What we do

The laboratory is divided into several sections according to the cell -communication system examined and the potential translational approach

  1. The role of gap junctional communication in the pathogenesis of several kinds of dementia (NeuroHIV, ALS, MS, Alzheimer’s and Parkinson’s disease). Our Laboratory is a pioneer on the examination of gap junctional communication in dementias and HIV. We recently described that several diseases, including neuroHIV, “highjack” this communication system to spread toxicity to neighboring cells. Our data demonstrate that bystander cell toxicity is essential to trigger and spread cognitive disease.  Normally, gap junctional communication is shut down in pathological conditions. However, dementias are different. Thus, our main goal is to block this exacerbated cell to cell communication or reduce the formation of the toxic molecules transmitted by gap junction channels into healthy cells to reduce the devastating consequences of dementia like diseases in the population.
  2.  The role of pannexin-1 channels, purinergic receptors, and ATP as the main target to prevent HIV infection, and associated diseases. Our unique studies identify that pannexin-1 channels are essential for HIV entry, spread, and viral reactivation.  In healthy conditions, pannexin-1 channels are mostly in a closed stage. Thus, pannexin-1 channels could be a perfect therapeutic target becasue is not active in the healthy population. However, upon HIV infection or reactivation the channel become open and active. We identified that this channel can be used as an alternative target to reduce HIV infection and its consequences. We are currently testing several compounds to block this channel to alleviate the devastating consequences of HIV infection. We expect to produce an additional treatment for antiretroviral treatment to avoid most of the aging complications observed in the HIV infected population.
  3. ATP as a biomarker of cognitive disease. Our data using samples from different kinds of dementia indicates that several metabolic pathways are altered in the brain of individuals with progressive brain function decline. We identified that ATP, that is a highly unstable molecule, is not degraded and could use a biomarker of cognitive disease. This discovery is unique and we expect to generate a standardized test to predict the onset of dementia to inform the physicians about potential protective treatments to avoid brain dysfunction and compromise.
  4. The role of gap junctional and tunneling nanotube communication in the pathogenesis of HIV and glioblastoma. This is a new area in the laboratory and was a result of the previous 3 points.  Glioblastomas (GB) are the most aggressive, heterogeneous, poor prognosis and treatment-resistant form of primary brain cancer. GB is a fatal type of cancer with a median survival of only 5-years, despite advances in treatments and molecular diagnoses. Furthermore, the HIV-infected population exhibits an alarming rate and aggressiveness of GB as compared to uninfected individuals. Currently, the suggested treatment is surgical resection, if accessible, with subsequent radiation and temozolomide (TMZ) regiment, which results in an incremental increase in 5% survival. Here, we propose that gap junctional and tunneling nanotubes (TNTs) communication contribute to tumor resistance by enabling DNA repair enzymes to diffuse into areas with low expression of these DNA repair enzymes resulting resistance to treatment.