

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