The CART Fund provides “seed” money for cutting edge, high impact studies in hopes of finding prevention of or a cure for Alzheimer’s disease. Capital Rotary supports CART – Coins for Alzheimer’s Research Trust – as a “home grown” project. It began in our District 7770 in 1995 and has since been adopted by Rotarians in Georgia and both Carolinas, plus a number of individual clubs throughout the United States.
Bright blue CART buckets adorn each table at our weekly meetings, ready to receive donations earmarked for Alzheimer’s projects in the United States. CART backs exploratory and developmental research that has the potential for substantial biomedical progress in new directions or applications. Grants awarded to date total approximately $5.2 million. For more information, visit http://www.cartfund.org
Below, our very own, Jimmy Gibbs, joins Dawdy Mercer Plank on WIS-TV to discuss the Capital Rotary Club and how our donations are helping research a cure for Alzheimer’s disease through Coins for Alzheimer’s Research Trust (CART).
Dr. Jack Bass, a Rotarian in Hilton Head who handles CART grants for the CART Board, provided the following. Here are the grants awarded as of May 2006:
1999 Investigator: Allan Levey, MD, PhD; Emory University.
Project: Validation of a Novel Diagnostic Test for Alzheimer’s Disease.
This project was to develop a diagnostic blood test to be sufficiently specific and sensitive for the diagnosis of AD. However, the results of the study were not adequate enough to overcome the technical problems and cost of the test itself. Nevertheless, a secondary finding was a difference in the function of a certain blood cell in patients with AD that may help the body’s defense against infection.
A $50,000 piece of equipment that was acquired for the grant can still be used for many and various laboratory tests in other field of aging research.
2001 Investigators: Karl Herrup, PhD/Gary Landreth, PhD – Case Western Reserve University – Project: Inflammatory Mechanisms in Alzheimer’s Disease.
This project was to locate genes that are regulated by exposure to amyloid plaques and inflammatory stimuli and to examine the role of this inflammatory process in neuronal cell death. Deposits of amyloid activate the inflammatory process that stimulates neurons to begin cell division that leads to cell death and clinical AD.
Investigators are now studying a specific protein that inhibits these neurons from dividing. Then they can investigate genes that are ‘turned-on’ by amyloid or ‘turned-off’ by anti-inflammatory drugs, e.g., ibuprofen. Next will be an investigation of a new class of anti-inflammatory drugs using the above technology.
Two members of our CART Board were briefed on this project during a site visit to their laboratory in July 2003.
Dr’s. Herrup and Landreth have five (5) journal publications with reference to support received from CART funds:
2002 Investigator: Philip Wong, PhD; Johns Hopkins University – Project: Nicastrin and gamma-Secretase in Alzheimer’s Disease.
The normal activity of certain enzymes are required for neuron function. In this project, a mouse model was engineered with a controlled set of genes that actively developed until given a ‘knock-out’ substance that caused a specific deficiency of an enzyme that led to amyloid plaques. This information can now direct a course to find a mechanism-based therapy for AD, none of which are now available.
As a result of a subsequent overlap grant funded by the National Institute of Health, our contract with Johns Hopkins required them to negate $187,000 of this award.
Dr. Wong has two (2) journal publications with reference of support received from CART funds:
2003 Investigator: Philip Wong, PhD. – Project: Development of a Conditional BACE1 Transgenic Mouse Model.
Award: $187,000. The money returned from a previous grant was approved by review of the peer committee to be awarded for this project.
This investigator initiated efforts to study whether the amyloid plaques in the AD brain are dependent upon a continuous supply of amyloid and whether these plaques can be cleared by inhibiting a specific enzyme. Given the current state of knowledge, new compounds that directly impact this enzyme will be developed and tested in animal models, and if successful then brought to clinical trials in an effort to prevent or cure AD.
Dr. Wong has had two (2) journal publications with reference of support by CART funds.
2003 Investigators: Domenico Pratico, MD / John Q. Trojanowski, MD, PhD; University of Pennsylvania School of Medicine – Project: Novel Therapeutics for Alzheimer’s Disease Amyloidosis.
This project was to determine if the accumulation of ‘fats’ from metabolic oxidation in the central nervous system could cause amyloid plaques. This effect was blocked through a genetic chemical receptor, leading to a significant reduction in the early phase of amyloid deposition.
Dr’s. Pratico and Trojanowski have one (1) journal publication with reference of support received from CART funds:
2004 Investigator: Robert Reenan, PhD; University of Connecticut Health Center – Project: Testing the Amyloid Hypothesis in Drosophila
This project was started by engineering flies [Drosophila] that are either amyloid secreting or non-secreting types of flies. This gene expression is silent until crossed with a stock of flies that activate the brain. Then they can compare any tissue abnormalities and behavioral changes in the two types of flies. This could lead to developing specific medications for AD.
2005 Investigator: Gary Small, MD; UCLA – Neuropsychiatric Institute – Project: Amyloid Plaque and Tangle Imaging in Mild Cognitive Impairment.
This investigator has developed a clinical marker that enables him to see Alzheimer’s plaques and tangles with a brain scan in a living patient. This could differentiate between mild cognitive impairment and cognitively intact controls, predicting early detection and prevention of AD.
2006 Investigator: Claudio Soto, PhD; University of Texas Medical Branch – Project: Deletion of Misfolded Ab Oligomers for Early Detection of Alzheimer’s Disease
At the time that clinical symptoms of AD appear, the extent of damage from amyloid-b plaques has already occurred in the brain. The major goal of this project is
to develop a biochemical assay to detect the early stages of these protein alterations that are characteristic of AD.
Their hypothesis is that small amyloid aggregates start many years before the onset of clinical symptoms with some of these structures circulating in blood and cerebral spinal fluid. Their objective is to identify minute quantities of these aggregates and assess their utility for the pre-clinical diagnosis of AD.