ViewpointIs amyloidogenesis during Alzheimer's disease due to an IL-1-/IL-6-mediated ‘acute phase response’ in the brain?☆
References (44)
- et al.
Cell
(1988) - et al.
Neurobiol. Aging
(1990) - et al.
Neuron
(1990) - et al.
Brain Res. Rev
(1987) - et al.
Neurosci. Lett
(1990) - et al.
- et al.
Science
(1984) - et al.
Nature
(1990) - et al.
Nature
(1991) - et al.
Nature
(1987)
Science
Nature
Nature
Nature
Nature
Nature
Science
Science
Science
Bio/Technology
Biochem J
Cited by (257)
Precision Nutrition in Aging and Brain Health
2023, Precision Nutrition: the Science and Promise of Personalized Nutrition and HealthAstrocyte subtype-specific approach to Alzheimer's disease treatment
2021, Neurochemistry InternationalCitation Excerpt :Contrarily, IL-6 like cytokines may have detrimental effects on neurogenesis during development (John et al., 2005). While some data suggest that IL-6 inhibits the expression of proinflammatory cytokines like IL-1β and TNFα (John et al., 2005), others show that it may induce APP synthesis (Vandenabeele and Fiers, 1991). In AD, it may trigger ERK1/ERK2 and STAT3 (Schumann et al., 1999) as well as induce the expression of acute phase proteins including α2-macroglobulin and metallothionine in neurons (Ganter et al., 1991; Bauer et al., 1993; Akiyama et al., 2000).
Eicosapentaenoic acid-enriched phospholipids improve Aβ1-40-induced cognitive deficiency in a rat model of Alzheimer's disease
2016, Journal of Functional FoodsCitation Excerpt :Accordingly, IL1β and TNFα are detected in AD brains (Dickson, Lee, Mattiace, Yen, & Brosnan, 1993; Goldgaber et al., 1989). These cytokines might be involved in the pathogenesis of AD, for example, by promoting local inflammatory responses (Vandenabeele & Fiers, 1991). An increasing body of research suggests that CNS inflammation, mediated by glial activation and the production of inflammatory mediators such as cytokines and complement proteins, plays a role in the pathophysiology of AD (Benveniste, Tang, & Law, 1995).
Emerging roles of the γ-secretase-notch axis in inflammation
2015, Pharmacology and TherapeuticsCitation Excerpt :Indeed, evidence suggests a central role of inflammation in the development of AD. For example, levels of pro-inflammatory cytokines such as TNF, IL-1, IL-6, and IL-18 are increased in various regions of the AD brain (Bauer et al., 1991; Cacabelos et al., 1994; Ojala et al., 2009; Vandenabeele & Fiers, 1991). Furthermore, the expression of monocyte chemoattractant protein-1 (MCP-1), IL-6, and IL-8 has been found to be higher in the brain of the PS1 mutant AD patients (Sokolova et al., 2009), indicating a link between PS1/γ-secretase and inflammation in AD.
Is there an association between peripheral immune markers and structural/functional neuroimaging findings?
2014, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :For example, elevated levels of interleukin-1β (IL-1β) are observed in patients with mild cognitive impairment (MCI), specifically in those with impairment in multiple cognitive domains (Forlenza et al., 2009). Also, interleukin-6 (IL-6) is strongly associated with AD senile plaques (Strauss et al., 1992) and there is evidence suggesting that amyloid plaque formation in AD might be mediated by interleukin-1 (IL-1)/IL-6 acute phase reaction (Vandenabeele and Fiers, 1991). More specifically, in AD, expression of IL-6 is increased in the parietal cortex and decreased in the temporal cortex, occipital cortex and cerebellum compared to age matched controls.
Multiplex analysis of intrathecal cytokines in patients with mild cognitive impairment
2011, Revista del Laboratorio Clinico
- ☆
Research in the authors' laboratory was supported by the Belgian FGWO, IUAP, ASLK and the National Lottery.
- ∗
We thank E. Van Mechelen for fruitful discussion and M. Vandecasteele for editorial assistance.