Alzheimer’s disease and other dementias affect 47 million people worldwide and the situation can only get worse…if we fail to act to prevent the disease first rather than to cure it.
Dementia is essentially the slow and progressive dying of brain cells, usually resulting from a neurodegenerative disease like Alzheimer’s. The main causes of dementia is the buildup of toxins, chemicals, drugs that block acetylcholine, and heavy metals in the brain, along with nutritional deficiencies. The statistics for potential increases in Alzheimer’s do not consider the wholesale poisoning of the environment with aluminum via chemtrails. Combating the ogre of Alzheimer’s is likely to restructure human society more towards the essentials of healthy living. Alzheimer’s disease is on the rise, with Alzheimer’s disease becoming the third leading cause of death in the United States behind cardiovascular disease and cancer. By 2050, it’s estimated that 160 million people globally will have the disease, including 13 million Americans, leading to potential bankruptcy of the Medicare system.
Integral Cognitive Repair: A study, by the Buck Institute for Research on Aging and the UCLA Easton Laboratories for Neurodegenerative Disease Research, is the first to objectively show that memory loss in Alzheimer’s patients can be reversed, and improvement sustained, using a complex 36-point therapeutic program that involves comprehensive personalized changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry. After several months on the protocol there was a clear improvement in patient’s recall, reading, math, navigating, vocabulary, mental clarity and facial recognition. Proving that an extensive broad-spectrum lifestyle change approach to cognitive decline is highly effective for reversing Alzheimer’s symptoms.
Synapse elimination, or “synaptic pruning,” is a normal process that occurs during brain development. However in Alzheimer’s the mechanisms involved in such pruning might be aberrantly turned back on or hijacked, so to speak, contributing to synapse loss. In the pruning process, microglia eat away at synapses to assist the immune system. Heparan sulfate, is a linear polysaccharide produced by mast cells, found on the surface of cells (including neurons), where they interact with a plethora of ligands. Heparan sulfate essentially “traps” amyloid peptides, causing them to aggregate and form deposits that will eventually lead to amyloid beta plaques and tangles in the brain that trigger inflammation and result in the loss of brain connections called synapses, the effect most strongly associated with cognitive decline, neurodegeneration and dementia.
The early vulnerability of ageing to the Locus coeruleus (LC), the major noradrenergic nucleus of the brain and to neurodegenerative disease like Parkinson’s and Alzheimer’s diseases is of considerable significance. Noxious stress and anxiety-provoking extremes cause heightened arousal and activation of the sympathetic nervous system, which overworks the dopamine and noradrenaline circuits thereby aging the protective neuromelanin pigmentation and causing nerve cell death.
Dr. Richard Deth found autism and other attention disorders like ADHD, schizophrenia and Alzheimer’s disease can be attributed to impaired function of the D4 subtype of dopamine receptor due to high oxidative stress and a reduction in folate-dependent methylation reactions, including their regulation by dopamine and growth factors, as well as their inhibition by neurodevelopmental toxins. Molliver et al. (1989) remarked on the similarity between serotonergic axons damaged by the drug Ecstasy and those seen in Alzheimer’s disease.