Sunday December 2 was the annual appreciation event for participants in the USC-Keck School of Medicine Alzheimer’s Disease Research Project. I attended as a member of the project’s Community Advisory Board. There are many developments in the field of Alzheimer’s studies.
Developments in Alzheimer’s Research
Phyto-SERMs (Selective Estrogen Receptor Modulator) are being explored as potential palliatives for Alzheimers. Because estrogen itself can raise the risk of breast cancer in women, research is being directed towards using SERMS from botanical sources that can help control the disease without causing the additional cancer risk.
Likewise, male androgen Phyto-SARMs (Selective Androgen Receptor Modulator) are being researched to avoid the potential of causing prostate cancer by increasing blood levels of Testosterone. Testosterone brain levels are half for Alzheimer’s patients compared to normal brains. Testosterone levels decline early in the disease. Animal neurons are shown in studies to have been saved by Testosterone. Whether low Testosterone is a cause of the disease or a consequence of it is not clear, but as with the Phyto-SERM studies, it is important to find a way to replace Testosterone without increasing a risk of cancer at the same time.
DHEA studies have been conducted on Alzheimer’s patients with very low levels of DHEA (one study I looked at was two 50mg doses daily). DHEA–which raises Testosterone levels–is derived from plants and its study on Alzheimer’s patients seems to have been tried (as far as I can tell) exclusively on people who already have the disease. One study showed some slightly less than significant improvement at a three month level and none after six months (the one with the 2 50mg dosages). But if low Testosterone is the cause rather than a consequence of Alzheimer’s perhaps a better long term study would be whether DHEA (Dehydroepiandrosterone) can help prevent Alzheimer’s in the first place rather than to attempt to reverse the disease once it has started.
For additional information on DHEA, go to: http://www.lifelinknet.com/siteResources/Products/DHEA.asp.
PET (Positron Emission Tomography) scans can see brain plaques but not the tangles that cause Alzheimer’s. MRI’s (Magnetic Resonance Imaging) can see millimeters not to the necessary resolution of micrometers. Consequently the Keck ADRC is working on PET to enable observation of the brain tangles.
Pharmaceutical company Eli Lilly spent $1 billion on Solenuzemab and now is not seeing enough success to get FDA approval. This underscores the expensive nature of funding in our society for Alzheimer’s research. There are currently 29 NIA (National Institute for Aging) funded projects working on Alzheimer’s. With the current crisis over the federal budget, NIH (National Institute for Health of which NIA is a part) will lose $2.4 billion in funding come January if a budget deal does not get through Congress.
NACC (National Alzheimer’s Coordinating Center) serves as the equivalent of the NIST (National Institute of Standards and Technology) for Alzheimer’s research protocols. Prior to the establishment of NACC by the NIA, different research projects couldn’t even merge their data because the questions being asked of patients and the statistics being kept were not even standardized. NACC established uniform data definitions. Currently NACC maintains 26,452 clinical records, (USC contributed 998 of those). Neuropathological records are 2,085 total 70 of which are from USC.
Helping to coordinate government responses to the impending epidemic of Alzheimer’s disease, the United States has established the website http://www.alzheimers.gov/. The Alzheimer’s patient population in the U.S. is predicted to rise from the current 5.4 million to 16 million by 2050. Care costs are mostly borne by taxpayers, and may rise from roughly $200 billion this year to $1.1 trillion in 2050.
If the budget fiasco sets back research, the disaster may be even worse.