Balaji Krishnan

This study shows that repeated VU0155069 treatment causes region- and stage-specific dendritic spine remodeling in female 3xTg-AD mice, affecting multiple brain circuits.

This paper identifies the PFKFB3-F2,6BP metabolic axis as a key driver of Alzheimer's disease by linking metabolic dysregulation to genomic stability and Tau proteostasis, showing that F2,6BP supplementation rescues AD phenotypes across multiple models.

This paper demonstrates that trophoblast-derived extracellular vesicles can restore P-gp function in brain endothelial cells, enhancing Aβ clearance and reducing neuroinflammation in Alzheimer's disease models.

This study shows that fructose-2,6-bisphosphate (F2,6BP) restores genome repair and motor function in TDP-43 pathology-driven motor neuron diseases.

This study investigates the role of PLD1 in tau pathology and synaptic dysfunction in FTD using postmortem brain samples and proteomic analyses.

This paper shows that F2,6BP restores mitochondrial genome integrity in Huntington's Disease by rescuing PNKP activity and mitochondrial function.

This study shows that modulating PLD1 affects synaptic integrity and cognition in aging and Alzheimer's disease models, with PLD1 attenuation improving synaptic function and memory in AD mice.

This study shows that the w1118 genetic background significantly affects ERG responses in Drosophila, with sex-specific differences and partial compensation by a UAS-hPLD1 construct.

This study shows that F2,6BP restores PNKP activity and alleviates neurodegenerative symptoms in HD and SCA3 by rescuing DNA repair and genome integrity.

This study shows that Alzheimer's disease circulating exosomes reduce VE-cadherin expression and impair brain endothelial barrier function through RNA cargo-dependent mechanisms.