ALZHEIMER'S RESEARCH LAB
Director
Sam Scott
Room
Grover Center W262
Note from the director
Not My research agenda at Ohio University focuses on particular brain changes that occur in Alzheimer's disease (AD), and how they might relate to the pattern of cognitive and functional deterioration seen within this disorder. As a neuroanatomist by training, my work addresses particular elements of the neuropathology of AD, a diagnosis presently achieved only via postmortem examination. Therefore the procedures implemented in my laboratory center around use of the microscope, stains that selectively identify particular elements in AD brain tissue, and quantitative assessment of how these changes could
underlie age-related cognitive dysfunction.
It has been known for many years that senile plaques and eurofibrillary tangles are the two major pathological hallmarks of AD. To this day, leading experts in AD neuropathology disagree regarding how these develop and indeed, whether they play a direct role in the loss of neurons and the synapses between them (both regarded as the direct substrate of senile dementia). However, it is generally accepted that once the clinical picture of AD develops within a loved one, little can be done to reverse the physical deterioration sustained within the brain. Therefore, a majority of current research focuses on means of preventing the development of AD rather than "curing" it per se.
The cascade of specific aims in my laboratory are generally predicated upon the assumption that senile plaques and neurofibrillary tangles are, by themselves, relatively benign structures. Instead, an inflammatory response within the brain to these same structures, which can take many years to develop, is one of several theories attempting to explain how plaques and tangles could relate to dementia. In particular, my agenda focuses on a certain cell type within the brain (microglia) and how the reaction of this cell to the buildup of plaques and tangles, theoretically by way of local neurotoxin release, may lead to frank dementia. The approach utilized in my laboratory for ascertaining such an hypothesis is to examine the microscopic relationship between plaque-associated microglia and local nerve cell loss, using thin sections of brain tissue from the brains of AD patients as well as those of similar age who died from some other cause.