by National Institute of Health:

Researchers may have discovered a mechanism behind the largest known genetic risk factor for late-onset Alzheimer’s disease. The finding suggests possible strategies for prevention as well as a potential new drug target.

Alzheimer’s disease is the most common cause of dementia in older adults, affecting more than 5 million Americans. A hallmark of the disease is a protein fragment called beta-amyloid, which is thought to be toxic and forms clumps, or plaques, within the brain. Past studies have revealed several genetic risk factors for Alzheimer’s disease. A gene called APOE has shown the strongest connection to the most common, late-onset form of the disease.

APOE encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body. The gene exists in 3 forms. APOE2 is thought to play a protective role against both Alzheimer’s and heart disease, APOE3 is believed to be neutral, and APOE4 confers a higher risk for both conditions. Outside the brain, the APOE4 protein appears to be less effective than the other versions at clearing away cholesterol. How it contributes to Alzheimer’s disease in the brain, however, has been a mystery.

by Robert Bazell, Chief science and medical correspondent for NBC News:

Should high school kids get a genetic test for the risk for Alzheimer’s disease before they’re allowed to play football? Two prominent scientists who study both Alzheimer’s and the traumatic brain injury suffered by some football players raise that ethically charged question in an editorial out Wednesday in the journal Science Translational Medicine.

We all carry a gene called APOE which comes in three forms. If we carry one copy of the form called E4, it triples our lifetime risk for Alzheimer’s. About 10 percent of the U.S. population falls in that category. If we have two copies of E4, the lifetime Alzheimer’s risk is 15 times greater. About 2 percent of us have that genetic makeup.

Although the connection between APOE E4 and Alzheimer’s risk has been known for years, few have suggested it as a screening tool because there’s no known way to prevent the mind-robbing disease. But, now as scientists want to test drugs as early as possible as potential methods of preventing Alzheimer’s, APOE is getting more attention, as are brain scans and other techniques that might determine who is at risk.

by Dementia Today

GENETIC RISK FACTORS

by University of California

Scientists at the UC San Francisco-affiliated Gladstone Institutes have enhanced the understanding of how a protein linked to Alzheimer’s disease keeps young brains healthy, but can damage them later in life — suggesting new research avenues for treating this devastating disease.

In the Journal of Neuroscience, available online today, researchers in the laboratory of Yadong Huang, M.D., Ph.D., have uncovered the distinct roles that the apoE protein plays in young vs. aging brains. These findings, which could inform the future of Alzheimer’s drug development, come at a time of unprecedented challenge and need.

“By the year 2030, more than 60 million people worldwide will likely be diagnosed with Alzheimer’s, but we are still grappling with the disease’s underlying biological mechanisms,” said Huang, an Alzheimer’s expert at the Gladstone Institute of Neurological Disease and an associate professor of neurology and pathology at UCSF. “However, with this research we’ve shed new light on these complex processes — and how we could modify these processes to fight this disease.”

by Dementia Today

People with AD gradually suffer memory loss and a decline in thinking abilities, as well as major personality changes. These losses in cognitive function are accompanied by changes in the brain, including the build-up of amyloid plaques and tau-containing neurofibrillary tangles, which result in the death of brain cells and the breakdown of the connections between them.

Amyloid plaques and neurofibrillary tangles are the primary hallmarks of Alzheimer’s disease. Plaques are dense deposits of protein and cellular material outside and around the brain’s nerve cells. Tangles are twisted fibers that build up inside the nerve cells.

Scientists have known about plaques and tangles since 1906, when a German physician, Dr. Alois Alzheimer, first identified them in the brain of woman who had died after suffering paranoid delusions and psychosis. Intensive research efforts of the last two decades have revealed much about their composition, how they form, and their possible roles in the development of Alzheimer’s disease.

by Tom Bills for In-Law Suite

Alzheimer’s disease is an illness that causes the brain’s neurons to deteriorate. This causes the sufferer to lose memory, loss of language skills, and changes in behavior. As the disease progresses to different areas of the brain, it affects different skills and abilities. Alzheimer’s is a degenerative illness, meaning that it progresses and gets worse as the person gets older.

Alzheimer’s disease is different from other types of senility, but it is the most common cause of dementia among senior citizens aged 65 and older. Not everyone gets Alzheimer’s, and it is a disease and not a form of aging. Currently, there is no cure for Alzheimer’s disease, nor is there any way to halt or reverse its progress through the brain.

Causes of Late-Onset Alzheimer’s Disease

Most cases of Alzheimer’s disease are late-onset, meaning that they affect people aged 65 and older. As of the time of this writing, scientists do not know for sure what factors cause late-onset Alzheimer’s disease. The greatest risk factor for late-onset Alzheimer’s disease is advanced age. The older a person gets, the more at risk they become for late-onset Alzheimer’s disease.

Those with a family history of Alzheimer’s are more likely to develop late-onset Alzheimer’s disease, which suggests that there may be a hereditary link. However, many people develop late-onset Alzheimer’s disease who do not have a family history of the disease. Scientists believe that one gene, Apolipoprotein E, or ApoE, is linked to late-onset Alzheimer’s disease. People with this gene are more likely to develop late-onset Alzheimer’s disease.

A Defective ApoE Gene, Called ApoE4, Can Contribute to Causing Alzheimer’s Disease by Failing to Synthesize the Synapse-Generating Enzyme, PKC Epsilon
by Blanchette Rockefeller Neurosciences Institute for PR Newswire

Researchers at the Blanchette Rockefeller Neurosciences Institute (BRNI) at West Virginia University in Morgantown, West Virginia reported a significant advance in understanding how different forms of the ApoE gene raise the risk for Alzheimer’s disease.

Among the earliest events in Alzheimer’s disease is the loss of the nerve cell connections known as synapses.  In a paper published in this week’s issue of the Journal of Biological Chemistry, Drs. Abhik Sen, Daniel Alkon and Thomas Nelson report that the normal ApoE3 gene stimulates the growth of synapses through a protein called PKC epsilon.  PKC epsilon also prevents the toxic Alzheimer’s disease protein, beta amyloid, from destroying synapses.  Loss of synapses in the brains of Alzheimer’s disease patients is known to closely correlate with the degree of dementia.

ApoE4, a defective version of the ApoE gene, could cause the early loss of synapses in Alzheimer’s disease by not stimulating the synthesis of the synaptogenic and neuroprotective protein, PKC epilson.  Evidence from past studies indicates that the brains of Alzheimer’s disease patients show PKC deficits.

The thought of losing your mind as you grow older is terrifying, made worse that there appeared to be little we could do about it
by Kirsty English for The Mirror

Alzheimer’s strikes fear in all of us. The thought of losing your mind as you grow older is terrifying and made worse by the fact that, before now, there appeared to be little we could do to slow down or avoid Alzheimer’s, the most common form of dementia.

This week, Mirror columnist Fiona Phillips, 51, talked openly about her experience of Alzheimer’s after losing first her mother Amy and, earlier this month, her father Neville to the disease. She fears that, like her mother who was struck down in her late 50s, she too will start to develop symptoms in the next five years.

Having witnessed Alzheimer’s first hand she knows how sufferers are stripped of self respect, leaving them incapable of performing even the most basic daily tasks.

But according to Jean Carper, 79, an American medical journalist, there could be hope. In her international best selling book, 100 Simple Things You Can Do To Prevent Alzheimer’s, a host of experts reveal scientifically-backed, easy tips about how to head off the disease, ranging from eating vinegar to surfing the net.

A widely available cancer drug has shown remarkable success in reversing Alzheimer’s disease in mice, raising hope of a breakthrough against incurable dementia in humans, US researchers said Thursday.
by Dawn News

Mice treated with the drug, known as bexarotene, became rapidly smarter and the plaque in their brains that was causing their Alzheimer’s started to disappear within hours, said the research in the journal Science.

“We were shocked and amazed,” lead author Gary Landreth of the Department of Neurosciences at Case Western Reserve University School of Medicine in Ohio told AFP. “Things like this had never, ever been seen before,” he said. The drug works by boosting levels of a protein, Apolipoprotein E (ApoE), that helps clear amyloid plaque buildup in the brain, a key hallmark of Alzheimer’s disease.

“Think of this as a garbage disposal,” Landreth said. “When we are young and healthy, all of us can basically get rid of this (amyloid) and degrade it and grind it into small bits and it gets cleared.

“Many of us will be unable to do this as efficiently as we age. And this is associated with mental decline or cognitive impairment.”Six hours after mice got the drug, soluble amyloid levels fell by 25 per cent, ultimately reaching 75 per cent reductions. The effect lasted up to three days, said the study.

Science is bringing some understanding of the heritability, prevalence, and inner workings of one of the most devastating diseases.
by Daisy Yuhas for Scientific American

This has been a big week in Alzheimer’s news as scientists put together a clearer picture than ever before of how the disease affects the brain. Three recently published studies have detected the disease with new technologies, hinted at its prevalence, and described at last how it makes its lethal progress through the brain.

The existence of two forms of Alzheimer’s—early- and late-onset—has long baffled scientists. Of the estimated five million Americans who suffer from Alzheimer’s, only a few thousand are diagnosed with an early-onset form of the affliction, which affects people before the age of 65. This rare early-onset form is thought to be hereditary and scientists have associated multiple genetic mutations contributing to its occurrence. Late-onset Alzheimer’s, although more common, has been the bigger mystery. One variant of the APOE gene-—sometimes known as the Alzheimer’s gene—is linked to the late-onset disease. But the APOE gene, unlike dominant early-onset genes, does not determine whether a person will ultimately have dementia.