Cancer and neurodegenerative diseases represent one of the most chronic physiological ailments. Aging, characterized by the deterioration of physiological functions necessary for survival and fertility, is considered as a major risk factor for the these disorders.
Cancer has been associated with generalized hallmarks such as sustenance of proliferative signaling, evasion of growth suppressors, resistance to cell death, acquisition of replicative immortality, induction of angiogenesis, and activation of invasion and metastasis. Interestingly, current research has indicated parameters such as deregulated cellular energetics and avoidance of immune destruction, as pertinent hallmarks. These features are effectuated by genome instability, mutations and/ or tumor-promoting inflammation.
Neurodegeneration is characterized by dysfunction and loss of neurons, impairment of synaptic plasticity, proteinopathies, which include misfolded amyloid-β (Aβ) and tau in Alzheimer’s disease (AD), α-synuclein in Parkinson’s disease (PD).
There is a significant overlap between the genes upregulated in the neurodegenerative diseases and downregulated in cancer, and between the genes downregulated in the neurodegenerative diseases and upregulated in cancer.
Multiple signaling pathways that regulate cell death and survival have been well investigated in tumorigenesis, including DNA damage, cell cycle aberrations, inflammation, immunity, and oxidative stress; these pathways have now been shown to be associated with neurodegenerative diseases as well.
Significant knowledge has been generated on the shared or distinct roles of overlapping molecules that have been significantly correlated with the pathophysiology of both cancer and neurodegenerative diseases, such as p53, cyclin D, cyclin E, cyclin F, and protein phosphatase 2A (PP2A).
Studying these signaling pathways and hyperinflammation, it is a natural progression for Innox to focus on drug development targeting cancer and neurodegenerative diseases. Specifically, our emphasis is on halting, preventing or slowing down the pro-inflammatory cycle to stop the disease progression.