On Nov. 4, 1906, a man named Alois Alzheimer stepped to a podium and delivered a lecture at the 37th Conference of South-West German Psychiatrists in Tübingen, Germany. Alois was a German-trained medical doctor who had interests in a variety of fields, but his lecture that day would be the one that immortalized him.
He described the progressive neurodegeneration of a 51-year-old female patient named Auguste D., and in doing so, he cemented his name in history, forever linked to his newly described disease. You can read more about Auguste and Alois in an article titled “Auguste D. and Alzheimer’s disease,” published in the May 1997 edition of The Lancet.
According to the 2018 Alzheimer’s Association Report, “Alzheimer’s disease facts and figures,” around 5.7 million people currently have Alzheimer’s disease in the U.S. The report also estimates this number will reach 13.8 billion by the year 2050. Over 15 years from 2000-15, the medical community saw a drop in heart disease, cancer and stroke-related deaths, but a 123% increase in deaths from Alzheimer’s. The report also covers some of the facts centered around the health care-related costs of Alzheimer’s, which neared $280 billion in 2018 alone.
The impact this disease has on a person and their loved ones are actually immeasurable.
The neural pathways formed by our genes and influenced by our environment are what make us the person that we are. Our hopes, personalities, beliefs, memories, talents and love are all stored within the electrical and chemical signaling of our adapted neural pathways.
As these pathways degrade, we lose ourselves and even end up forgetting fundamental facts that were once impossible to forget, such as the face and name
of your child. Alzheimer’s disease steals our identity and takes our loved ones along for the ride.
For those who are unfortunate enough to be touched by Alzheimer’s disease, there is hope, and science is desperately trying to find solutions to the problem.
A recent article from the journal “Nature Medicine” titled “Resistance to autosomal dominant Alzheimer’s disease in an APOE3 Christchurch homozygote: a case report,” details a discovery that may lead to new treatments for the disease. For decades now, a large extended family from Columbia has suffered from very early-onset Alzheimer’s, typically in their 40s. The family carries a unique mutation that causes the disease to begin early, but one 73-year-old member who carries this same mutation is not suffering from the disease.
A team of scientists found she possesses another variation in a gene called APOE3, which is involved in fat metabolism. While she does have a massive build-up of the famous amyloid protein in her brain from Alzheimer’s, she does not have much of another protein build-up known as tau. This suggests that her mutation in APOE3 may be preventing the tau protein tangles, and therefore may be protecting her from the severe impact of Alzheimer’s. Further investigation is needed, but targeting tau tangles and APOE3 is now more on the radar of researchers.
Hope exists, and if you search just a bit, you will find many new discoveries and potential treatments for this horrible disease. A new drug, Oligomannate, recently approved in China and derived from seaweed and is showing promise, as are the vaccines UB 311 and AADvac1.