Unusual Occurrence of Peripheral Ossifying Fibroma in an Elderly Male

The present case is a scenario of occurrence of relatively common peripheral ossifying fibroma in an uncommon site of occurrence. It was noted in the maxillary posterior region incontrast to its usual occurrence in anterior maxillary region. The lesion was observed in elderly male subject aged 64 years, contradictory to its usual predilection for young females in thesecond or third decade of life. As this case contradicts the common norms of predilection of the lesion with regard to age, gender and site, it emphasizes the need for looking beyond theconventional norms for proper diagnosis and prompt treatment.&nbsp

What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research

Experimental models that faithfully mimic the developmental pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated