Molecular Basis of Alzheimer’s Disease
At Reddy Laboratory, we investigate the role of abnormal mitochondrial dynamics and therapeutic approaches in neurodegenerative diseases such as Alzheimer’s (AD) and Huntington’s Disease (HD). Our research utilizes cutting-edge live-cell imaging to study axonal transport of mitochondria and synaptic degeneration in primary neurons.
A key strength of our lab is the development of transgenic and knockout mouse models for aging and neurodegenerative diseases, including AD, HD, and Parkinson’s Disease (PD). Recent work has focused on microRNA-455-3p (miR-455-3p) and RLIP76, a stress-responsive protein that regulates oxidative stress and mitochondrial function. Our findings indicate that Rlip interacts with AD-related proteins, suggesting it as a promising therapeutic target.
Additionally, we have established that VDAC1, a mitochondrial protein, interacts with amyloid beta and phosphorylated tau, contributing to AD pathology. Our experiments show that partial reduction of VDAC1 can alleviate cognitive deficits in transgenic mouse models. Through ongoing research, we aim to identify innovative biomarkers such as miR-455-3p and therapeutic strategies to mitigate AD progression, enhance cognitive function, and improve the quality of life for those impacted by neurodegeneration.
Relevant Publications
Reduced VDAC1, Maintained Mitochondrial Dynamics and Enhanced Mitochondrial Biogenesis in a Transgenic Tau Mouse Model of Alzheimer's Disease.
Vijayan M, Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/35955694/
A partial reduction of VDAC1 enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model.
Vijayan M, Alvir RV, Alvir RV, Bunquin LE, Pradeepkiran JA, Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/35801276/
Reduced VDAC1 protects against Alzheimer's disease, mitochondria, and synaptic deficiencies.
Manczak M, Sheiko T, Craigen WJ, Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/23948905/
Is the mitochondrial outer membrane protein VDAC1 therapeutic target for Alzheimer's disease?
Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/22995655/
Rlip76 in ageing and Alzheimer's disease: Focus on oxidative stress and mitochondrial mechanisms.
Bandaru M, Sultana OF, Islam MA, Rainier A, Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/39617058/
The role of RLIP76 in oxidative stress and mitochondrial dysfunction: Evidence based on autopsy brains from Alzheimer's disease patients.
Bose C, Kshirsagar S, Vijayan M, Kumar S, Singh SP, Hindle A, Reddy PH.
https://pubmed.ncbi.nlm.nih.gov/37926360/
Abnormal interaction of Rlip with mutant APP/Abeta and phosphorylated tau reduces wild-type Rlip levels and disrupts Rlip function in Alzheimer's disease.
Baig J, Sawant N, Rawat P, Reddy AP, Reddy PH, Kshirsagar S.
https://pubmed.ncbi.nlm.nih.gov/37633469/
Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer's Disease?
Hindle A, Singh SP, Pradeepkiran JA, Bose C, Vijayan M, Kshirsagar S, Sawant NA, Reddy PH.
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