Distribution of interleukin‐1‐immunoreactive microglia in cerebral cortical layers: implications for neuritic plaque formation in Alzheimer’s disease

Sheng, Jin; Griffin, W. Sue T.; Royston, M.C.; Mrak, Robert E.

doi:10.1046/j.1365-2990.1998.00122.x

Cited by 101 publications

(52 citation statements)

References 15 publications

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“…Moreover, brains from Alzheimer's patients contain more IL-1-positive microglia cells than control brains [429]. These observations support the concept of a cytokine cycle in which neuronal injury stimulates microglia to release IL, which triggers astrocytes to become reactive and to release cytokines and other neurotrophic factors and neurons to process more β-amyloid precursor protein, favoring additional deposition of β-amyloid, and so on [430][431][432].…”

Section: Alzheimer's Diseasesupporting

confidence: 66%

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Hertz¹,

Chen²,

Gibbs³

et al. 2004

CDTCNSND

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Considerable attention has recently been paid to astrocyte functions, which are briefly summarized. A large amount of data is available about adrenoceptor expression and function in astrocytes, some of it dating back to the 1970's and some of it very recent. This material is reviewed in the present paper. The brain is innervated by noradrenergic fibers extending from locus coeruleus in the brain stem, which in turn is connected to a network of adrenergic and noradrenergic nuclei in the medulla and pons, contributing to the control of (nor)adrenergic, serotonergic, dopaminergic and cholinergic function, both in the central nervous system (CNS) and in the periphery. In the CNS astrocytes constitute a major target for noradrenergic innervation, which regulates morphological plasticity, energy metabolism, membrane transport, gap junction permeability and immunological responses in these cells. Noradrenergic effects on astrocytes are essential during consolidation of episodal, long-term memory, which is reinforced by β-adrenergic activation. Glycogenolysis and synthesis of glutamate and glutamine from glucose, both of which are metabolic processes restricted to astrocytes, occurs at several time-specific stages during the consolidation. Astrocytic abnormalities are almost certainly important in the pathogenesis of multiple sclerosis and in all probability contribute essentially to inflammation and malfunction in Alzheimer's disease and to mood disturbances in affective disorders. Noradrenergic function in astrocytes is severely disturbed by chronic exposure to cocaine, which also changes astrocyte morphology. Development of drugs modifying noradrenergic receptor activity and/or down-stream signaling is advocated for treatment of several neurological/psychiatric disorders and for neuroprotection. Astrocytic preparations are suggested for study of mechanism(s) of action of antidepressant drugs and pathophysiology of mood disorders.

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Section: Alzheimer's Diseasesupporting

confidence: 66%

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Hertz¹,

Chen²,

Gibbs³

et al. 2004

CDTCNSND

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“…Degeneration of these neurons could then result in increased secretion of APP and formation of Aβ deposits within these layers [4]. Second, interleukin-immunoreactive microglia (IL-Mg) have a similar laminar distribution as APP-immunoreactive NP [46]. Hence, the laminar distribution of microglia could be a factor determining the distribution of the Aβ deposits.…”

Section: Discussionmentioning

confidence: 99%

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

Armstrong¹

2015

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A b s t r a c t To determine whether genetic factors influence frontal lobe degeneration in Alzheimer's disease (AD), the laminar distributions of diffuse, primitive, and classic β-amyloid (Aβ) peptide deposits were compared in early-onset familial AD (EO-FAD) linked to mutations of the amyloid precursor protein (APP) or presenilin 1 (PSEN1) gene, late-onset familial AD (LO-FAD), and sporadic AD (SAD). The influence of apolipoprotein E (Apo E) genotype on laminar distribution was also studied. In the majority of FAD and SAD cases, maximum density of the diffuse and primitive Aβ deposits occurred in the upper cortical layers, whereas the distribution of the classic Aβ deposits was more variable, either occurring in the lower layers, or a double-peaked (bimodal) distribution was present, density peaks occurring in upper and lower layers. The cortical layer at which maximum density of Aβ deposits occurred and maximum density were similar in EO-FAD, LO-FAD and SAD. In addition, there were no significant differences in distributions in cases expressing

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“…IL-1b is increased in AD but mostly associated with microglial activation suggesting a role for Csp-1 in inflammation. 20,[23][24][25] On the other hand, significant evidence from studies using Csp-1 inhibitors, a Csp-1 DN construct and Csp-1 null cells indicates that Csp-1 can be involved in cell death. [26][27][28][29] The increase of Csp-1 in AD raises the possibility that Csp-1 also activates Csp-6 in vivo.…”

Section: Discussionmentioning

confidence: 99%

Caspase-1 activation of caspase-6 in human apoptotic neurons

et al. 2005

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Active caspase-6 (Csp-6) induces cell death in primary cultures of human neurons and is abundant in the neuropathological lesions of Alzheimer's disease. However, the mode of Csp-6 activation is not known. Here, we show that the Csp-1 inhibitor, Z-YVAD-fmk specifically prevents activation of Csp-6 and cell death in human neurons. A transient increase in Csp-1-like activity and an increase in the p23Csp-1 subunit occur early after serum deprivation. Recombinant active Csp-1 (R-Csp-1) cleaves recombinant and neuronal pro-Csp-6 in vitro resulting in Csp-6 activity. However, R-Csp-1 does not induce cell death when microinjected in human neurons despite the inhibition of serum-deprivation induced cell death with a Csp-1 dominant negative construct. These results show that Csp-1 is an upstream positive regulator of Csp-6-mediated cell death in primary human neurons. Furthermore, these results suggest that the activation of Csp-1 must be accompanied by an apoptotic insult to induce Csp-6-mediated cell death.

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Distribution of interleukin‐1‐immunoreactive microglia in cerebral cortical layers: implications for neuritic plaque formation in Alzheimer’s disease

Cited by 101 publications

References 15 publications

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Astrocytic Adrenoceptors: A Major Drug Target in Neurological and Psychiatric Disorders?

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

Caspase-1 activation of caspase-6 in human apoptotic neurons

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