Cancer and Alzheimer’s disease (AD) are two common disorders for which the final pathophysiological mechanism is not yet clearly defined. Several studies in the past have reported bidirectional inverse associations between the two disorders- how overexpressed genes in central nervous system diseases (Alzheimer’s disease, Parkinson’s disease, and schizophrenia) were underexpressed in cancer (lung, colon, and prostate), and vice versa.
Therefore, now through a study, scientists at the Spanish National Cancer Research Centre (CNIO) started analysing the basic molecular footing of these processes in hopes that it would lead them to valuable information regarding the causes of each of these diseases and respective possible therapeutic strategies.
The team analyzed more than 1000 samples from patients to identify 198 genes whose function is altered significantly in three cases- Alzheimer’s, lung cancer and brain cancer . Of these, 112 had a similar pattern in Alzheimer’s disease and glioblastoma and the opposite pattern in lung cancer.
Later, by comparing the biological processes altered through the deregulation of these genes, they confirmed the role of mitochondrial dysfunction in the development of Alzheimer’s which could also lead to an increased risk of brain tumours in the patients, through the emergence of chronic inflammation in the brain
. The decrease in the energy supply and the generation of reactive oxygen species (ROS) due to alterations in the mitochondrial function would, in turn, be related to the protection against lung cancer in patients with Alzheimer’s.“A functional analysis of the sets of deregulated genes points to the immune system, up-regulated in both Alzheimer’s disease and glioblastoma, as a potential link between these two diseases. Mitochondrial metabolism is regulated oppositely in Alzheimer’s disease and lung cancer, indicating that it may be involved in the inverse co-morbidity between these diseases.” Read the paper which appeared on June 30 in the journal Scientific Reports.
“These results could help to suggest drug repurposing and drug combination strategies in the future. Initial relevant examples could include combinations of proteasome and chaperone inhibitors, anti-oxidants and oxidative phosphorylation or TCA cycle [tricarboxylic acid or Krebs cycle] inhibitors for LC [lung cancer] treatment.”
