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Inflammasome Therapeutics - Alzheimer's Disease

Alzheimer's Disease

Inflammasomes & Alzheimer's Disease

Alzheimer's Disease is the most common form of dementia, affecting 5.7M people in the US and 1 in 10 people over 70 years of age. There are no satisfactory treatments for the disease.

It has long been recognized that in AD, amyloid-β and tangles of tau protein accumulate in the brain, triggering inflammation and nerve cell death, which then triggers further inflammation and amyloid-β accumulation.

Biochemically, AD is a multifactorial disease. Amyloid-β and tau protein tangles have long been therapeutic targets in the AD as they are present in the brains of patients with AD. Also present in brains of patients with the disease are elevated levels of Alu-RNA, complement, iron, and reactive oxygen species. These different factors all induce inflammasome activation, which triggers production of caspase-1 and the inflammatory cytokines, IL-1β and IL-18. In AD, inappropriate inflammasome activation causes nerve cell death.

In animal studies it has been found that inhibition of caspase-1 and inflammasome activation alleviates cognitive impairment and neuropathy in an Alzheimer’s disease mouse model.