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Last year, I blogged<\/a> on a CDC report that Alzheimer\u2019s Disease<\/a> is more prevalent than previous epidemiology had acknowledged. \u00a0Last month at the Rejuv Biotech conference, I heard Chas Bountra<\/a> tell us that<\/p>\n Boutra is in a position to direct many millions of research dollars for AD, and he says he won\u2019t go near either of the two large branches of research on the disease. \u00a0Study of (1) beta amyloid<\/a> plaques and (2) tau proteins has absorbed tens of billions of research dollars over half a century, and yet there is no agreement even about what ultimately causes AD, let alone a program for cure. \u00a0So he will only fund long-shot ideas at the fringes of Alzheimer\u2019s research.<\/p>\n There is no shortage of dark horses in this field. \u00a0In recent blog posts, I described two: \u00a0Tony Wyss-Coray<\/a> is beginning clinical trials using plasma transfusions from young donors, and Bioviva<\/a> will soon be trying gene therapy to activate telomerase.<\/p>\n Further along than either of these is Dale Bredesen\u2019s innovative approach<\/a> based on the\u00a0sustained\u00a0application of common sense. \u00a0Bredesen reports on a trial with just 10 patients, but 9 of them showed major improvement. \u00a0This was not the kind of result that you need a cognitive test to measure; the patients came out of nursing care and went back to their jobs. \u00a0He calls the program MEND, for M<\/b>etabolic E<\/b>nhancement forN<\/b>eurod<\/b>egeneration.<\/p>\n Bredesen\u2019s starting point is a model in which AD results from a change in hormonal signaling. \u00a0There is turnover of neurons throughout our lives (this alone is a relatively new acknowledgment), and late in life, the destruction of neurons outpaces the growth of new ones. \u00a0Bredesen defines AD as the tail of the distribution, in which the destruction of neurons has become so severe as to precipitate\u00a0obvious cognitive decline. \u00a0He draws an analogy to osteoporosis, which is understood as a loss of the healthy balance between the creation and destruction of bone cells (osteoblasts) that renews bone tissue and keeps bones strong. \u00a0Nerve cells in the brain do not turn over as frequently as bone cells, but the principle is the same.<\/p>\n Body homeostasis is maintained generally by signaling with negative feedback loops. \u00a0Biology derives its robustness from \u00a0processes that are self-limiting. \u00a0But positive feedback loops act like \u201cswitches\u201d; they can take the body from one state to another. \u00a0Beta amyloid is at the center of a positive feedback loop; it is a mis-folded protein that tends to cause more proteins to misfold, similar in dynamics to a prion<\/a>, though the feedback\u00a0of beta amyloid is not so direct as in prion diseases.<\/p>\n In the case of beta amyloid, the protein that is misfolded is called APP, for amyloid precursor protein. \u00a0Bredesen sees APP as a switch that turns AD on, and can just as well turn AD off. \u00a0It is both a signal protein and the gunk that accumulates around neurons in the Alzheimer\u2019s brain.<\/p>\n The (missing) punch line<\/b><\/p>\n So what is the program that Bredesen has used so successfully to reverse Alzheimer\u2019s symptoms in ten patients? \u00a0It is multi-faceted, not easily summarized, addressing multiple risk factors through multiple modalities. \u00a0The program is also personalized, as a doctor works with each patient\u2019s particular symptoms and particular strengths, desiging a program the patient can commit to. \u00a0This is not traditional allopathic medicine, and prescription drugs play a minor role. \u00a0Bredesen describes a program for one of the 10 patients.<\/p>\n (1) she eliminated all simple carbohydrates, leading to a weight loss of 20 pounds; (2) she eliminated gluten and processed food from her diet, and increased vegetables, fruits, and non-farmed fish; (3) in order to reduce stress, she began yoga, and ultimately became a yoga instructor; (4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day; [5<\/a>] she took melatonin 0.5mg po qhs; (6) she increased her sleep from 4-5 hours per night to 7-8 hours per night; (7) she took methylcobalamin 1mg each day; (8) she took vitamin D3 2000IU each day; (9) she took fish oil 2000mg each day; (10) she took CoQ10 200mg each day; (11) she optimized her oral hygiene using an electric flosser and electric toothbrush; (12) following discussion with her primary care provider, she reinstated HRT (hormone replacement therapy) that had been discontinued following the World Health Inst report in 2002; (13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime; (14) she exercised for a minimum of 30 minutes, 4-6 days per week. [<\/em>same ref above<\/a>]<\/em><\/p>\n<\/blockquote>\n (Do you ever wonder about the code language used by doctors on their prescription pads, that only pharmacists can read? \u00a0\u201cpo qhs\u201d is prescription-ese for \u201cby mouth at bedtime\u201d. \u00a0Methyl cobolamin is vitamin B12.)<\/p>\n Bredesen\u2019s results<\/b><\/p>\n The good news is that AD was dramatically reversed, especially in its early stages, with a low-cost program that does not require superhuman life style changes. \u00a0This worked in 9 cases out of 10, and the 10th case was advanced AD. \u00a0The bad news is that crafting an individualized program for the patient requires a doctor with broad knowledge both of medicine and of the patient\u2019s history and temperament, as well as blood tests and cognitive tests. \u00a0Patience. \u00a0This is likely to be expensive and difficult to replicate in modern, assembly-line medicine where doctors are fungible cogs in a health care factory. \u00a0But then, perhaps the bad news isn\u2019t bad\u2013it\u2019s pointing in the direction of the future of medicine.<\/p>\n Ultrasound<\/b><\/p>\n This is just vibration, but at a higher frequency than human ears can hear. \u00a0Ultrasound is commonly used (at low intensity) as an imaging tool<\/p>\n Prof. J\u00fcrgen G\u00f6tz and Gerhard Leinenga of the Clem Jones<\/a> Centre for Ageing Dementia Research, Queensland, Australia have pioneered the use of ultrasound at higher intensity to break up the beta amlyloid plaques in the brain, with dramatic benefits in mice. \u00a0Mice normally don\u2019t get AD, but they can be genetically engineered to come down with AD reliably. \u00a0It was these mice that the Queensland doctors worked with, and in most mice they were able to clear up the plaques. \u00a0There is still controversy (after 40 years) whether amyloid plaques actually cause AD or whether they are a symptom or side-effect. \u00a0So it was important to verify that the mice showed actual memory improvements, and not just better results on the diagnostic tests. \u00a0The next step is to get experience in larger animals, before the first human trials. \u00a0[Read more from Medical News Today<\/a>] \u00a0[In-depth nterview with Norman Swan<\/a>. \u00a0The episode also includes an interview with Saul Vileda of Stanford about planned plasma transfusion experiments in Alzheimer\u2019s patients.]<\/p>\n <\/p>\n Alzheimer\u2019s as an Immune Disorder<\/b><\/p>\n A promising line of research regards AD as an immune attack on nerve cells that producers amyloid plaques as a side-effect. \u00a0It is not the neurons byt glial cells<\/a>, the \u201cin-between\u201d cells in the brain, that trigger the immune attack. \u00a0In active brains with lots of nerve firings, the glial cells are kept in check, while inactive neurons allow the neighboring glial cells to turn themselves into immune provocateurs.<\/p>\n This is a link between decline of the immune system with age, increase in inflammation, and AD. \u00a0Strong circumstantial support for this perspective comes from the fact that anti-inflammatories such as NSAIDs and curcumin offer some of the best protection against Alzheimer\u2019s risk that we currently have available.<\/p>\n Conversely, the healthy immune system attacks<\/i><\/b> amyloid beta and breaks it up. \u00a0Biogen Corp purchased a drug based on antibodies produced by healthy humans that attacks A-beta. \u00a0Just this year, a new drug called Aducanumab<\/a>, aka BIIB037, wasreported<\/a> to be effective in reversing cognitive decline in small, initial trials with human trials\u2013not just mice.<\/p>\n <\/p>\n DFMO and Arginine<\/b><\/p>\n Arginine is one of the 20 amino acids used to build proteins, and it has been found that the AD brain consumes inordinate quantities of arginine<\/a>. \u00a0This begs the question whether arginine is part of the problem or part of the body\u2019s natural solution. \u00a0Carol Colton and her Duke Univ lab are betting on the latter. \u00a0DFMO=difluoromethylornithine is a drug that blocks arginase, the enzyme that breaks down arginine. \u00a0In case that\u2019s too many negatives for you: more DFMO means more arginine. \u00a0DFMO has already been approved as a cancer treatment, and now it has been tested in mice, and found to both decrease plaques and improve cognitive performance. [News article<\/a>, Research article<\/a>]<\/p>\n Another protein component called taurine was found last year to be beneficial for the mice genetically engineered for susceptibility to AD. \u00a0Taurine was added to their drinking water in quantities huge by human standards, equivalent to more than 2 ounces per day of pure taurine. \u00a0But improvements in cognitive performance were dramatic. \u00a0Results were reported<\/a> from the Korean lab of YoungSoo Kim.<\/p>\n <\/p>\n Current \u201cbest practices\u201d<\/b><\/p>\n There are currently 5 FDA-approved drugs for AD, but all of them provide symptomatic relief only, and work only for a few months. \u00a0None is able to slow progression of the disease. \u00a0[Read more from Carl Sundquist<\/a>] \u00a0Last year, there was a breathless announcement by Eli Lilly about early successes with a new drug called solanezumab, but later results deflated the bubble<\/a>.<\/p>\n <\/p>\n What you can do to lower your long-term risk of AD<\/b><\/p>\n Fortunately, the greatest risk factors for AD are the same as for other diseases of old age, so there are broad benefits from the above program. \u00a0General risk factors are cholesterol levels in the blood, insulin resistance, and inflammation.<\/p>\n <\/p>\n ###<\/p>\n This article previously appeared in Josh’s blog Aging Matters here<\/a>. Republished with permission.<\/p>\n The post Promise of Novel Alzheimer\u2019s Treatments<\/a> appeared first on h+ Media<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":" Last year, I blogged on a CDC report that Alzheimer\u2019s Disease is more prevalent than previous epidemiology had acknowledged. \u00a0Last month at the Rejuv Biotech conference, I heard Chas Bountra tell us that Alzheimer\u2019s Disease is currently #3 among diseases of old age Demographics are increasing the prevalence of AD at an inexorable rate Far … <\/p>\n\n
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