Publications by authors named "A Kanthasamy"
Disease monitoring informs the opportunities for intervention by natural resource agencies tasked with managing chronic wasting disease (CWD) in wild cervids. However, allocating funds toward testing can reduce those available for education, outreach, and disease reduction. Implementation of more efficient testing strategies can help meet both an expanding need by resource managers and a burgeoning demand from the hunting public in North America.
View Article and Find Full Text PDFThe Alzheimer's disease and Parkinson's disease risk locus FYN kinase is implicated in neurodegeneration and inflammatory signaling. To investigate in vivo mechanisms of Fyn-driven neurodegeneration, we built a zebrafish neural-specific Gal4:UAS model of constitutively active FynY531F signaling. Using in vivo live imaging, we demonstrated that neural FynY531F expression leads to dopaminergic neuron loss and mitochondrial aggregation in 5 day larval brain.
View Article and Find Full Text PDFExcessive exposure to manganese (Mn) increases the risk of chronic neurological diseases, including Parkinson's disease (PD) and other related Parkinsonisms. Aggregated α-synuclein (αSyn), a hallmark of PD, can spread to neighboring cells by exosomal release from neurons. We previously discovered that Mn enhances its spread, triggering neuroinflammatory and neurodegenerative processes.
View Article and Find Full Text PDFNuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson's and other related neurodegenerative diseases.
Mol Neurodegener
November 2024
Article Synopsis
- * Key features of neurodegenerative diseases include mitochondrial dysfunction, oxidative stress, and protein aggregation, particularly affecting dopaminergic neurons, which are crucial in PD progression.
- * The review explores how disruptions in NPCs, nuclear transport, and the nuclear envelope may contribute to PD, emphasizing the need for further research on how these mechanisms interact with oxidative stress in the disease.
Mitochondrial Stress Disassembles Nuclear Architecture through Proteolytic Activation of PKCδ and Lamin B1 Phosphorylation in Neuronal Cells: Implications for Pathogenesis of Age-related Neurodegenerative Diseases.
bioRxiv
November 2024
Article Synopsis
- - Mitochondrial dysfunction and oxidative stress are significant factors in age-related neurodegenerative diseases, and PKCδ isoform in dopaminergic neurons is critical for cell death during these stress events through caspase-3 activation.
- - The study revealed that upon mitochondrial dysfunction, PKCδ gets activated and moves to the nucleus, where it interacts with Lamin B1, causing nuclear damage and contributing to neuronal cell death.
- - Experiments showed that blocking PKCδ activation or modifying Lamin B1 can prevent nuclear damage, confirming PKCδ's role as a major player in neurodegenerative processes linked to mitochondrial stress.