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Neuroinflammation as a potential therapeutic target in dementia with Lewy bodies
  1. Hiroshige Fujishiro
  1. Correspondence to Dr Hiroshige Fujishiro, Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan; fujishiro17{at}hotmail.co.jp

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The more reliably identifiable prodromal phase of dementia with Lewy bodies than Alzheimer’s disease provides a critical opportunity for intervention

There is a great deal of evidence suggesting a fundamental role of central and peripheral inflammation in the pathogenesis of Alzheimer’s disease (AD).1 Neuropathological and neuroradiological studies have indicated that activated microglia and inflammation-related mediators is observed in the cerebral neocortex of patients with early AD before extensive tau-related neurofibrillary pathology develops. Numerous epidemiological studies have revealed that treatment with non-steroidal anti-inflammatory drugs decreases the risk for developing AD. However, several prospective clinical trials showed no benefit from anti-inflammatory drugs in patients with symptomatic AD. These results imply that therapies should be initiated during earlier stages of AD pathology. Although it has been established …

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Footnotes

  • Contributors The author is the sole contributing writer of this manuscript.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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