Experimental therapy for Alzheimer’s disease enabled the normalization of energy metabolism in the brain and the restoration of cognitive functions even in late stages of the ailment—for now, in experiments on mice. Scientists reported that the novel approach led to the complete elimination of symptoms in the animals. The work’s findings were published in the journal Cell Reports Medicine and spurred considerable interest within the scientific community.
Since the Alzheimer’s disease description over 100 years ago, it was considered an irreversible pathology, and the majority of research aimed at slowing its progression. The new study proposes a different strategy: the authors established a previously uncharacterized mechanism linked to impaired energy exchange and tested a medication that not only prevented the disease’s development when administered preventatively but also led to the near-complete recovery of already afflicted mice.
The experience was conducted on two lines of animals modeling different genetic variations of the human condition—those dominated by amyloid plaque deposits and pathological tau protein. The compound P7C3-A20 was aimed at normalizing the level of the NAD⁺ coenzyme in the brain. This coenzyme is necessary for cellular energy metabolism, and its shortage is viewed as one of the primary factors in neurodegeneration.
The treatment restored the brain’s energetic equilibrium in both mouse lines, despite variations in the pathology’s development mechanisms. Improvement in behavioral metrics was noted: the creatures exhibited normal orientation and learning, which researchers interpreted as a sign of functional recovery.
Previously, P7C3-A20 demonstrated a positive outcome in models of severe traumatic brain injury. This suggests its potential application in other neurodegenerative disorders, including Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis. The subsequent phase will involve clinical trials on humans. The authors anticipate that correcting NAD⁺ levels might not only decelerate but also partially reverse the advancement of Alzheimer’s disease, though this conclusion still requires validation in studies involving patients.
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