Though the longstanding treatment focus for patients with Alzheimer’s disease (AD) has been on amyloid-beta and tau protein accumulation in the brain, recent evidence continues to spotlight neuroinflammation as a key contributor to AD progression. The presence of toxic amyloid-beta species along with excess and chronic systemic inflammatory responses fuels a cycle of amyloid-beta plaque and tau tangle accumulation along with activation of microglia in the brain. Multidirectional relationships among these and other processes chronically promotes the damage and neurodegeneration that are characteristic of AD. Clinicians and multidisciplinary care teams must be appraised on the rapidly maturing science of neuroinflammation as a disease-modifying target for AD to understand emerging treatments of value.

In the second activity of this three-part CME Outfitters Snack series, expert faculty will guide learners through evaluating the role of neuroinflammation in the pathology and progression from mild cognitive impairment (MCI) to AD and dementia.

Learn more at: [ Ссылка ]

свернуть