A team of American scientists claim they have done something miraculous: they “cured” lab mice suffering from Alzheimer’s disease, which has robbed more than seven million Americans, typically 65 years old and up, of their identity and cognitive ability.
The researchers achieved this feat by administering the rodents with the powerful compound P7C3-A20, which they announced in a new paper in the journal Cell Reports Medicine. Scientists from Ohio’s Case Western Reserve University (CWRU), University Hospitals, and the Louis Stokes Cleveland VA Medical Center undertook the study.
“The key takeaway is a message of hope — the effects of Alzheimer’s disease may not be inevitably permanent,” said Andrew A. Pieper, the study’s principal investigator and a CWRU neuroscience professor, in a statement about the research. “The damaged brain can, under some conditions, repair itself and regain function.”
This research is part of a growing wave of very promising lab studies that point to a tantalizing future where Alzheimer’s and other neurological issues could be a thing of the past. Besides this P7C3-A20 research, others have scored remarkable lab results using different compounds and treatments.
This has made normally cautious scientists so excited that they are making bold predictions. University of Edinburgh neuroscience professor Tara Spires-Jones, who wasn’t part of this P7C3-A20 study, told the BBC this month she thinks scientists are closer than ever to a “truly life-changing” treatment — in as little as five to 10 years; instead of a slow death where people lose themselves, she forecasts that new tests will detect the condition early and innovative treatments will “really make your life normal.”
Scientists are also closer to understanding what causes Alzheimer’s, which seems to be sparked by different factors such as genetics, environment and other stressors — which means that future patients may receive personalized cocktail of anti-Alzheimer’s treatment and drugs suited for their own situation.
Regardless of the cause, previous research has suggested that Alzheimer’s is a form of inflammation. That means lessening or zeroing out inflammation in the brain would be key rather than managing symptoms.
In the P7C3-A20 study, the scientists focused on the impact of the crucial molecule NAD+, a coenzyme important for driving cellular metabolism and which decreases as we age, according to the study. Patients with Alzheimer’s suffer from a significant decrease of NAD+ in the brain, and hence their brain cells have trouble maintaining normal functionality, staving off inflammation, and canceling other physical hallmarks of the disease.
For the study, the team first took two types of lab mice that have been genetically bred to be predisposed to Alzheimer’s; one cohort had mutations for the amyloid protein and the other had tau protein mutations. Both proteins are important to cellular function, but they can become dangerous if they accrete in the brain in the form of amyloid plaques and tau tangles — causing a breakdown in normal cellular processes.
The team injected P7C3-A20 into both mice cohorts at two months of age, later finding out that this treatment successfully prevented them from developing the disease. But the big news was when they injected the compound into another batch of lab mice, who were suffering from a relatively advanced stage of Alzheimer’s at six months of age; after getting injections, these mice completely recovered their cognitive ability and NAD+ levels were restored to homeostasis leve;s
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