by Science Daily:

During Alzheimer’s disease, ‘plaques’ of amyloid beta (Ab) and tau protein ‘tangles’ develop in the brain, leading to the death of brain cells and disruption of chemical signaling between neurons. This leads to loss of memory, mood changes, and difficulties with reasoning.

New research published in BioMed Central’s open access journal Alzheimer’s Research & Therapy, has found that up-regulating the gene Hes1 largely counteracted the effects of Ab on neurons, including preventing cell death, and on GABAergic signaling.

The exact mechanism behind how Ab contributes to Alzheimer’s disease is not yet fully understood, however researchers from Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) in Spain recently discovered that Ab interferes with the normal activity of nerve growth factor (NGF). One of the actions of NGF is activating the protein Hes1, a transcription factor required to turn on other genes. Without this factor GABAergic signaling within the brain decreases.

by John Phillip for Natural News

Alzheimer’s disease is characterized by an initial loss of short term memory and the ability to form rational and permanent thoughts. Protein tangles known as tau aggregates strangle neural synapses, blocking the vital flow of neurotransmitter and electrical signals necessary to form memories and personality. Once considered a disease of the aging, this form of dementia is increasing at a startling rate in younger individuals, largely due to a processed and refined food diet, environmental factors and long-term chronic stress.

Researchers from the University of California, San Diego School of Medicine have published the result of a study in the Proceedings of the National Academy of Sciences, explaining the mechanism behind continual exposure to stressors so common in our rapid-paced lifestyle, and the unnatural accumulation of insoluble tau protein aggregates in brain tissue.

They explain that neurofibrillary tangles are one of the physical hallmark signs of Alzheimer’s disease, and have been shown to contribute to disease progression in people under chronic stress conditions during the course of past studies.

by News Medical

In Alzheimer’s disease, brain neurons become clogged with tangled proteins. Scientists suspect these tangles arise partly due to malfunctions in a little-known regulatory system within cells. Now, researchers have dramatically increased what they know about this particular regulatory system in mice. Such information will help scientists better understand Alzheimer’s and other diseases in humans and could eventually provide new targets for therapies.

In a study released online in the Proceedings of the National Academy of Sciences Early Edition this week, the team at least doubled the number of proteins found to be subject to a type of regulation based on a sugar known as O-GlcNAc (oh-GLIK-nak). The O-GlcNAc system likely adds another layer of control to the proteins that serve as a brain cell’s widgets and gears — control that might be muddled in Alzheimer’s brains known to have problems in sugar metabolism.

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.

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.

Alzheimer’s researchers create new antibody that enables detailed analysis of brain.
by Christopher Wright for Daily Rx

There is no cure for Alzheimer’s disease, and watching a loved one’s mental health degrade is an experience that no one should endure. Thankfully new research may lead to advancements in Alzeimer’s treatment.

A key distinctive sign of Alzheimer’s disease is the change in behavior of a protein called ‘tau.’ This protein is essential to neuron health and to the proper functioning of the brain.

Until recently this change has been a mystery but new antibody will allow for much deeper analysis of the tau protein. The study was led by Rakez Kayed, Ph.D., from the University of Texas Medical Branch at Galveston.

Research could lead to better understanding of the origins of Alzheimer’s
by Randy Dotinga at Health day News

A new study suggests that a brain-clotting plaque linked to Alzheimer’s disease may cause cognitive decline even in healthy people, potentially setting the stage for the development of the devastating illness later in life. The findings don’t point to any new treatment for Alzheimer’s disease, which is incurable, and the detected decline in brain function is so small that affected people probably wouldn’t notice anything in their daily lives.

Still, “I think they certainly are at higher risk of Alzheimer’s,” said study co-author Denise Park, A cognitive neuroscientist at the Center for Vital Longevity at the University of Texas at Dallas. She added that the test that turned up signs of the brain plaque could eventually help doctors figure out if someone’s at risk for the disease long before they reach old age.

At least three AD biomarkers are ready to be incorporated into AD clinical trials.
by Dennis J. Selkoe and John C. Morris for The Scientist

There’s been a lot of discussion about the need for biomarkers to diagnose and monitor the progression of Alzheimer’s disease (AD). That discussion should continue, for sure, but the aging of our society means that researchers in the AD field need to move from talk to action.

Although some biomarkers have been under study for more than a decade, the continuing absence of truly effective therapies for preventing, moderating, or curing AD spurred the publication in December of a special supplemental issue of Neurobiology of Aging about the latest research and expert opinion on AD biomarkers in an effort to advance trials of experimental agents for the disease.

by James P. Richardson, MD, MPH for KevinMD

Mark Twain, the American author and humorist once said, “It ain’t what you don’t know that gets you into trouble.  It’s what you know for sure that just ain’t so.”  In my experience as a geriatrician, I’ve encountered many misunderstandings about this degenerative neurologic disease that devastates both patients and their families.  Countering these can help patients, families, professionals, and all those who have someone in their lives with Alzheimer’s disease.

1. There’s no difference between Alzheimer’s disease and dementia.  The confusion here is understandable, as Alzheimer’s disease is the cause of at least 60% – and perhaps a much larger proportion – of all those diagnosed with dementia.  Although the terms are used interchangeably, dementia is the umbrella which covers all diseases that cause cognitive decline in adulthood, including Alzheimer’s disease.  The next most common cause of dementia is vascular disease, such as occurs after multiple strokes or one very large one. 

by James Urquhart for RSC

Parkinson’s and Alzheimer’s could be caused by an accumulation of iron in regions of the brain, Australian researchers say. Following this discovery, the team went on to actually prevent neurodegeneration in transgenic mice by giving them an iron chelator. The finding could offer new avenues of investigation for finding treatments for these incurable diseases.

Tangles of tau protein inside the brain have been linked to Alzheimer’s and Parkinson’s before. ‘The field has been inclined to think of these tangles as poisonous junk. But there is no proof that tangles are the sole culprit in nerve death in these incurable disorders,’ says Ashley Bush who led the research at the University of Melbourne. ‘Genetic studies have implicated tau in both Alzheimer’s and Parkinson’s, but there is no certainty about what goes wrong.’