Preventing Neurodegenerative Disease
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. The coronavirus is no match for the Alzheimer’s epidemic, yet. That’s because scientists finally confirmed that Alzheimer’s disease and other forms of neurodegenerative disease are forms of prion disease, which means that they are highly infectious. Caregivers, family members and billions of innocent people are caught in the crossfire of this explosive epidemic. Few, if any, mammals are immune.
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 many millions more will be diagnosed, misdiagnosed and undiagnosed. The epidemic is more severe in some countries than others.
Until recently, few have considered the possibility that Alzheimer’s disease is a transmissible disease. As it turns out, all evidence suggests that it is a prion disease (infectious proteins). In fact, there is no evidence to the contrary. This denial and misinformation has been fueling a public health crisis around the world for years. It’s gaining momentum.
Billions of dollars and years of research have been wasted on Alzheimer’s disease. Unfortunately, hope for treatment is beyond our vision and grasp. To close that gap we need to overcome two major sticking points that are preventing progress and putting millions of people in harm’s way. The first fact that we must accept is that Alzheimer’s disease is a prion disease. The second fact that we must accept is that all forms of prion disease are transmissible–the scientific name for prion disease is transmissible spongiform encephalopathy (TSE). The operative word is transmissible.
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.
“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.
Prusiner’s most recent study confirms that Alzheimer’s is a prion disease, which means that millions of people with Alzheimer’s disease (and millions who died ahead of them) are highly infectious. Alzheimer’s disease is currently defined based on the presence of toxic protein aggregations in the brain known as amyloid plaques and tau tangles, accompanied by cognitive decline and dementia.
A variety of factors can trigger neurodegenerative disease, including genetics, head trauma and neurotoxins. But attempts to treat the disease by clearing out these proteins have been unsuccessful, so far. The new evidence that active Aß and tau prions could be driving the disease – published May 1, 2019 in Science Translational Medicine — could lead researchers to explore new therapies that focus on prions directly. Hopefully, it will lead to many reforms to safeguard public health.
“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain,” said Stanley Prusiner, MD, the study’s senior author and director of the UCSF Institute for Neurodegenerative Diseases, part of the UCSF Weill Institute for Neurosciences. “The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease. We need a sea change in Alzheimer’s disease research, and that is what this paper does. This paper might catalyze a major change in AD research.”
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.
Prions + Pathways = Victims
Since prion disease is clearly a pathway disease, minimizing and managing prion pathways is an essential first step to safeguard human health and the health of other mammals that are vulnerable to prions. It’s a tall task and one that has been grossly mismanaged around the world for years.
However, as Prusiner suggested, clearing prions from our brains and bodies is an important fallback strategy that demands more research.
Current Alzheimer’s treatments temporarily improve symptoms of memory loss and problems with thinking and reasoning, but they aren’t cures. These treatments don’t stop the the death of brain cells. As more cells die, Alzheimer’s disease progresses.
Experts are cautiously hopeful about developing Alzheimer’s treatments that can stop or significantly delay the progression of Alzheimer’s disease. A growing understanding of how the disease disrupts the brain has led to potential Alzheimer’s treatments that short-circuit basic disease processes.
Future Alzheimer’s treatments may include a combination of medications, similar to how treatments for many cancers or HIV/AIDS include more than a single drug. The following treatment options are being studied today:
Some of the new Alzheimer’s treatments in development target microscopic clumps of the protein beta-amyloid (plaques). Plaques are a characteristic sign of Alzheimer’s disease.
Strategies aimed at beta-amyloid include:
- Recruiting the immune system. Several drugs — known as monoclonal antibodies — may prevent beta-amyloid from clumping into plaques or remove beta-amyloid plaques that have formed and help the body clear the beta-amyloid from the brain. Monoclonal antibodies mimic the antibodies your body naturally produces as part of your immune system’s response to foreign invaders or vaccines.The monoclonal antibody solanezumab did not demonstrate any benefit for individuals with mild or moderate Alzheimer’s disease. It’s possible that solanezumab may be more effective when given earlier in the course of the disease. The drug seemed safe in recent studies, and solanezumab continues to be evaluated in the preclinical stage of the disease.
- Preventing destruction. Researchers learned that beta-amyloid interacts with another protein called Fyn. When combined with beta-amyloid, Fyn is over-activated, which triggers a destruction of connections between nerve cells (synapses) in the brain. Studies are currently in progress for drugs that inhibit the Fyn protein.A drug initially developed as a possible cancer treatment — saracatinib — is now being tested in Alzheimer’s disease. In mice, the drug turned off Fyn, which allowed synapses to start working again, and the animals experienced a reversal of some memory loss. Human trials for saracatinib as a possible Alzheimer’s disease treatment are in progress.
- Production blockers. These therapies may reduce the amount of beta-amyloid formed in the brain. Research has shown that beta-amyloid is produced from a “parent protein” in two steps performed by different enzymes. Several experimental drugs aim to block the activity of these enzymes. They’re known as beta- and gamma-secretase inhibitors. Recent studies showed that the beta-secretase inhibitor verubecestat did not slow down cognitive decline and was associated with several side effects in those with mild or moderate Alzheimer’s.
Leukine is currently being investigated as a potential treatment for cognitive treatment for Alzheimer’s disease. Leukine is a recombinant human granulocyte-macrophage colony stimulating factor (rhu GM-CSF). White blood cells such as granulocytes and macrophages are key components that allow the immune system to fight off infections by attacking and digesting foreign organisms. These cells are produced in the bone marrow (a sponge-like substance that fills the center of some bones in the body) with the help of growth factors such as GM-CSF.
Alzheimer’s disease is marked by abnormal protein deposits called beta-amyloid plaques in the brain that are harmful to nerve cells. GM-CSF is thought to stimulate macrophages in the blood and local brain immune cells (microglia) to “eat” these proteins, and possibly slow or stop disease progression.
The therapy is also reported to have the added benefit of not causing microglial cells to become overactive — a phenomenon that can harm the brain, as excessively stimulated microglia release inflammatory chemicals that are toxic to nerve cells. At the same time, GM-CSF is thought to promote the secretion of other immune-related chemicals that work to protect the brain.
Tau and Tangles
A vital brain cell transport system collapses when a protein called tau twists into microscopic fibers called tangles, which are another common brain abnormality of Alzheimer’s. Researchers are looking at a way to prevent tau from forming tangles.
Tau aggregation inhibitors and tau vaccines are currently being studied in clinical trials.
Alzheimer’s causes chronic, low-level brain cell inflammation. Researchers are studying ways to treat inflammatory processes at work in Alzheimer’s disease. The drug sargramostim (Leukine) is currently in research. It’s thought that the drug may stimulate the immune system to protect the brain from harmful proteins.
Researchers studied the diabetes drug pioglitazone (Actos) because it may lessen beta-amyloid and inflammation in the brain, but this trial was negative.
Researchers are studying the effects of insulin on the brain and brain cell function, and insulin changes in the brain that may be related to Alzheimer’s. A trial testing an insulin nasal spray to determine whether it slows the progression of Alzheimer’s was recently reported as negative.
The heart-head connection
Growing evidence suggests that brain health is closely linked to heart and blood vessel health. The risk of developing Alzheimer’s appears to increase as a result of many conditions that damage the heart or arteries. These include high blood pressure, heart disease, stroke, diabetes and high cholesterol.
A number of studies are exploring how best to build on this connection. Strategies under investigation include:
- Current drugs for heart disease risk factors. Researchers are investigating whether drugs such as blood pressure medications now used to treat vascular disease may also help people with Alzheimer’s or reduce the risk of developing the disease.
- Drugs aimed at new targets. Additional projects are looking more closely at how the connection between heart disease and Alzheimer’s works at the molecular level to find new drug targets.
- Lifestyle choices. Research suggests that lifestyle choices with known heart benefits, such as exercising on most days and eating a heart-healthy diet, may help prevent Alzheimer’s disease or delay its onset.
In one study, taking estrogen-based hormone therapy for at least a year during perimenopause or early menopause appeared to protect thinking and memory in women with a higher risk of Alzheimer’s disease.
But further research has been conflicting, with some studies indicating that estrogen didn’t offer any benefit. More research and a better understanding of the relationship between estrogen and cognitive function are needed before any recommendations can be made.
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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is “transmissible.”