ABSTRACT
The pharmacological interventions for Alzheimer disease should be based in its pathogenic mechanisms such as amyloidogenesis, tau hyperphosphorilation, disturbances in neurotransmission and changes in neuronal trophism. Other therapies derive from epidemiological observations, such as antioxidants and anti-inflammatory drugs, estrogens, statins and anti hypertensive drugs. Some life style interventions, such as changes in diet, exercise and brain stimulation could also be beneficial for the prevention of Alzheimer disease. Ongoing research on pathogenic mechanisms promises the discovery of more effective therapies. Healthy life style should always be recommended due to its benefit and lack of untoward effects.
Subject(s)
Animals , Humans , Alzheimer Disease/therapy , Life Style , Amyloid beta-Peptides/metabolism , Amyloidosis/drug therapy , Amyloidosis/prevention & control , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antihypertensive Agents/therapeutic use , Diet , Disease Models, Animal , Exercise , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic useABSTRACT
This study comprised 80 Syrian Gold hamsters, 70 of them were infected with Schistosoma mansoni and 10 uninfected hamsters served as negative controls. Of the schistosome infected hamsters, 10 served as positive controls [infected but untreated] and the rest [60 hamsters] received treatment for 9-week duration. In 30 hamsters treatment was given early [9 weeks after infection], before the appearance of hepatic amyloidosis, and in the other 30 hamsters treatment was given late [15 weeks after infection] after the appearance of hepatic amyloidosis. Each treatment group was subdivided into three subgroups [ten hamsters each], in which treatment was either colchicine alone, combined colchicine and praziquantel, or praziquantel alone. All hamsters were sacrificed nine weeks after treatment, liver biopsies were taken and evaluated semiquantitatively for amyloid deposits. In the group with combined therapy there is significant reduction in hepatic amyloid deposits, together with reduction of proteinuria serum bilirubin, SGPT with an increase of total serum protein and serum albumin. This improvement was nearly complete with early treatment and only partial when treatment was given late. When colchicine was given alone, a partial, but insignificant reduction of hepatic amyloid deposits was documented. It was concluded that, colchicine is effective for the prevention and reduction of schistosome induced hepatic amyloidosis in Syrian Gold hamsters