The Alzheimer’s Disease Epidemic
Neurodegenerative disease has been surging around the world for the past 30 years. It’s the fastest-growing cause of death and it will soon be the leading cause of death.
Alzheimer’s disease alone is taking the lives of 50-100 million people around the world now. Millions will die of the disease this year, while millions more will be diagnosed, misdiagnosed and undiagnosed. The epidemic is more severe in some countries than others. No one really knows the scope of the epidemic.
A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins. Misinformation and mismanagement are fanning the flames.
Despite millions of deaths, experts suggest that the prevalence of the disease will quadruple by 2050, if not sooner. Unfortunately, there is a growing stack of evidence that Alzheimer’s disease, Parkinson’s disease and other brain diseases are transmissible. Deadly, self-replicating proteins appear to be one of the common threads. Similar proteins appear to be associated with autism and the childhood cases of Creutzfeldt-Jakob disease.
The epidemic is worse in some regions of the world than others. Finland and Iceland were at the top of the list just a few years ago. Now, countries in the Middle East and Persian Gulf states have soared to the top of the list.
Prions (PREE-ons) are a deadly and unstoppable form of protein that migrates, mutates, multiplies and kills with unparalleled efficiency. Prions cause fatal neurodegenerative disease in humans and other mammals by converting the cellular version of prion protein into a toxic form that erodes the brain and body. Prion disease often is described as a wasting disease that causes a loss of body mass and brain mass.
Dr. Stanley Prusiner, an American neuroscientist from the University of California at San Francisco, earned a Nobel Prize in 1997 for discovering and characterizing prions and prion disease. President Obama awarded Prusiner the National Medal of Science in 2010 to recognize the importance of his research. Important reforms to policies to protect public health, however, have been elusive.
Prion disease also is known as transmissible spongiform encephalopathy (TSE). The operative word is “transmissible.” Prusiner claims that all forms of TSE are caused by infectious prions.
“Alzheimer’s disease (AD) is the most common neurodegenerative disease in humans and will pose a considerable challenge to healthcare systems in the coming years,” Prusiner said. Aggregation of the β-amyloid (Aβ) peptide within the brain is thought to be an initiating event in AD pathogenesis. Many recent studies in transgenic mice have provided evidence that Aβ aggregates become self-propagating (infectious) during disease, leading to a cascade of protein aggregation in the brain, which may underlie the progressive nature of AD. The ability to self-propagate and the existence of distinct strains reveals that Aβ aggregates exhibit many properties indistinguishable from those of prions composed of PrPSc proteins. The evidence that Aβ can become a prion during disease, Aβ prions may be important for understanding the pathobiology of AD.”
Like prion diseases, misfolded alpha-synuclein and tau protein associated with Parkinson’s disease and Alzheimer’s disease, respectively, have been reported in skin tissues of patients with these conditions. Skin could serve as a screen for early diagnosis, but also for monitoring the accumulation of the misfolded proteins in the brain of these neurodegenerative diseases. It also could be another pathway of transmission.
“There has been a resurgence of this sort of thinking, because there is now real evidence of the potential transmissibility of Alzheimer’s disease,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s disease researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins (prions).”
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