High-Dose Statins Following a Stroke Can Prevent a Second
Patients with cardiovascular disease are less likely to have a stroke if they are taking statins.

Loading up on a statin within six months of a stroke or transient ischemic attack reduced the risk of recurrent stroke or TIA, according to results of a major trial published today.....

skin test for Alzheimer's disease::
PRESS RELEASE: Blanchette Rockefeller Neurosciences Institute (BRNI)
"A painless skin test for Alzheimer%u2019s disease? It may seem unlikely, but scientists at the Blanchette Rockefeller Neurosciences Institute (BRNI) have isolated a substance in skin cells that may provide doctors with a quick and accurate yes-or-no answer when they suspect a patient is showing early signs of the disease. The test could be performed easily by a nurse or medical technician in a doctor%u2019s office or outpatient clinic."

Osteoporosis Treatment Now Approved in Europe & US for Men ! "The US Food and Drug Administration (FDA) this week approved Actonel 35mg (risedronate sodium tablets) for treatment to increase bone mass in men with osteoporosis. This follows the positive outcome in July 2006 of the European application for the additional indication of %u2018treatment of osteoporosis in men at high risk of fracture. ...."

A journey through the known---and unknown: "Alzheimer’s patient Dorothee Lundgren, 60, sits at the kitchen table chewing her bottom lip and staring blankly out the window. She was 49 when she began noticing symptoms."

Diets High in Copper and Fats Linked to Cognitive Decline - CME Teaching Brief- MedPage Today:
"A diet high in saturated and trans fats along with a high intake of dietary copper may be associated with an accelerated decline in thinking, learning, and memory, according to researchers here.

In a study of 3,718 participants, ages 65 and older, enrolled in the Chicago Health and Aging Project (CHAP), high copper intake from food and supplements was linked to a significantly faster rate of cognitive decline. However, the association held only for those who also consumed a diet high in saturated and trans fats, found a study in the August issue of the Archives of Neurology.

Organ meats, such as liver, and shellfish are foods with the highest copper levels, followed by nuts, seeds, legumes, whole grains, potatoes, chocolate, and some fruits. Drinking water delivered through copper pipes may also add trace amounts of the metal. The recommended dietary allowance of copper for adults is 0.9 mg/d, said Martha Clare Morris, Sc.D., of Rush here, and colleagues......."

Many different reversible conditions can cause an older person to appear to have dementia:
"At the first sign of memory loss and confusion we think of Alzheimer's disease and anticipate hearing, 'It's Alzheimer's disease: there's nothing you can do.' These inaccurate words are spoken too often to older people and their families. Instead of accepting this misinformation, consider these alternatives.Maybe it's not Alzheimer's disease!!! There are reversible conditions that can cause an older person to appear to have dementia....."

Neur-Hitech signs agreement with Xel to develop Alzheimer transdermal patch treatment: "The therapeutic agent is Huperzine A, a molecule currently undergoing U.S. phase II clinical testing as an orally administered treatment for mild-to-moderate Alzheimer disease....."

Stigma, denial may delay Alzheimer diagnosis by average of over 2 years, new survey shows: "Concern about stigma and denial of symptoms can delay a diagnosis of Alzheimer disease by more than 2 years (28.7 months) on average after symptoms appear, according to a new survey from the Alzheimer's Foundation of America (AFA)......"

Slipping Away-Self-portraits of an artist's progression into Alzheimer's to be focus of series of community education programs
Alzheimer's disease took O.C. "Shorty" Blackburn's wife. It's now taking Don Rowe's wife.

The other day they joined the director of a day-care center for people with Alzheimer's at an exhibit of self-portraits made by artist William Utermohlen as he descended into Alzheimer's. The expressions of frustration, anger, despair, fear, sadness, resignation and - in the end - blankness were all too familiar to them.

Looking at a painting that shows Utermohlen peering through bars, Rowe said, "He thinks he is in prison."

"He is in prison," said Jean Small, the director of Senior Services' Elizabeth & Tab Williams Adult Day Center, where Rowe's wife, Jo, goes during the day.....

The Scripps Research Institute
By disrupting the aging process in an organism, scientists at The Scripps Research Institute and the Salk Institute for Biological Studies have discovered two mechanisms in an animal model of Alzheimer’s disease that protect cells against protein aggregation that leads to damage called “proteotoxicity.” Since proteotoxicity appears to cause the neurodegeneration in disorders such as Alzheimer’s and Parkinson’s diseases, these findings have important therapeutic implications.

The research, led by Professor Jeffery Kelly of Scripps Research and Professor Andrew Dillin of the Salk Institute’s Molecular and Cell Biology Laboratory, is being published August 10, 2006 as an article in an advanced, online edition of the journal Science.
Alzheimer’s disease now strikes more than one in 30 Americans, and about half the population that lives past 85 acquires Alzheimer’s. Approximately one million Americans have Parkinson’s disease, including three out of every 100 people over age 60. Aging is the most important risk factor for both of these diseases.

The new study—conducted in a C. elegans model, a roundworm that expresses a protein whose aggregation appears to cause Alzheimer’s disease—showed that toxicity from protein aggregation is “drastically reduced” when aging is slowed by modulating the insulin growth factor (IGF) signaling pathway.

Moreover, the researchers found two novel independent activities promoting this cellular survival. The first protective mechanism disassembles and cuts up protein aggregates. Surprisingly, the second protective mechanism enables the formation of larger aggregates from smaller ones that appear to be more toxic.
Unexpected Findings

Kelly, who is Lita Annenberg Hazen Professor of Chemistry at The Scripps Research Institute, a member of its Skaggs Institute of Chemical Biology, and dean of graduate and postgraduate studies, stresses that this novel work was a synergetic collaboration between the research groups at the two institutions.

The Dillin lab at Salk was interested in investigating the connection between cell aging and the onset of proteotoxicity. So, the group set out to determine if the aging process in the worm could be slowed by using RNA interference (RNAi), a naturally occurring process known to suppress certain gene activity in living cells, to lower the activity of the IGF signaling pathway. Indeed, this approach worked and the researchers discovered that if aging was delayed, the onset of proteotoxicity was also postponed.
“In switching this pathway on and off, we also found that we altered the high molecular weight aggregates—the plaque buildup in the animals,” explains Dillin.

But the researchers also noticed an unexpected phenomenon. “Curiously,” Dillin continues, “some animals were totally protected from proteotoxicity despite having high molecular weight aggregation buildup, while other animals were extremely sensitive to proteotoxicity even though they had no detectable high molecular weight aggregates.”
Dillin was eager to further investigate these unexpected findings, so he contacted Kelly at Scripps Research, whose lab had the expertise to examine and analyze these aggregates.
Opposite Activities

Intrigued, Kelly’s colleague Jan Bieschke in collaboration with Ehud Cohen of the Dillin laboratory did additional experiments perturbing individual components of the IGF signaling pathway. They focused on two downstream transcription factors, heat shock factor-1 (HSF-1) and DAF 16, to see what effect they had on aggregation. The results were surprising.
“When we inhibited only HSF-1, the result was a tremendous amount of aggregate buildup; when we selectively inhibited DAF 16, there were almost no aggregates observed,” Kelly says. “That clued us in to the fact that these two transcription factors must be controlling effectively opposite activities.”

His group had been using aggregation assays for a long time, and it occurred to him and his colleagues to add samples of the worm’s ground-up tissue to these assays as a way of even more sensitively detecting how these transcription factors were controlling aggregation in the animal. The Scripps Research team subjected the worm contents to aggregation assays, using fluorescent dyes that emit light when amyloid is present to read out the extent of aggregation. “It turned out that this worked really well,” Kelly says.
When Cohen and Bieschke examined the results, they expected to see less aggregation in the worms when insulin signaling was inhibited. “In fact, what they saw was more.”

Teasing apart the results, the researchers concluded that two mechanisms were protecting the worms against protein-aggregation-associated proteotoxicity. One mechanism was taking the aggregates apart and degrading them into small pieces; the second mechanism was taking smaller, lower-molecular-weight aggregates and transforming them into high molecular weight aggregates of lower toxicity.
Kelly says that this second finding is “quite surprising” in that heavier aggregates seem to be protective for the cell, albeit in a transient fashion—until the cell can “re-group” to dispose of the aggregates. “What we expected was that the amount of aggregates would correlate with toxicity in these worms, but there was no correlation.”

“This second finding is clearly a shift in paradigm,” says Dillin. “For nearly a year in this work, we assumed that large aggregates were the toxic species; however, our data proved otherwise. These results further support a shift in thinking for this field regarding the toxicity of small aggregates and lays the framework for new avenues to combat age-onset protein aggregation diseases, such as AD, Parkinson’s, Huntington’s, and ALS owing to the protective biological activities discovered.”

“Now, we want to use this mechanistic information to discover the macromolecular basis for these activities and to discover small molecules that will delay the aging program and thus delay the onset of proteotoxicity associated with these diseases by modulating aggregation and disaggregation activities,” Kelly states. “The hope is that, by manipulating the protective mechanism inherent in cells, we can find a single entity—a single drug—that would be useful for a variety of neurodegenerative diseases where protein aggregation leads to neurodegeneration.”

In addition to Kelly and Bieschke at Scripps Research and Dillin and Cohen at Salk, Technician Rhonda Perciavalle of the Salk Institute also made significant contributions to the Science study, titled “Opposing Activities Protect from Age Onset Proteotoxicity.”