Getty Images SHUBHANGI GANESHRAO KENE
In July 2000, when the World Alzheimer's Congress was held in Washington, DC, there was a moment – a "diminutive feeling that scientists might emerge the edge of curbing the epidemic," wrote the journal as Treatment of the disease was imminent. Science has put heads and money into solving this devastating problem that can lead to a total collapse of nerves, shattering families and going bankrupt.
Spoiler alarm: no. Almost two decades later, the heartbreaking and costly illness that Alois Alzheimer first recognized in 1906 is more common than ever. Nearly six million Americans are currently on the grim path of Alzheimer's disease progression, a figure that is expected to reach nearly 14 million by 2050. While Alzheimer's often becomes noticeable only in the 70's or later, the brain changes beginning decades earlier. The sums of money that inspired this optimism have failed to produce a drug that produces more than a modest, transient relief of the symptoms when they emerge – if so.
The lack of progress causes some researchers to rethink everything they have learned about Alzheimer's disease and how it works. Although the number of these scientists is small, the idea of uniting them is a big idea: Alzheimer's is caused by germs. And not some exotic new germ, but the same microscopic organisms that cause things like gum disease and cold sores. Most brains accumulate pathogens with age – blood vessels leak, making the blood-brain barrier more porous. These scientists believe that some of the germs that infiltrate the brain may be the instigators of the changes that become Alzheimer's.
When this so-called microbial protective hypothesis emerges – and the evidence for it proves – this will point the way to a new and radical approach to stopping the construction of a protein called beta-amyloid. These proteins accumulate in the brains of Alzheimer's patients and form telltale deposits called plaques associated with dementia. For 30 years, scientists thought beta-amyloid was a dysfunctional rogue protein and tried to stop it by breaking it down or blocking its production. The new Guardian looking for bugs believes that this old hypothesis knocks on the wrong cell doors. Maybe beta-amyloid is not the real problem. Maybe it's a symptom of something else.
Could Alzheimer's germinate?
In his Cambridge lab, Harvard Medical School's Professor of Morality, Robert Moir, has shown that showed some with experiments showing that beta-amyloid can act as an antimicrobial agent – it kills pathogens in petri dishes and in the brains of mice. The presence of beta-amyloid in the brain of people with Alzheimer's disease suggests that it is there to fight an underlying infection. To target beta-amyloid without tackling the infection, Moir says, "It's like trying to extinguish a forest fire without wiping out the match that caused it."
Moir has made progress despite limited support from the National Institutes of Health, which has favored investigations that view beta-amyloid as the sole cause of Alzheimer's disease. Since completing his first and only NIH scholarship in 2014, Moir has had trouble landing a second country despite his pioneering work. This lack of funding could change soon, thanks to the efforts of individuals such as Drs. med. Leslie Norins, a retired publisher of medical bulletins, offers $ 1 million worth of microbes to Alzheimer's disease to those eligible for a role.
The former infectious disease researcher, Norins, highlights some of the evidence in the medical literature that has convinced him that the microbe idea needs more research. It has been reported that neurosurgeons routinely treating brain tissue die of Alzheimer's at an unusually high rate. One study found that married people who take care of spouses with dementia are more likely to experience similar cognitive impairments than those who care for spouses for other reasons. Autopsy revealed viral DNA in amyloid plaques. Various studies have associated with antibiotics or antivirals a significant improvement in symptoms or outcomes.
Norins fits in with the pattern of a certain type of germ – the kind that is tuberculosis, leprosy, or HIV that thrives in very special circumstances, escaping detection. Competing research teams point to several suspects, with Herpes simplex 1, Chlamydia, and Toxoplasma gondii on the shortlist. Silicon Valley is not waiting for a consensus. A startup called Cortexyme is currently enrolling volunteers for a Phase II study of a drug targeted for a pathogen called Porphyromonas gingivalis . Better known as the cause of gum disease, P. gingivalis was found in the brain of Alzheimer's patients and causes the unique pathology of the disease in mice. In a previous study, members of the (very small) treatment group showed a trend toward improving cognitive function after just 28 days.