There is growing evidence that immune mechanisms are important in the pathogenesis of a number of neurodegenerative disorders, such as Alzheimer disease (AD), and that this may have therapeutic implications. In a recent study, Shepherd et al1 evaluated the role of inflammation in dementia with Lewy bodies (DLB) by counting activated microglial cells in postmortem tissue. While the number of microglial cells was increased in AD, they found no significant increase in DLB compared with nondemented controls and concluded that "anti-inflammatory strategies are not likely to be effective for pure DLB." This result contrasts with my findings; I found a significant degree of microglial activation in patients with DLB, even in the absence of any AD pathology (so-called "pure" DLB).2 Although the design of these 2 studies was very similar, 2 important differences may explain the discrepant results.
Mackenzie IRA. Cortical Inflammation in Dementia With Lewy Bodies. Arch Neurol. 2001;58(3):519–520. doi:
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