Path Is Found for the Spread of Alzheimer’s

[OKIsItJustMe]

http://www.nytimes.com/2012/02/02/health/research/alzheimers-spreads-like-a-virus-in-the-brain-studies-find.html?_r=1

[font face=Times, Serif][font size=5]Path Is Found for the Spread of Alzheimer’s[/font]

By GINA KOLATA
Published: February 1, 2012

[font size=3]Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau.

…

Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning.

But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer.

The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.

…[/font][/font]

[Marnie]

1. Ever since the discovery of prions,

an abnormal configuration of a molecule in the body which, in the brain can stimulate normal prion molecules to alter to the abnormal configuration, there has been suspicion that Alzheimer's plaques might have a similar cause.

Looks like that is the case.

Abnormal prions cause a variety of expressions of brain cell destruction including Scrapie in sheep, Mad Cow Disease in cattle, Kuru, Creutzfeldt-Jakob Disease, Gerstmann-Straussler-Scheinker Syndrome, Fatal Familial Insomnia, and Kuru.

[dixiegrrrrl]

2. What would be interesting is finding out why there is such an increase in the disease.

[msongs]

3. maybe there is no increase, just better diagnosing of what used to be called senility nt

[LeftishBrit]

4. Also, a lot more people nowadays live to reach the age where Alzheimers is common

[LeftishBrit]

5. I really hope that this results in a cure or prevention for Alzheimers!

[OKIsItJustMe]

6. Study Shows Alzheimer’s Disease May Spread by ‘Jumping’ from One Brain Region to Another

http://www.cumc.columbia.edu/news-room/2012/02/study-shows-alzheimer%E2%80%99s-disease-may-spread-by-%E2%80%98jumping%E2%80%99-from-one-brain-region-to-another/

[font face=Times,Times New Roman,Serif][font size=5]Study Shows Alzheimer’s Disease May Spread by ‘Jumping’ from One Brain Region to Another[/font]

Published: February 1, 2012

[font size=4]Findings open new opportunities for studying Alzheimer’s and testing potential therapies[/font]

[font size=3]New York, NY (February 1, 2012) — For decades, researchers have debated whether Alzheimer’s disease starts independently in vulnerable brain regions at different times, or if it begins in one region and then spreads to neuroanatomically connected areas. A new study by Columbia University Medical Center (CUMC) researchers strongly supports the latter, demonstrating that abnormal tau protein, a key feature of the neurofibrillary tangles seen in the brains of those with Alzheimer’s, propagates along linked brain circuits, “jumping” from neuron to neuron.

The findings, published today in the online journal PloS One, open new opportunities for gaining a greater understanding of Alzheimer’s disease and other neurological diseases and for developing therapies to halt its progression, according to senior author Karen E. Duff, PhD, professor of pathology (in psychiatry and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at CUMC and at the New York State Psychiatric Institute.

Alzheimer’s disease, the most common form of dementia, is characterized by the accumulation of plaques (composed of amyloid-beta protein) and fibrous tangles (composed of abnormal tau) in brain cells called neurons. Postmortem studies of human brains and neuroimaging studies have suggested that the disease, especially the neurofibrillary tangle pathology, begins in the entorhinal cortex, which plays a key role in memory. Then as Alzheimer’s progresses, the disease appears in anatomically linked higher brain regions.

“Earlier research, including functional MRI studies in humans, have also supported this pattern of spread,” said study coauthor Scott A. Small, MD, professor of neurology in the Sergievsky Center and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at CUMC. “But these various findings do not definitively show that Alzheimer’s spreads directly from one brain region to another.”

…[/font][/font]

http://dx.doi.org/10.1371/journal.pone.0031302

[OKIsItJustMe]

7. Untangling the mysteries of Alzheimer’s Researchers tease out toxic role of tau oligomers

http://www.utmb.edu/newsroom/article7448.aspx

[font face=Times,Times New Roman,Serif]Published Thursday, Feb. 2, 2012, 10:18 AM
[font size=5]Untangling the mysteries of Alzheimer’s Researchers tease out toxic role of tau oligomers [/font]

[font size=3]One of the most distinctive signs of the development of Alzheimer’s disease is a change in the behavior of a protein that neuroscientists call tau. In normal brains, tau is present in individual units essential to neuron health. In the cells of Alzheimer’s brains, by contrast, tau proteins aggregate into twisted structures known as “neurofibrillary tangles.” These tangles are considered a hallmark of the disease, but their precise role in Alzheimer’s pathology has long been a point of contention among researchers.

Now, University of Texas Medical Branch at Galveston researchers have found new evidence that confirms the significance of tau to Alzheimer’s. Instead of focusing on tangles, however, their work highlights the intermediary steps between a single tau protein unit and a neurofibrillary tangle — assemblages of two, three, four, or more tau proteins known as “oligomers,” which they believe are the most toxic entities in Alzheimer’s.

“What we discovered is that there are smaller structures that form before the neurofibrillary tangles, and they are much more toxic than the big structures,” said Rakez Kayed, UTMB assistant professor and senior author of a paper on the work now online in the FASEB Journal. “And we established that they were toxic in real human brains, which is important to developing an effective therapy.”

According to Kayed, a key antibody developed at UTMB called T22 enabled the team to produce a detailed portrait of tau oligomer behavior in human brain tissue. Specifically designed to bond only to tau oligomers (and not lone tau proteins or neurofibrillary tangles), the antibody made it possible for the researchers to use a variety of analytical tools to compare samples of Alzheimer’s brain with samples of age-matched healthy brain.

…[/font][/font]

http://dx.doi.org/10.1096/fj.11-199851