For instance, using immuno-histochemical, sandwich ELISA, and dot blot analyses, several groups determined that AD brains express significantly increased levels of Hsp27 in the frontal, parietal, and temporal cortices, but not in occipital cortex when compared to age-matched non-demented controls; specifically, Hsp27 co-localized with areas affected by senile plaques and cerebral amyloid angiopathy [53, 93, 107, 109]. The gene discussed is HSPB1; the disease is Alzheimer disease.