New Method to Slow Brain AgeingWinter SE 2016 – 2017
Alzheimer’s was viewed as an incurable consequence of ageingIn a stunning development, two natural factors have been discovered that protect against structural brain damage. Published studies reveal a simple strategy to improve cognitive unction, slow Alzheimer’s progression, and possibly reverse it. These innovations provide an affordable way to thwart senile changes that were once thought to be unavoidable.
By William Faloon And Cynthia Richards
- Beta amyloid accumulation: Amyloid plaques are senile protein “clumps” that damage areas involved in memory consolidation. These plaques are highly toxic to neurons (brain cells).
- Tau protein dysfunction: Healthy neurons are held together by a cellular skeleton made up of tau proteinmicrotubules. When tau proteins are dysfunctional and abnormally accumulate, the consequence is cellular death.
- Neurofibrillary tangles: As damaged tau proteins accumulate, neurons become clogged with neurofibrillary tangles. This renders neurons dysfunctional.
GSK-3: The Age-Accelerating Enzyme
- Accelerated ageing in heart and muscle, showing profound dysfunction.
- Increase in pro-inflammatory cytokines.
- Accelerated ageing in the skeletal system, leading to degenerative joint disease.
- Accelerated ageing in the stomach and liver.
- Development of structurally abnormal cell organelles including disrupted mitochondria.
- Dysfunctional autophagy, meaning inability to clear “debris” that accumulates inside aging cells.
- Development of type II diabetes, Alzheimer’s and other disorders.
How GSK-3 Contributes to Alzheimer’s diseaseAlzheimer’s disease brains undergo structural changes that result in accumulations of beta amyloid plaque and damaged tau proteins. This in turn creates neuron fibrillate tangles that lead to brain shrinkage and cell death associated with Alzheimer’s dementia. These structural alterations in brain cells correlate with increased activity of the GSK-3 enzyme. GSK-3 converts tau proteins into destructive tangled clumps that poison brain cells. The abnormal expression of tau proteins caused by GSK-3 can lead to neurofibrillary tangle formation and eventual dementia. Evidence suggests that impaired glucose/insulin action increases accumulations of beta alkaloid and damaged tauproteins. These observations have led to the term “type III diabetes” being used to describe Alzheimer’s disease. That’s because so many Alzheimer’s patients also present with glucose impairment and insulin resistance. Studies have shown that by inhibiting GSK-3 activity, one can effectively lower blood glucose in diabetic animals, while increasing insulin sensitivity. Since Alzheimer’s patients frequently suffer from abnormal sugar and insulin action in their brains, this has led to the idea that GSK-3 inhibition might be a useful approach in Alzheimer’s disease. In fact, the title of a comprehensive scientific report on this topic is:
“GSK-3 is essential in the pathogenesis of Alzheimer’s disease”
WHAT YOU NEED TO KNOW
Preventing Alzheimer’s with Lithium and Proline-Rich Polypeptide
- Alzheimer’s disease threatens aging Americans with progressive erasure of memories, cognitive function, and normal social interactions.
- Mainstream medicine offers little hope for those with or at risk for Alzheimer’s, providing only temporary symptomatic relief with no ability to reverse the disease’s progress.
- Lithium, an element used as a drug for decades to achieve brain changes in psychiatry, is now showing tremendous promise, at micro doses, in inhibiting the GSK-3 enzyme, thereby preventing the chemical changes to tau proteins that cause them to aggregate into defibrillation tangles.
- Colostrum-derived proline-rich polypeptide can modify gene expression to reduce the amount of beta amyloid precursor production and damage to tau proteins.
- Lithium and proline-rich polypeptide have been shown in recent human studies to stabilize cognitive decline in people with mild cognitive impairment or early Alzheimer’s disease. Colostrum-derived proline-rich polypeptide is capable of reversing cognitive decline.
- Lithium and proline-rich polypeptide work more powerfully in the earliest stages of Alzheimer’s.
Lithium: A GSK-3 InhibitorYou don’t have to wait for pharmaceutical research to resolve the devastating impact inflicted by excess GSK-3. That’s because a GSK-3 inhibitor already exists and holds tremendous promise in the fight against Alzheimer’s. This GSK-3 inhibitor is the trace element lithium. Lithium has a long history in medicine as a psychoactive drug. It has also been shown to be an important component for cognitive and mental health. Epidemiological studies show a strong association between low lithium levels in drinking water and high rates of suicide and homicide, suggesting that insufficient lithium contributes to mental destabilisation Because lithium intake from natural sources varies widely, this has led to speculation that many of us are failing to consume the element in quantities large enough to provide natural neuron protection. And that, in turn, means that there may be real benefits in increasing our regular consumption of lithium by tiny amounts, on a regular basis. We now have persuasive evidence on how microdose lithium exerts robust brain-protective effects.
LITHIUM AND LONGEVITY
“We could discover new ways of controlling the ageing process in mammals, including humans.”
Lithium Reduces Brain Plaque Accumulation
ONLY “TINY” DOSES OF LITHIUM
Human Study Shows that Lithium Preserves Cognition
Proline-Rich Polypeptide Reverses Neurologic Decline
Proline-Rich Polypeptide Lowers Beta Amyloid and Abnormal Tau LevelsIn a lab study, proline-rich polypeptide altered the expression of genes involved in beta amyloid protein production and in the changes to tau proteins that trigger formation of neurofibrillary tangles. At the same time, proline-rich polypeptide altered the expression of genes to increase the production of enzymes that break down and eliminate beta amyloid as part of the natural clearance process. This study demonstrated additional protective effects of proline-rich polypeptide, including enhanced defences against chemical stresses and decreased expression of cytokines that promote inflammation, a process long implicated in Alzheimer’s disease. Together, these properties of proline-rich polypeptide change the expression of molecular networks that lead to beta amyloid formation and tau alterations. This mother’s milk-derived compound thus has the potential to prevent some of the fundamental structural causes of Alzheimer’s disease!
Proline-Rich Polypeptide Improves Cognitive PerformanceCompelling laboratory studies demonstrate that proline-rich polypeptide, when applied to nerve cellsgrowing in culture, triggers a cascade of events very similar to that produced by natural nerve growth factor. These structural effects include important brain benefits such as enhanced differentiation of premature cells into functioning adult neurons, and increased outgrowth of neuritis, the tiny projections on nerve cells where cell-to-cell communication takes place. A study was done on senescence-accelerated mice, which age at a much higher rate than do normal mice. They were fed either colostrum-derived pro-line-rich polypeptide, colostrum, or a mixture of cow-derived proteins. The mice were then subjected to a battery of behavioural tests to study spatial learning and memory. In the group fed colostrum-derived proline-rich polypeptide, but not the others, learning and memory capabilities were found to be significantly improved as the animals aged, and the median lifespan was extended by 26%.
Reversal of Cognitive Decline in Human Alzheimer’s Patients
LITHIUM AND ALZHEIMER’S
Multiple Mechanisms of Cellular ProtectionLithium has an established role in the treatment of major psychiatric problems, especially bipolar disorder. Recently, enticing data from experimental studies suggest that lithium provides neuron protective benefits. Animal studies and cell models suggest lithium increases nerve cell viability through a combination of mechanisms that includes:
- Regulation of cell lifespan,
- Removal of dysfunctional cellular components,
- Increased mitochondrial function, and
- Synthesis of nerve growth factors.
- Cerebral cortex thickening,
- Increased gray matter density, and
- Hippocampal enlargement.