An Alzheimer’s treatment could be closer than you think
Ken Blaker
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June is Alzheimer’s and Brain Awareness Month. That may seem unnecessary since few of us are unaware of Alzheimer’s. The name invokes one of our greatest health fears: the fear of being mentally impaired. And it is common knowledge that Alzheimer’s is an incurable descent into unremitting isolation and confusion.
Over 55 million people live with varying forms of dementia, with Alzheimer’s being the most common form. Every month news stories of cultural and political heroes displaying known or suspected neurodegeneration break the public’s heart.
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For me, the face of neurodegeneration was my uncle Marty. For most of his life, he was fearless. He’d fought in WWII and built a successful career. He had endless stories and deep wisdom. When he became forgetful, he also became short-tempered. Finally, in the middle of one of his trademark stories, he looked at me quizzically and asked, “How do I know you?” The last time I saw him he was almost unrecognizable, helplessly begging me to take him away from the care facility where he soon died.
Dr. Alois Alzheimer first described the illness in 1906, in the case of Auguste D., a patient who suffered from memory and language loss and other psychological problems. After the woman’s untimely death at 50, her postmortem brain examination showed abnormalities, including “senile plaque” and nerve tangles.
To this day, most drug treatments for Alzheimer’s disease focus on the same plaques. Progress has been made in slowing the progression of the disease and even sparking short-term improvements in memory formation. But in the end, there is no cure, and the disease always prevails over the drugs. Our Martys die, often not knowing who we are. And current drug therapies come with a sad offset: a wide range of side effects, from minor to severe, brain bleed and inflammation being the worst. Short-term gains are measured against the other suffering.
In recent decades, researchers have widened their scope beyond just the plaques to an examination of the neuroinflammation that may lead to them, as well as potential treatments for that inflammation. Dr. Avindra Nath, head of the NIH’s National Institute of Neurological Disorders and Stroke, told me in an email that “many systemic infections may unmask or accelerate the process of Alzheimer’s disease, and that is most likely through the process of neuroinflammation.”
But he also points out that “many drugs targeting inflammation have been considered for treatment of Alzheimer’s disease; however, to date, there is no FDA-approved anti-inflammatory drug with that indication.” In clinical testing, well-known anti-inflammatory agents such as Celebrex, Aleve, and Aspirin have failed to heal or even slow the disease. In fact, over 99% of all drugs tested for Alzheimer’s prevention have failed, which is the worst yield of any group reported in Food and Drug Administration data.
But research into Alzheimer’s and other neurodegeneration is not slowing down, and understanding of the processes that lead to dementia and other neurological impairments is growing. Prospective treatments continue to be advanced and studied.
In 2015, a team at Pfizer published Phase 2 testing of their autoimmune drug Enbrel, showing that in some Alzheimer’s patients, the drug not only slowed cognitive decline but actually improved cognition. Enbrel works by inhibiting the protein TNF-alpha, thereby slowing inflammation. The pursuit of Enbrel for Alzheimer’s treatment was eventually dropped, but other potential treatment studies continue.
Pharmaceutical start-up BioVie focuses not on inhibiting TNF-alpha, like Enbrel, but on working earlier in the inflammation cascade. Its experimental treatment, NE3107, is in Phase 3 testing, inhibiting a different protein called inflammatory ERK. Inflammatory ERK is produced before TNF-alpha production, and leads to it. Phase 1 and 2 testing show promising cognitive results, and encouragingly the treatment has very low toxicity, making it exciting as a potential clinical treatment with low side effects.
Other research teams are mapping out the ways that neuroinflammation activates specific immune cell responses in the central nervous system, searching for the right keys to counter the degenerative effects.
After 117 years of discouraging results in treating Alzheimer’s disease, worldwide research targeting neuroinflammation is a cause for real hope. Combating inflammation holds the potential for preventing further decline and perhaps even reversing some effects of Alzheimer’s and other neurodegenerative diseases that can be associated with inflammation.
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This June, I am paying attention to Alzheimer’s and Brain Awareness Month. Don’t be surprised to see me in my purple “#ENDALZ” T-shirt. I’ve got one, and you should, too.
Ken Blaker is a healthcare and technology consultant focused on medical devices and FDA compliance.