Journal
CURRENT ALZHEIMER RESEARCH
Volume 14, Issue 4, Pages 412-425Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567205013666160930110551
Keywords
Alzheimer's disease; BACE1; etanercept; inflammation; neuroinflammation; thalidomide; TNF-alpha
Categories
Funding
- NIA [P30 AG 019610, K01AG047279]
- Alzheimer's Association [NIRG-12-237512]
- Banner Sun Health Research Institute
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Alzheimer's disease (AD) affects an estimated 44 million individuals worldwide, yet no therapeutic intervention is available to stop the progression of the dementia. Neuropathological hallmarks of AD are extracellular deposits of amyloid beta (A beta) peptides assembled in plaques, intraneuronal accumulation of hyperphosphorylated tau protein forming tangles, and chronic inflammation. A pivotal molecule in inflammation is the pro-inflammatory cytokine TNF-alpha. Several lines of evidence using genetic and pharmacological manipulations indicate that TNF-alpha signaling exacerbates both A beta and tau pathologies in vivo. Interestingly, preventive and intervention anti-inflammatory strategies demonstrated a reduction in brain pathology and an amelioration of cognitive function in rodent models of AD. Phase I and IIa clinical trials suggest that TNF-alpha inhibitors might slow down cognitive decline and improve daily activities in AD patients. In the present review, we summarize the evidence pointing towards a beneficial role of anti-TNF-alpha therapies to prevent or slow the progression of AD. We also present possible physical and pharmacological interventions to modulate TNF-alpha signaling in AD subjects along with their limitations.
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