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elfuzzy.bsky.social
ElFuzzy
@elfuzzy.bsky.social
450 followers 210 following 1.8K posts
He/Him

League of Legends Enthusiast

Dimir player

Clan lead of the official unofficial Loading Ready Run Warframe Clan.
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Reposted by ElFuzzy
niminightmare.bsky.social
Thank you for your beautiful art!!

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December 28, 2025 at 9:41 PM
Reposted by ElFuzzy
sailorrooscout.bsky.social
In preclinical models, treatment repaired brain pathology, restored cognitive function, and normalized Alzheimer’s biomarkers (in HUMAN models as well).
• case.edu/news/new-stu...

The study has been published in Cell. YES, it is PEER-REVIEWED.
• www.cell.com/cell-reports...

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Highlights •Severity of Alzheimer's disease (AD) correlates with NAD+ homeostasis dysregulation •Preserving brain NAD+ homeostasis prevents AD in mice • Restoring brain NAD+ homeostasis reverses advanced AD in mice • Multiomics across human and mouse AD brain identifies nodes for human AD reversal Summary Alzheimer's has long been considered irreversible, but new research challenges that assumption. Scientists discovered that severe drops in the brain's energy supply help drive the disease-and restoring that balance can reverse damage, even in advanced cases. In mouse models, treatment repaired brain pathology, restored cognitive function, and normalized Alzheimer's biomarkers. The results offer fresh hope that recovery may be possible. Abstract Alzheimer's disease (AD) is traditionally considered irreversible. Here, however, we provide proof of principle for therapeutic reversibility of advanced AD. In advanced disease amyloid-driven 5xFAD mice, treatment with P7C3-A20, which restores nicotinamide adenine dinucleotide (NAD+) homeostasis, reverses tau phosphorylation, blood-brain barrier deterioration, oxidative stress, DNA damage, and neuroinflammation and enhances hippocampal neurogenesis and synaptic plasticity, resulting in full cognitive recovery and reduction of plasma levels of the clinical AD biomarker p-tau217. P7C3-A20 also reverses advanced disease in tau-driven PS19 mice and protects human brain microvascular endothelial cells from oxidative stress. In humans and mice, pathology severity correlates with disruption of brain NAD+ homeostasis, and the brains of nondemented people with Alzheimer's neuropathology exhibit gene expression patterns suggestive of preserved NAD+ homeostasis. Forty-six proteins aberrantly expressed in advanced 5xFAD mouse brain and normalized by P7C3-A20 show similar alterations in human AD brain, revealing targets with potential for optimizing translation to patient care. Graphical Abstract (CREDIT: Cell Reports Medicine)
December 28, 2025 at 5:03 PM