We are analyzing https://link.springer.com/article/10.1007/bf03033906.

Title:
Glial cell dysregulation: a new perspective on Alzheimer disease | Neurotoxicity Research
Description:
Alzheimer disease (AD) is a major cause of dementia. Several mechanisms have been postulated to explain its pathogenesis, beta-amyloid (Aß toxicity, cholinergic, dysfunction, Tau hyperphosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques, among others. Glial cells are the major producers of inflammatory mediators, and cytotoxic activation of glial cells is linked to several neurodegenerative diseases; however, whether inflammation is a consequence or the cause of neurodegeneration is still unclear. I propose that inflammation and cellular stress associated with aging are key events in the development of AD through the induction of glial dysfunction. Dysregulated inflammatory response can elicit glial cell activation by compounds which are normally poorly reactive. Inflammation can also be the major cause of defective handling of Aß and the amyloid precursor protein (APP). Here I review evidence that support the proposal that dysfunctional glia and the resulting neuroinflammation can explain many features of AD. Evidence supports the notion that damage caused by inflammation is not only a primary cause of neurodegeneration but also an inducer for the accumulation of Aß in AD. Dysfunctional glia can result in im paired neuronal function in AD, as well as in many progressive neurodegenerative disorders. We show that microglial cell activation is enhanced under pro-inflammatory conditions, indicating that glial cell responses to Aß related proteins can be critically dependent on the priming of glial cells by pro-inflammatory factors.
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Keywords {🔍}

google, scholar, pubmed, cas, article, alzheimers, disease, neurosci, amyloid, microglial, glial, aging, res, cells, brain, alzheimer, expression, microglia, neuronal, neurol, inflammation, activation, protein, astrocytes, bernhardi, role, van, growth, precursor, plaque, hippocampal, βamyloid, inflammatory, neurons, human, increased, biol, transgenic, cell, response, sci, griffin, interleukin, receptor, transforming, med, cytokine, proinflammatory, acad, usa,

Topics {✒️}

c-jun-ap-1 protective pathway amyloid-β-induced chemokine production β-amyloid-induced neuronal death nonsteroidal anti-inflammatory drugs beta-amyloid-induced glial expression month download article/chapter microglia-dependent amyloid-ß toxicity transforming growth factor-β1 amyloid ß-protein neurotoxicity amyloid-β attenuates alzheimer-disease steroidal anti-inflammatory drugs transforming growth factor-betas amyloid β-protein fibrillogenesis increased β-secretase activity surface-bound ß-amyloid amyloid ß-peptide toxicity jb el khoury lesion-induced neuronal alteration region-specific neurotrophin imbalances phosphatidyl-serine-mediated recognition amyloid β-peptide generation β-amyloid neurotoxicity perspectives amyloid-β fibril formation ß-amyloid fibrils ifn-γ-mediated pathways flurbiprofen target ψ-secretase disease amyloid β-protein ay abramov large-scale microarray studies inhibiting nf-κb signaling increased intrathecal tgf-β1 ifn-γ signaling pathways alzheimer ß-amyloid peptides pro-inflammatory cytokine profiles long-term potentiation brain-derived neurotrophic factor rommy von bernhardi amyloid-ß peptide β-amyloid protein amyloid β-protein amyloid precursor protein amyloid precursor protein microglia/brain macrophagesin vitro amyloid-β peptide amyloid β-peptide full article pdf β-amyloid neurotoxicity microglial interleukin-1α expression glial cell dysregulation normal adult mouse

Questions {❓}

Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
Nguyen MD, J-P Julien and S Rivest (2002) Innate immunity: the missing link in neuroprotection and neurodegeneration?
Vitkovic L, J Bockaert and C Jacque (2000) “Inflammatory” Cytokines: neuromodulators in normal Brain?
Wyss-Coray T (2006) Inflammation in Alzheimer disease: driving force, bystander or beneficial response?
Von Bernhardi R and G Ramirez (2001) Microglia-astrocyte interaction in Alzheimer’s disease: friends or foes for the nervous system?

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      headline:Glial cell dysregulation: a new perspective on Alzheimer disease
      description:Alzheimer disease (AD) is a major cause of dementia. Several mechanisms have been postulated to explain its pathogenesis, beta-amyloid (Aß toxicity, cholinergic, dysfunction, Tau hyperphosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques, among others. Glial cells are the major producers of inflammatory mediators, and cytotoxic activation of glial cells is linked to several neurodegenerative diseases; however, whether inflammation is a consequence or the cause of neurodegeneration is still unclear. I propose that inflammation and cellular stress associated with aging are key events in the development of AD through the induction of glial dysfunction. Dysregulated inflammatory response can elicit glial cell activation by compounds which are normally poorly reactive. Inflammation can also be the major cause of defective handling of Aß and the amyloid precursor protein (APP). Here I review evidence that support the proposal that dysfunctional glia and the resulting neuroinflammation can explain many features of AD. Evidence supports the notion that damage caused by inflammation is not only a primary cause of neurodegeneration but also an inducer for the accumulation of Aß in AD. Dysfunctional glia can result in im paired neuronal function in AD, as well as in many progressive neurodegenerative disorders. We show that microglial cell activation is enhanced under pro-inflammatory conditions, indicating that glial cell responses to Aß related proteins can be critically dependent on the priming of glial cells by pro-inflammatory factors.
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