Mrutyunjaya Panda

Dottorato in Infiammazione, Immunità e Cancro - 39° ciclo (1 ottobre 2023 - 30 settembre 2026)

Programma di ricerca dottorato

Alzheimer’s Disease (AD) is the most common cause of dementia and is characterized by a progressive loss of cognitive function. The common AD phenotype includes aggregation of beta-amyloid (Aβ) peptides, which form extracellular amyloid plaques, and hyperphosphorylated tau (pTau) protein, which forms intracellular neurofibrillary tangles in the brain. Mitochondrial dysfunction and defects in autophagy are major causes and effects of AD pathophysiology. Recent research has shown a possible correlation between circadian rhythm and mitophagy. Circadian clock proteins regulate the expression of genes involved in mitophagy and control the timing and efficiency of mitochondrial clearance. Disruptions in the circadian clock, as observed in AD, can impair mitophagy, leading to the accumulation of dysfunctional mitochondria and increased oxidative stress. Aberrant mitochondrial turnover contributes to neurodegenerative processes observed in AD. Understanding the circadian regulation of mitochondria-specific autophagy provides valuable insights into the mechanisms underlying neuronal degeneration and offers new avenues for therapeutic intervention. Targeting the circadian factors involved in mitophagy modulation may help restore mitochondrial homeostasis, mitigate neurodegeneration, and potentially slow the progression of AD. However, further research is required to unravel the intricate molecular mechanisms governing the circadian control of mitophagy in AD and to develop targeted strategies that exploit this pathway for therapeutic benefit. The aim of this project is to elucidate the role of circadian rhythm dysfunction in modulating mitophagy and metabolic dysfunction in AD. 

Referente dottorato

Prof. Nektarios Tavernarakis

Tutori dottorato

Prof. Nektarios Tavernarakis (IMBB, FORTH), Prof. Gaberiela Constantin (UNIVR)