Abstract:
Oxidative stress plays an important role in the neuropathology of many progressive
neurodegenerative disorders such as Alzheimer’s Disease and Parkinson’s Disease.
An excess of aggregated beta amyloid is one of the major markers of Alzheimer’s
Disease, and this causes an increase in the oxidative stress. Moreover, in a positive
feedback loop, oxidative stress seems to increase the production of beta amyloid as
well. Thus, it would be very interesting to be able to study the real-time changes in
the redox state of the cell in response to oxidative stress, first in cell lines, and
eventually in primary neurons to get a better understanding of the disease. To this
end, we performed live-cell imaging experiments on human embryonic kidney cells,
and observed an interesting phenomenon upon addition of an external oxidativestress causing agent (tert-Butyl Hydroperoxide), wherein the oxidative state of the
cell seems to come back to normal after an hour or two. This is potentially due to
some antioxidant mechanisms present in the cells. This rebound phenomenon was
however not observed in Neuroblastoma cells. It remains to be seen how primary
neurons will react to oxidative stress, and whether wild type neurons will show a
different oxidative state as compared to neurons transgenic for Alzheimer’s
mutations which might have an intrinsically higher level of oxidative stress due to the
presence of excess beta amyloid.
