Hypersensitive cytokine response to beta-amyloid 25-35 in astroglial cells from IL-1 receptor type I-deficient mice.

Eriksson, Gun; Zetterström, Maria; Toro, Veronica Cortés; Bartfai, Tamás; Iverfeldt, Kerstin

doi:10.3892/ijmm.1.1.201

Cited by 5 publications

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“…1989). In addition, in vitro experiments have shown that treatment of cultured rat cortical astrocytes with β‐amyloid peptides induce up‐regulation of IL‐1β (Eriksson et al . 1998; Hu et al .…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, it has been found that IL-1 levels are higher in the brain of Alzheimer patients than in controls (Griffin et al 1989). In addition, in vitro experiments have shown that treatment of cultured rat cortical astrocytes with b-amyloid peptides induce up-regulation of IL-1b (Eriksson et al 1998;Hu et al 1998) and that IL-1b is involved in glia proliferation (Ait-Ikhlef et al 1999;Parish et al 2002). On the other hand, recent studies have shown that endozepines can modulate the immune response (Cosentino et al 2000;Marino et al 2003), suggesting that Ab-induced stimulation of endozepine secretion may participate to the propagation of the inflammatory process and thus to the progression of Alzheimer's disease.…”

Section: Discussionmentioning

confidence: 99%

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Beta‐amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Tokay

Masmoudi

Gandolfo

et al. 2005

Journal of Neurochemistry

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Accumulation of b-amyloid peptide (Ab), which is a landmark of Alzheimer's disease, may alter astrocyte functions before any visible symptoms of the disease occur. Here, we examined the effects of Ab on biosynthesis and release of diazepam-binding inhibitor (DBI) There is now clear evidence that, in the brain, the DBI gene is primarily expressed in glial cells (Tong et al. 1991;Lihrmann et al. 1994;Alho et al. 1995;Bürgi et al. 1999) and the presence of DBI-related peptides has been visualized by immunohistochemistry in astroglial cells in various regions of the central nervous system, notably in the cerebral cortex (Tonon et al. 1990), in ependymocytes lining the third ventricle (Tonon et al. 1990;Malagon et al. 1993;Do-Rego et al. 2001), in tanycytes in the median eminence (Tonon et al. 1990;Malagon et al. 1993) and in Bergmann cells in the cerebellum (Tonon et al. 1990;Vidnyanszky et al. 1994;Yanase et al. 2002). In vitro studies have shown that cultured rat astrocytes contain and release substantial amounts of endozepines (Lamacz et al. 1996;Patte et al. 1999;Masmoudi et al. 2003Masmoudi et al. , 2005 and that endozepines act as autocrine factors modulating intracellular calcium concentration in astroglial cells (Gandolfo et al. 1997(Gandolfo et al. , 2001Leprince et al. 1998Leprince et al. , 2001).Alzheimer's disease is a neurogenerative disorder characterized by the presence of senile plaques in the brain

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Beta‐amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Tokay

Masmoudi

Gandolfo

et al. 2005

Journal of Neurochemistry

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“…Aβ 25–35 , a neurotoxic fragment of the Alzheimer β‐amyloid peptide, acts as a strong inducer of proinflammatory cytokines, such as IL‐1 and IL‐6, in astroglial cells (Eriksson et al, 1998; Toro et al, 2001). The mechanisms involved in the activation of astrocytes by Aβ remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…Typical hallmarks of AD are the progressive extracellular deposit of β‐amyloid peptide (Aβ), the major constituent of senile plaques (Kang et al, 1987), and the appearance of reactive astrocytes in the area surrounding the amyloid‐containing plaques (Arelin et al, 2002; Nagele et al, 2004). It is now clearly established that, in astrocytes, Aβ activates the synthesis and secretion of various proinflammatory mediators, including interleukin‐1 (IL‐1) and IL‐6 (Eriksson et al, 1998; Toro et al, 2001). We have recently shown that Aβ stimulates both the expression of the DBI gene and the release of endozepines from cultured rat astrocytes (Tokay et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Beta‐amyloid peptide stimulates endozepine release in cultured rat astrocytes through activation of N‐formyl peptide receptors

Tokay

Hachem

Masmoudi-Kouki

et al. 2008

Glia

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Astroglial cells synthesize and release endozepines, a family of neuropeptides derived from diazepam-binding inhibitor (DBI). The authors have recently shown that beta-amyloid peptide (Abeta) stimulates DBI gene expression and endozepine release. The purpose of this study was to determine the mechanism of action of Abeta in cultured rat astrocytes. Abeta(25-35) and the N-formyl peptide receptor (FPR) agonist N-formyl-Met-Leu-Phe (fMLF) increased the secretion of endozepines in a dose-dependent manner with EC(50) value of approximately 2 microM. The stimulatory effects of Abeta(25-35) and the FPR agonists fMLF and N-formyl-Met-Met-Met (fMMM) on endozepine release were abrogated by the FPR antagonist N-t-Boc-Phe-Leu-Phe-Leu-Phe. In contrast, Abeta(25-35) increased DBI mRNA expression through a FPR-independent mechanism. Abeta(25-35) induced a transient stimulation of cAMP formation and a sustained activation of polyphosphoinositide turnover. The stimulatory effect of Abeta(25-35) on endozepine release was blocked by the adenylyl cyclase inhibitor somatostatin, the protein kinase A (PKA) inhibitor H89, the phospholipase C inhibitor U73122, the protein kinase C (PKC) inhibitor chelerythrine and the ATP binding cassette transporter blocker glyburide. Taken together, these data demonstrate for the first time that Abeta(25-35) stimulates endozepine release from rat astrocytes through a FPR receptor positively coupled to PKA and PKC.

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“…Additionally, it has been demonstrated that Aβ peptide raises IL-6 generation by astrocytes either directly or indirectly through an IL-1β-dependent pathway. Therefore, it appears that IL-6 acts as a secondary mechanism, enhancing the inflammatory reaction triggered by IL-1 [ 367 , 368 , 369 , 370 ]. Proinflammatory cytokines such as IL-1 and IL-6 are prevented from being produced in vitro by IL-10 cytokines [ 371 ].…”

Section: The Role Of Immune System In Admentioning

confidence: 99%

Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer’s Disease

Afsar

Castro

Soladogun

et al. 2023

IJMS

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that leads to dementia and patient death. AD is characterized by intracellular neurofibrillary tangles, extracellular amyloid beta (Aβ) plaque deposition, and neurodegeneration. Diverse alterations have been associated with AD progression, including genetic mutations, neuroinflammation, blood–brain barrier (BBB) impairment, mitochondrial dysfunction, oxidative stress, and metal ion imbalance.Additionally, recent studies have shown an association between altered heme metabolism and AD. Unfortunately, decades of research and drug development have not produced any effective treatments for AD. Therefore, understanding the cellular and molecular mechanisms underlying AD pathology and identifying potential therapeutic targets are crucial for AD drug development. This review discusses the most common alterations associated with AD and promising therapeutic targets for AD drug discovery. Furthermore, it highlights the role of heme in AD development and summarizes mathematical models of AD, including a stochastic mathematical model of AD and mathematical models of the effect of Aβ on AD. We also summarize the potential treatment strategies that these models can offer in clinical trials.

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Hypersensitive cytokine response to beta-amyloid 25-35 in astroglial cells from IL-1 receptor type I-deficient mice.

Cited by 5 publications

References 0 publications

Beta‐amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Beta‐amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Beta‐amyloid peptide stimulates endozepine release in cultured rat astrocytes through activation of N‐formyl peptide receptors

Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer’s Disease

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