Two new medical studies show caffeine consumption may help prevent and treat Alzheimer’s disease.

Researchers at the Florida Alzheimer’s Disease Research Center found that 500 milligrams of caffeine, which is the equivalent of five 8 oz. cups of coffee, reversed memory issues in mice bred to develop Alzheimer’s.

In fact, after two months on caffeine, the Alzheimer’s mice scored just as well as normal mice on memory tests.

The studies also found caffeine cut the animals’ levels of beta amyloid, the protein linked to plaque found in human Alzheimer’s patients.

“Caffeine is the most widely used psychoactive drug in the world and it might protect against Alzheimer’s,” said Gary Arendash, a researcher at the Byrd Alzheimer Institute in Tampa, Fla..

Forgetfulness is a possible sign of the onset of Alzheimer’s, and researchers say the study indicated caffeine could protect the brain from small changes in one’s memory capability.

The study found that Alzheimer’s disease strikes nearly 50 percent of Americans 85 years old and older.

The study is published in the Journal of Alzheimer’s Disease.

Technorati Tags: alzheimers, caffeine, disease, improve, prevent

Those with less schooling were diagnosed later but with more severe disease.
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Theres a new clue in the search to identify the harbingers of Alzheimers disease.

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Technorati Tags: aging, alzheimers, MRI, PET

Alzheimer’s Research Yields Potential Drug Target

ScienceDaily (July 3, 2009) — Scientists at UC Santa Barbara and several other institutions have found laboratory evidence that a cluster of peptides may be the toxic agent in Alzheimer’s disease. Scientists say the discovery may lead to new drugs for the disease.

In an article published the week of June 29 in Nature Chemistry, the researchers explain the process in which the toxic Amyloid Beta 42 peptides aggregate, and outline the new technology they use to study these peptides. The findings come out of the laboratory of Michael T. Bowers, professor of chemistry and biochemistry at UCSB.

“We believe that we have put a face, a structure, on the molecular assembly that is responsible for Alzheimer’s disease,” said Bowers. His research group used an innovative technology called ion mobility-based mass spectroscopy, a method that allows researchers to investigate the structure, aggregation, and energetics of protein and peptide systems.

The Amyloid Beta (AB) 42 peptide is clipped from a much larger protein, the amyloid precursor protein (APP), and is composed of 42 amino acid residues. A second peptide, AB40, is 10 times more abundant than AB42 in healthy human brains and is also clipped from APP. It is identical to AB42 except it is missing the last two amino acids. Both peptides aggregate, but AB42 more so than AB40.

AB40 never grows beyond a tetramer –– a cluster of four AB40 peptides. As a consequence, it is nontoxic. By contrast, AB42 grows to form rings of six units each. Two of these “six-mer” rings stack to form a dodecamer, or “twelve-mer,” according to Bowers, and then the aggregation stops. These dodecamer clusters are long-lived, but may eventually rearrange to form so-called B-sheet structures, which lead to the large fibrils that form the plaques found in the brains of those with Alzheimer’s disease and other neurodegenerative diseases.

In related studies, transgenic mice, implanted with the gene that expresses human APP (and hence able to form AB42 in their brains), are found to quickly develop memory deficits –– as if they have Alzheimer’s disease. Since mice have a much faster metabolism than humans, the disease progresses more quickly. Of importance is the fact that the only AB species found in the brains of the transgenic mice correlates with the dodecamer of AB42 characterized in the Bowers lab experiments. These two pieces of data together strongly implicate the dodecamer of AB42 as the toxic agent in Alzheimer’s disease.

“Our group, along with our collaborators, are searching for drug candidates that can prevent AB42 from aggregating to form the toxic dodecamer,” said Bowers. “While it is early in the search, we are hopeful good candidates can be found. As a consequence, there is a need to find an early marker for Alzheimer’s disease so that we can use these drugs to radically slow down the disease progression.”

Bowers explained that this research method is new, but is gaining acceptance in the biological community. He said that to fully understand the disease, effects of the oligomerization process would have to be observed at the cellular level, however.

“These latest results are a very hopeful thing,” said Bowers. “I’m more hopeful now than I have ever been that we can make some real progress on this terrible disease.”

The National Institutes of Health funded the study. When Bowers first received the funding, he explained: “In biology, structure and function are tightly coupled. When it became clear that small soluble oligomers were most probably the toxic agents in Alzheimer’s disease, I realized our ion mobility methods could contribute, since we could measure the oligomer distribution and shapes of these peptides for the first time.”

This illustrates the progression of AB42 to a toxic dodecamer, or, “twelve-mer” aggregation, (blue — above). Below, the AB40 oligomer only becomes a nontoxic tetramer aggregation. (Credit: UCSB)

Summer L. Bernstein, a doctoral student of Bowers at UCSB, is the first author on the paper. Co-author David B. Teplow, a professor with UCLA’s David Geffen School of Medicine, provided the proteins for the study. Joan-Emma Shea, a professor in UCSB’s Department of Chemistry and Biochemistry, headed the theoretical modeling aspect of the project. Other co-authors from the Bowers group are Nicholas F. Dupuis and Thomas Wyttenbach. Additional co-authors are Noel D. Lazo, of the Carlson School of Chemistry and Biochemistry, Clark University; Margaret M. Condron and Gal Bitan, of UCLA’s David Geffen School of Medicine; and Brandon T. Ruotolo and Carol V. Robinson, of the Department of Chemistry, University of Cambridge.

Technorati Tags: alzheimers, chemistry, dementia, nature, peptide, research

New triggers found for Alzheimer’s
By Tom Blackwell, National Post

For decades, scientists have struggled to understand what causes Alzheimer’s disease, once even suspecting that exposure to aluminum pots and pans played a role. Much is still unknown.

New Canadian research, however, offers a novel clue, concluding that infectious diseases such as bacterial pneumonia and the virus behind cold sores may make people more susceptible to the devastating illness — and indicate a way to guard against Alzheimer’s.

If borne out with more study, the findings would make it even more important to aggressively treat infection, while raising the possibility that vaccines against certain bacteria or viruses could actually prevent Alzheimer’s, says a paper published in the journal Alzheimer’s and Dementia.

“It is kind of counter-intuitive. You think an infection is gone and that is it, right?” said Dr. Paul Verhoeff, a psychiatrist at Toronto’s Baycrest brain-research facility. “But think about those cold sores. Whenever your immune system is compromised, those cold sores come back … We think that some infections can really increase the chance someone could develop Alzheimer’s if the person already has other predisposing factors.”

About 500,000 Canadians suffer from Alzheimer’s disease and that number is expected to double within 25 years, with women being disproportionately afflicted. The main known risk factors for the degenerative brain condition include old age, diabetes, family history and cardiovascular disease.

Dr. Verhoeff and colleagues at Toronto’s Sunnybrook Health Sciences Centre reviewed several studies conducted over the last decade or so that explored a link between various infections and Alzheimer’s.

The most convincing evidence involves Chlamydia pneumoniae, a common bacteria estimated to be present in more than half of American adults and to cause 10-20% of the pneumonia cases outside of hospital.

One autopsy-based study found the bug in the brains of 90% of 19 Alzheimer’s patients, and in just 5% of the brains of non-Alzheimer’s subjects. Another detected the bacteria located close to the amyloid plaques considered a hallmark of Alzheimer’s brains.

The C. pneumoniae microbe does not appear to cause the disease, but may make people more vulnerable to it and accelerate the progress of Alzheimer’s, the researchers concluded.

Other studies have unearthed a link between the Herpes simplex virus — another widespread bug that causes cold sores — and Alzheimer’s in people with APOE-4, a gene that itself is a risk factor for the disease.

How those and other infections might speed on the onset of Alzheimer’s is unclear, but is likely related to the inflammatory effects of the pathogens, Dr. Verhoeff said.

It could be that treating infection will one day help stave off the ravages of Alzheimer’s, and that vaccines for the relevant bugs might help prevent it, concludes the paper. The evidence so far, much of it from animal studies, is far from conclusive but “strongly supports” doing more research, the scientists say.

Dr. Jack Diamond, scientific director for the Alzheimer’s Society of Canada, said the group’s conclusions are “compelling,” and may help explain one of the newest twists in the science of the disease. Those plaques, which eventually become toxic to brain cells, and so-called “tangles,” which choke off crucial brain processes, have long been considered the direct source of the dementia brought on by Alzheimer’s. But recent post-mortem studies have discovered people whose brains had the tell-tale signs, but who didn’t suffer from dementia while alive, raising more vexing questions about what triggers the disease, he said.

It is possible that certain infections are an added factor that must be present for symptoms to appear, said Dr. Diamond.

“Could it be this is one of the things that causes the full-blown Alzheimer’s disease?” he asked. “Maybe this answers some of the unknowns.”

National Post

Technorati Tags: alzheimers, canadian, dementia, disease, infections, reaserch, viral

Current treatment for Alzheimers disease offer symptomatic relief only, but this may soon be changing. Recent discoveries by Nazneen Dewji, PhD, UCSD School of Medicine, support the development of two totally new drugs that would potentially treat the cause. Join us for this exciting discussion of what the future may hold in treating Alzheimers disease. Series: Sam and Rose Stein Institute for Research on Aging (SIRA) [11/2008] [Health and Medicine] [Show ID: 14205]

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Technorati Tags: alzheimers, dementia, loss, memory, treating

Images of Borrelia DNA in Alzheimer’s Disease brain tissue- Including Specific DNA probes for Borrelia Flagellin DNA ( A DNA sequence which is NOT present in the human genome) which glows Green when it finds its Target DNA in Alzheimer’s brain tissue. Also illustrated in this short video are the concepts of TRANSSYNAPTIC transmission of infection in Rabies,and in Herpes Zoster/Shingles. Infections INSIDE of a nerve cell are transmitted Across Synapse connections to neighboring Nerve cells. Borrelia spirochetes gain access to the interior regions of nerve cells and are also\ capable of “JUMPING’ across Synapses to infect neighboring Nerve cells. Networks of Connected nerve cells (NEURAL CIRCUITS) then become infected by Trans-synaptic transmission. This “NETWORK” of infected nerve cells in the brain explains the PATTERN of Sequential destruction of Brain tissue in the Braak Stages of Alzheimer’s Disease through the Braak stages I,II,III, IV, V , VI.

Duration : 0:2:26

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Technorati Tags: alzheimers, Borrelia, DNA, Infection