Pfizer’s current research on a potential blockbuster anti-Alzheimer drug is currently back to drawing-board status. According to the pharma company

[T]he drug, called Dimebon, had shown virtually no effect after six months in treating the cognitive decline or behavioral problems associated with Alzheimer’s when compared with a placebo.

Apparently, Wall Street has been watching the results of this Phase I study; the verdict is still out on whether Pfizer will continue to fund the research for this agent — designed to work better and longer at inhibiting some of the most distressing symptoms related to the disease. | LINK

• Popular anticonvulsant (with a multitude of off-label pain uses) gains approval to go generic.
• A Web-based provider of care analytics has come up with a prostate cancer screen. The cynic in me says it’s a new look to an old unresolved problem.

Through a web-based tool, men enter the results of their PSA test history and personal information such as height, weight and health history. This information is compared with up to a million case studies and outcomes from other men with various prostate conditions. Finally, the system may suggest a medical detective process for doctors and their patients in their efforts to detect non-cancerous prostate conditions and improve prostate cancer screening, the company said.

• Lilly is trying very hard to get a novel neuroleptic to market; it’s not going too well.
• Crestor, an popular cholesterol drug, to protect against venous blood clots? | VIDEO
• CA spice company linked to Salmonella outbreak. | LINK

One of the mysteries of Alzheimer dementia (AD) has been the normal function of the amyloid precursor protein (APP);  these specialized proteins are concentrated at the points where neurons connect within the brain. Even though the sticky amyloid plaques (which have been viewed as a hallmark sign of AD) result from APP, it seems unlikely that APP exists simply to cause AD. In a recent study, scientists from the U.S. and France show that APP binds to netrin-1, a protein that helps to guide nerves and their connections in the brain, as well as helping nerve cells to survive. When netrin-1 was given to mice that have a gene for AD, their symptoms were reversed, and the sticky amyloid was reduced.

These results suggest that the long-held belief that AD is caused by brain cell damage inflicted by the amyloid plaques may be wrong; instead, it is beginning to appear that the disease stems from an imbalance between the normal making and breaking of connections in the brain, with netrin-1 supporting the connections and the amyloid breaking the connections — both by binding to APP and activating normal cell functional programs.  One thing about novel molecular nanoresearch is that it always keeps things interesting. | LINK

In the wake of serious cuts which threaten public universities in Minnesota (largely aimed at the sprawling University of Minnesota system), is now the time to get involved in investing in knowledge capital? The U of M is being blamed for its lack of advancement in the field of bio-tech R&D. A report highlights the problems Minnesota has with maintaining an environment which fosters medical technical advancement and, more importantly in attracting those types of jobs — ones that can sustain a vibrant economy. Although the state is regarded as a pioneer in certain biotech spheres (notably cardiac devices), the report criticized Minnesota as focusing too much on a singular area and remaining stagnant. | LINK  | Report PDF LINK