Characterization of inflammatory biomarkers and candidates for diagnosis of Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia, several genetic, non-genetic, and environmental factors could be involved in disease progression. Association was suggested between inflammation and AD progression. Since neuroinflammation can be involved in neurodegeneration, studies suggested that several inflammatory molecules (cytokines) might enhance the inflammation or suppress the immune system. Altered cytokine levels might reflect the neuropathological changes in patients. This review summarizes the validated and potential inflammatory biomarkers in AD, and it is focusing on interleukins (ILs), interferons (IFNs) and tumor necrosis factors (TNFs). Interleukins have dual role in the AD progression: Several ILs (such as IL1, IL6 or IL8) can promote the disease-associated inflammatory pathways, while the others (such as IL1ra, IL4 or IL10) might be involved in the neuroprotection and dementia prevention. Conflicting reports are available on the role of IFNs (IFNα, IFNβ and IFNγ) in AD progression. Several studies reported that they might have neuroprotective effects, but the others suggested that they can contribute to neurotoxiciy by inducing the pro-inflammatory cytokines. TNFα can be expressed with other pro-inflammatory cytokines and induce the neurodegeneration. Both TNFα and TNFR were suggested as successful markers for AD and dementia. Several cytokines can be used to distinguish the AD patients from the healthy individuals, since their expression might be up-or down-regulated in the brain of AD patients. Some cytokines might be useful to measure the severity of the disorder. Overproduction of pro-inflammatory molecules could result neuroinflammation and enhance the neurotoxicity. Inhibiting the pro-inflammatory- and/ or inducing the anti-inflammatory molecules might improve the therapies for AD.