Biography & Research:
Our pioneering studies of the role of early neuron-glial interactions with elevated synthesis and release of proinflammatory cytokines, in particular IL-1, together with other studies from our lab and from many others, were key to a new understanding of neuropathogenesis of AD. For example, we showed that neuronal stress-induced glial activation with elevated synthesis and release of IL-1 gives rise to the synthesis of the each of the protein precursors of Aβ plaques (βAPP) and of tangles (hyperphosphorylated tau) in AD, and of Lewy bodies (α-synuclein) in PD. These findings, together with evidence of roles for neuroinflammatory-induced cellular and molecular events, including decreased synthesis of synaptophysin – a marker of synaptic distress; failures of proteostasis; and neuronal insulin resistance formed the basis for acceptance of neuroinflammation as a key element in the neuropathogenesis of AD and other conditions and diseases that are characterized by gliosis and elevated cytokine expression. In 2004 Dr. Robert E. Mrak and I established the Journal of Neuroinflammation as Editors-in-Chief.