Publications

MEK1/2 Inhibition Rescues Neurodegeneration in Alzheimer’s Disease Models by Enhancing Autophagy

Genuv presented three posters at the Keystone Virtual Symposium “Neurodegenerative Disease: Genes, Mechanisms and Therapeutics,” that show promising preclinical results for our new drug candidate, SNR1611. In mouse models of Alzheimer’s Disease, SNR1611 showed positive neurogenesis and neuroprotective effects. In one of the studies of a mouse model of Alzheimer’s, orally administered drug led to reduced beta amyloid plaque deposits and recovery of impaired neuronal structures and cognitive functions. The studies are an important validation of our ATRIVIEW® platform, which screens for compounds that induce differentiation of neurons without neuronal cell death in simulated disease conditions.

MEK1/2 Inhibition by Trametinib Rescues Memory Deficits via Activation of Adult Neurogenesis in Alzheimer’s Disease Mice

Genuv presented three posters at the Keystone Virtual Symposium “Neurodegenerative Disease: Genes, Mechanisms and Therapeutics,” that show promising preclinical results for our new drug candidate, SNR1611. In mouse models of Alzheimer’s Disease, SNR1611 showed positive neurogenesis and neuroprotective effects. In one of the studies of a mouse model of Alzheimer’s, orally administered drug led to reduced beta amyloid plaque deposits and recovery of impaired neuronal structures and cognitive functions. The studies are an important validation of our ATRIVIEW® platform, which screens for compounds that induce differentiation of neurons without neuronal cell death in simulated disease conditions.

Mechanisms That Activate 26S Proteasomes and Enhance Protein Degradation

Hyoung Tae Kim, Chief Science Officer and head of GENUV’s Neuroscience Research Center, co-authored a paper showing the mechanisms that activate 26S proteasomes and enhance protein regulation in Biomolecules.

Global Gene Expression of T Cells Is Differentially Regulated by Peritoneal Dendritic Cell Subsets in an IL-2 Dependent Manner

Chae Gyu Park, Managing Director of the Antibody Research Center, co-authored a paper in Frontiers which shows that the global gene expression of T Cells is differentially regulated by peritoneal Dendritic Cell subsets in an IL-2 dependent manner.

2021 SfN_MEK1/2 inhibition rescues neurodegeneration by activation of autophagic lysosomal function in Alzheimer’s Disease

We report that administration of trametinib, a MEK1/2 specific inhibitor, ameliorates memory deficits and synaptic dysfunction and reduces Aβ deposition in various Alzheimer’s disease models. The mechanism of neuroprotection by trametinib is achieved through an enhancement of protective autophagy, a conserved cellular process for clearing dysfunctional organelles and protein aggregates. Thus, we demonstrate that trametinib contributes to the recovery of damaged neuronal functions, representing a potential treatment for Alzheimer’s disease. .

2021 SfN_Trametinib protects motor neurons from degeneration by enhancing autophagy in the SOD1-G93A amyotrophic lateral sclerosis model mice

Administration of trametinib, a MEK1/2 specific inhibitor, is shown to improve survival and motor functions of the Amyotrophic lateral sclerosis (ALS) model animals. Enhancement of neuroprotective autophagy is the mechanism of trametinib’s therapeutic effects for ALS. Trametinib is currently in clinical trial (Phase I/IIa) for the indication of ALS in Korea (NCT04326283).

2021 SfN_Trametinib restores memory deficits by activating endogenous neurogenesis in mouse model of Alzheimer’s disease

Repairing damaged neural tissues in patient’s brain is a plausible therapeutic approach for Alzheimer’s disease (AD) and other neurodegenerative diseases. In this study, we report that inhibition of Mitogen-activated protein kinase (Extracellular Receptor Kinase) signaling by trametinib induces generation of new neurons from endogenous neural stem cells in the brain regions affected by the disease and recovers cognitive functions of AD model animals. We propose that trametinib is a promising therapeutic candidate for Alzheimer’s disease.