Abstract
Aside from the well-known amyloid beta and tau pathologies found in Alzheimer’s disease (AD), neuroinflammation is a well-established aspect described in humans and animal models of the disease. Inflammatory perturbations are evident not only in neurons, but also in non-neuronal cells and cytokines in the AD brain. Although the amyloid hypothesis implicates amyloid beta (Aβ) as the prime initiator of the AD, brain inflammation in AD has a complex relationship between Aβ and tau. Using our work with the 5-lipoxygenase protein as an example, we suggest that at least in the case of AD, there is an interdependent and not necessarily hierarchical pathological relationship between Aβ, tau and inflammation.
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Joshi, Y.B., Praticò, D. Neuroinflammation and Alzheimer’s disease: lessons learned from 5-lipoxygenase. Translat.Neurosci. 5, 197–202 (2014). https://doi.org/10.2478/s13380-014-0225-7
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DOI: https://doi.org/10.2478/s13380-014-0225-7