Progress and Promise –
INTERNATIONAL RESEARCH CONFERENCE

Millions received news about research progress during the Alzheimer’s Association’s July 2008 International Conference on Alzheimer’s Disease (ICAD), the largest-ever gathering of leaders in research and care.  Part of the Association’s research program, ICAD is a catalyst for generating new knowledge and fostering a vital, collegial research community.

Here’s a glimpse at the rich ICAD 2008 trove – for details call the Helpline (800-272-3900), and see Research at www.alz.org/norcal to sign up for new E-Bulletins, “Research Scoops” –

Diverse approaches to therapies continue to show progress.  Results from clinical trials of three potential AD therapies raise hope for new and better treatments, including: 18-month data from an open-label extension of a pivotal trial of Dimebon in mild-to-moderate Alzheimer’s; nine-month data from an interim analysis of the first U.S. Phase II trial of intravenous immunoglobulin, or IVIg, in AD; and results of a Phase II study of a monoclonal antibody (LY2062430) in mild-to-moderate Alzheimer’s.  Also, research suggested that persistent anti-dementia drug use contributes to longer life in people with AD – now the sixth leading cause of death in the U.S.  

Lifestyle factors contribute to lowering/raising risk.  One study suggests those in midlife who are unmarried or not living with a partner could have increased AD risk.  Another indicates people who ruminate about their problems may be less likely to develop AD, while people with metabolic, cardiovascular-related syndrome are at higher risk.  Analysis of nine European risk factor surveys confirmed well-recognized AD risk factors, including memory complaint, severe head trauma, diabetes, stroke and low education.  Other research shows people with better physical fitness have less brain atrophy during early AD.

MCI – More people have Mild Cognitive Impairment than previously thought.  While that’s bad news, there’s significant controversy over what percentage will progress to AD.  Increasingly scientists believe that in two to three years we’ll be able to identify people with AD pathology before symptoms present. 

Four AD Clinical Trials address a variety of treatment targets.  Promising reports came from:  (1) a Phase IIa trial of PBT2 (reduces the toxic form of amyloid by preventing amyloid interaction with copper and zinc in the brain); (2) an 84-week, Phase II trial of Rember™, a tau aggregation inhibitor targeting toxic “tangles;” and (3) a “proof of concept” clinical trial of Souvenaid, a “medical food” product that encourages formation of brain synapses, possibly reducing beta amyloid.  While disappointed with the 4th results (Flurizan – an amyloid therapy), many scientists believe that doesn’t mean other similar-targeted therapies in the clinical trial pipeline aren’t valid, asking whether even this well done study had the correct dosage, or started intervention early enough in the disease process.

ICAD 2009 will be held in July in Vienna, Austria; information at www.alz.org.