US EditionAlzheimer’s fighting infusion delivered in Canada for the first time
The neuroprotective compound P7C3-A20 restored brain NAD+ levels and reversed cognitive decline in advanced Alzheimer’s mouse models, showing biomarker improvements, researchers say.
- Recently, a research team led by Case Western Reserve University reported that P7C3-A20 restored brain NAD+ balance and reversed cognitive decline in two genetically engineered Alzheimer’s mouse models, with findings published in Cell Reports Medicine.
- NAD+ levels naturally fall with age and human Alzheimer’s brain samples showed a 30% reduction, disrupting energy metabolism, DNA repair, and increasing oxidative stress and inflammation.
- Laboratory measures showed that treated mice had restored blood–brain barrier integrity, reduced oxidative stress and DNA damage, decreased neuroinflammation, enhanced synaptic plasticity, and normalized phosphorylated tau 217 levels.
- The researchers called for well‑controlled clinical trials and further lab work to clarify brain energy mechanisms, while Andrew A. Pieper, MD, PhD, noted mouse results do not guarantee human benefit.
- By avoiding direct NAD+ supplementation, the study promotes the salvage pathway to prevent excess NAD+, potentially reducing cancer risk and offering a safer brain energy balance approach.
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South Florida ReporterExperimental treatment restores memory in mice - Health Care Today
For many years, scientists have considered Alzheimer’s disease to be irreversible. For this reason, much research has focused on preventing or slowing disease progression, rather than reversal. However, a recent study in mice investigated a compound with neuroprotective properties that may repair damage and recover cognitive function. In the animal models of advanced Alzheimer’s disease, the compound could restore levels of a vital cellular ener…
A new study reveals that a compound, P7C3-A20, could reverse the advanced cognitive decline associated with Alzheimer's disease. By restoring the energy balance of the brain via the NAD+ molecule, this treatment allowed, on animal models, to repair brain functions without removing the amyloid plaques, opening a promising path towards recovery.
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