Immune actions in the nervous system: A brief review with special emphasis on Aalzheimer's disease

Rogers, Joseph; Luber-Narod, Judith

doi:10.1002/ddr.430150214

Cited by 27 publications

(5 citation statements)

References 53 publications

(35 reference statements)

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“…Vascular factors continue to be an important element of the risk supported by many pathological studies of the vasculature [95]. New risk factors have also been identified including those associated with diet such as obesity [31,71,125,185], diabetes [4,118,124] and factors associated with the immune system [12,128,141,158]. With reference to metal exposure, the case for aluminium is less strong but other metals such as zinc and copper have been implicated, and the interactions among different metals emphasised [16,86,147,156].…”

Section: Discussionmentioning

confidence: 99%

“…Various disorders and co-morbidities associated with AD were discussed in earlier reviews [76] but there was little specific discussion of the involvement of the immune system. Nevertheless, several lines of evidence support the presence of immune system dysfunction in AD [128,141,158]. Hence, complement proteins associated with the 'classical' pathway [141], brain reactive antibodies [128], immunoglobulins [46,88], circulating immune complexes (CIC) in peripheral tissue and cerebral blood vessels [73], helper/inducer and cytotoxic/suppressor T-cells [128], and abundant reactive microglia [128] have all been observed in AD.…”

Section: Immune Systemmentioning

confidence: 99%

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Risk factors for Alzheimer’s disease

Armstrong¹

2019

375

238

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Early reviews identified over 20 risk factors associated with Alzheimer's disease (AD) including age, familial inheritance, exposure to aluminium, traumatic brain injury (TBI), and associated co-morbidities such as vascular disease and infection. In the light of recent evidence, this review reconsiders these risk factors, identifies those currently regarded as important, and discusses various hypotheses to explain how they may cause AD. Rare forms of early-onset familial AD (EO-FAD) are strongly linked to causal gene mutations, viz. mutations in amyloid precursor protein (APP) and presenilin (PSEN1/2) genes. By contrast, late-onset sporadic AD (LO-SAD) is a multifactorial disorder in which age-related changes, genetic risk factors, such as allelic variation in apolipoprotein E (Apo E) and many other genes, vascular disease, TBI and risk factors associated with diet, the immune system, mitochondrial function, metal exposure, and infection are all implicated. These risk factors may act collectively to cause AD pathology: 1) by promoting the liberation of oxygen free radicals with age, 2) via environmental stress acting on regulatory genes early and later in life ('dual hit' hypothesis), or 3) by increasing the cumulative 'allostatic load' on the body over a lifetime. As a consequence, lifestyle changes which reduce the impact of these factors may be necessary to lower the risk of AD.

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Section: Discussionmentioning

confidence: 99%

Section: Immune Systemmentioning

confidence: 99%

Risk factors for Alzheimer’s disease

Armstrong¹

2019

375

238

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“…In multiple sclerosis lesions, TNF-a has been localized within astrocytes (Hofman et al, 1989;Selmaj et al, 1991). In Alzheimer's disease, both TNF-a an IL-1 are elevated in the cerebral spinal fluid (Fillit et al, 1991;Griffin et al, 1989), abnormal major histocompatibility complex antigen expression occurs (Rogers and Luber-Narod, 1988), and IL-1 has been shown to be a promoter of b amyloid gene expression (Forloni et al, 1992). In patients with AIDS-related dementia, cerebral spinal fluid of these cytokines are also elevated (Perrella et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of tumour necrosis factor‐α secretion from rat astrocytes by Sesim‐Tang

Kim

Shin

Lee

et al. 2002

Phytotherapy Research

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Substance P (SP) can stimulate secretion of tumour necrosis factor-alpha (TNF-alpha) from astrocytes stimulated with lipopolysaccharide (LPS). In this study, we have examined whether an aqueous extract of Sesim-Tang inhibits the secretion of TNF-alpha from primary cultures of rat astrocytes. Sesim-Tang (10-1000 microg/mL) significantly inhibited the TNF-alpha secretion by astrocytes stimulated with LPS and SP. Interleukin-1 (IL-1) has been shown to elevate TNF-alpha secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore examined whether IL-1 mediated inhibition of TNF-alpha secretion from primary astrocytes by Sesim-Tang. Treatment with Sesim-Tang (10-1000 microg/mL) of astrocytes stimulated with both LPS and SP decreased IL-1 secretion significantly. Moreover, the secretion of TNF-alpha by LPS and SP in astrocytes was progressively inhibited with increasing amounts of IL-1 neutralizing antibody. Our results suggest that Sesim-Tang may inhibit TNF-alpha secretion by inhibiting IL-1 secretion and that Sesim-Tang has an antiinflammatory activity in the central nervous system.

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“…In multiple sclerosis lesions, TNF-α has been localized within astrocytes (20,21). In Alzheimer's disease, both TNF-α and IL-1 are elevated in the cerebral spinal fluid (22,23), abnormal major histocompatibility complex antigen expression occurs (24), and IL-1 has been shown to be a promoter of β amyloid gene expression (25). In patients with AIDS-related dementia, cerebral spinal fluid levels of these cytokines are also elevated (26).…”

Section: Discussionmentioning

confidence: 99%

INHIBITORY EFFECT OF TUMOR NECROSIS FACTOR-α SECRETION FROM RAT ASTROCYTES BY CHILBOKEUM

Kim

Shin

2001

Immunopharmacology and Immunotoxicology

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Substance P (SP) can stimulate secretion of tumor necrosis factor-alpha (TNF-alpha) from astrocytes stimulated with lipopolysaccharide (LPS). In this study, we have examined whether an aqueous extract of Chilbokeum inhibits secretion of TNF-alpha from primary cultures of rat astrocytes. Chilbokeum (10 microg/ml) significantly inhibited the TNF-alpha secretion by astrocytes stimulated with LPS and SP. Interleukin-1 (IL-1) has been shown to elevate TNF-alpha secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore examined whether IL-1 mediated inhibition of TNF-alpha secretion from primary astrocytes by Chilbokeum. Treatment of Chilbokeum (10 and 100 microg/ml) to astrocytes stimulated with both LPS and SP decreased IL-1 secretion significantly. Moreover, the secretion of TNF-alpha by LPS and SP in astrocytes was progressively inhibited with increasing amount of IL-1 neutralizing antibody. Our results suggest that Chilbokeum may inhibit TNF-alpha secretion by inhibiting IL-1 secretion and that Chilbokeum has an antiinflammatory activity in the central nervous system.

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Immune actions in the nervous system: A brief review with special emphasis on Aalzheimer's disease

Cited by 27 publications

References 53 publications

Risk factors for Alzheimer’s disease

Risk factors for Alzheimer’s disease

Inhibition of tumour necrosis factor‐α secretion from rat astrocytes by Sesim‐Tang

INHIBITORY EFFECT OF TUMOR NECROSIS FACTOR-α SECRETION FROM RAT ASTROCYTES BY CHILBOKEUM

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