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After 13 months, the rats begin to show signs of dementia including reduced cognitive ability and memory impairment (McGill University, 2010).
Amyloid B. immunotherapy
Past research
Past research on the effects of active or passive a? immunization on a? buildup and AD progression provided evidence that such immunization "protects against the progressive loss of synaptophysin in the hippocampal molecular layer and frontal neocortex of a transgenic mouse model of AD" (Buttini & al, 2005). This provided further support for the amyloid hypothesis.
Current research
Since the discovery of a? immunotherapy effectiveness in the treatment of AD in mice, the AN1792 a? vaccine was developed and tested on humans (Lemere & Masliah, 2010). Unfortunately, clinical trials were discontinued when around 6% of the subjects developed meningoencephalitis (Lemere & Masliah, 2010). However, since some subjects showed improvements in a? plaque clearance, several new a? immunotherapies have been developed and are currently undergoing clinical trials (Lemere & Masliah, 2010). Based on preliminary results from these clinical trials, scientists predict that a? immunotherapy will be most effective in "preventing or slowing the progression of AD when patients are immunized before or in the very earliest stages" of the onset of AD (Lemere & Masliah, 2010). Therefore, current research is also focused on identifying biomarkers to predict the "presymptomatic" stages of AD (Lemere & Masliah, 2010).
Conclusion
Research on AD has made tremendous progress in the past decade, strengthening the amyloid hypothesis and providing evidence to support the development of a? immunotherapies. Further studies taking advantage of the a? rat model may provide more clues to direct the development of effective a? immunotherapies. In addition, anti-inflammatory medications and therapies should be considered for patients with AD, since numerous studies show a link between inflammation reduction and improvement in AD symptomatology.
The future also shows exciting promise for novel approaches to AD treatment. One new causal theory...
This hypothesis suggests that AD results not from the a? cascade, but from three key contributing events: "an initiating injury, a chronic neuroinflammatory response, and a discontinuous cellular change of state involving most, if not all, of the cell types of the brain" (Herrup, 2010). Herrup doesn't dispute the role of the amyloid cascade; rather, he modifies its action as an amyloid deposition cycle (Herrup, 2010). This hypothesis, if proven to have merit, suggests changes to areas of research, diagnostic criteria, and treatment approaches for AD, taking into account the "three obligatory steps" leading to the onset of the disease (Herrup, 2010).
References
Basi, G., & al, e. (2010). Amyloid precursor protein selective gamma-secretase inhibitors for treatment of Alzheimer's disease. Alzheimer's Research & Therapy, 2 (36).
Buttini, M., & al, e. (2005). Amyloid Immunotherapy Prevents Synaptic Degeneration in a Mouse Model of Alzheimer's Disease. The Journal of Neuroscience, 25 (40), 9096-9101.
Ganguly, R., & al, e. (2005). Effect of Moringa Oleifera in Experimental Model of Alzheimer's Disease: Role of Antioxidants. Annals of Neurosciences, 12, 33-37.
Herrup, K. (2010). Reimagining Alzheimer's Disease -- an Age-Based Hypothesis. The Journal of Neuroscienc5y7e, 30 (50), 16755-16762.
McGill University. (2010, 03-30). Alzheimer's rat created for human research. Retrieved 02-10, 2011, from ScienceDaily: http://www.sciencedaily.com? / releases/2010/03/100329133602.htm
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