Immunophenotypes in the circulation of patients with mild cognitive impairment

Magaki, Shino; Yellon, Steven M.; Mueller, Claudius; Kirsch, Wolff M.

doi:10.1016/j.jpsychires.2007.01.004

Cited by 21 publications

(18 citation statements)

References 42 publications

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“…In addition, changes in lymphocyte subsets have been observed in patients with mild cognitive impairment and Alzheimer's disease. Patients with mild cognitive impairment or Alzheimer's disease showed lower percentages of B cells [28,47] but increased expansion of late-differentiated T cells (CD28-), especially in CD4+ cells [48,49,50]. These data are in line with our findings and give further support to the role of peripheral lymphocytes in human cognition.…”

Section: Discussionsupporting

confidence: 90%

Premature Immunosenescence Is Associated with Memory Dysfunction in Rheumatoid Arthritis

Petersen

Grassi‐Oliveira

Siara

et al. 2014

Neuroimmunomodulation

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Background: Rheumatoid arthritis (RA) has been associated with premature immunosenescence and an increased prevalence of age-related morbidities including poor cognitive function. Objective: We explored the relationships among lymphocyte subsets and memory in RA. Methods: Thirty patients with RA and 19 age-matched healthy controls took part in this study. Cognitive function stress and depression scores were evaluated by structured clinical questionnaires. Lymphocytes were isolated and immunophenotyped by flow cytometry to investigate the following subsets: B cells, activated and naïve/memory T cells, regulatory FoxP3+ T (Treg) cells, Th17+ cells, NK cells and senescence-associated CD28- T cells. Results: RA patients were more depressed than controls, but stress levels were similar in the 2 groups. Patients had impaired memory performance compared to controls, demonstrated by lower Mini-Mental State Examination scores and logical and working memories (all p < 0.0001). These group effects remained significant after correcting for depression and age. Patients had expansion of regulatory T cells, naïve CD4+ T cells and CD8+CD28- cells but reduced percentages of B cells and memory CD8+CD45RO+ T cells compared to controls. CD8+CD28- and CD8+CD45RO+ T cells were found to be negatively associated with memory. Conclusion: RA patients had reduced memory performance compared to healthy controls. Expansion of activated and senescence-associated T cells was correlated with poor memory performance.

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Section: Discussionsupporting

confidence: 90%

Premature Immunosenescence Is Associated with Memory Dysfunction in Rheumatoid Arthritis

Petersen

Grassi‐Oliveira

Siara

et al. 2014

Neuroimmunomodulation

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“…Finally, it was recently found a decrease in the percentage of total lymphocytes and a concomitant increase in granulocytes in MCI subjects compared to controls [75], consistent with evidences of a decrease in the proliferative ability of lymphocytes [117], and of increased granulocyte activity [69] in AD patients, suggesting an inflammatory state specific not only for AD, but also for MCI.…”

Section: Biomarkerssupporting

confidence: 60%

Mild Cognitive Impairment: A Systematic Review

Mariani

Monastero

Mecocci

2007

JAD

212

182

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Abstract. MCI is a nosological entity proposed as an intermediate state between normal aging and dementia. The syndrome can be divided into two broad subtypes: amnestic MCI (aMCI) characterized by reduced memory, and non-amnestic MCI (naMCI) in which other cognitive functions rather than memory are mostly impaired. aMCI seems to represent an early stage of AD, while the outcomes of the naMCI subtypes appear more heterogeneous -including vascular dementia, frontotemporal dementia or dementia with Lewy bodies-but this aspect is still under debate. MCI in fact represents a condition with multiple sources of heterogeneity, including clinical presentation, etiology, and prognosis. To improve classification and prognosis, there is a need for more sensitive instruments specifically developed for MCI as well as for more reliable methods to determine its progression or improvement. Current clinical criteria for MCI should be updated to include restriction in complex ADL; also the diagnostic and prognostic role of behavioral symptoms and motor dysfunctions should be better defined. A multidisciplinary diagnostic approach including biological and neuroimaging techniques may probably represent the best option to predict the conversion from MCI to dementia. In this review we discuss the most recent aspects related to the epidemiological, clinical, neuropathological, neuroimaging, biochemical and therapeutic aspects of MCI, with specific attention to possible markers of conversion to dementia.

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“…Besides the Ab-mediated systemic adaptive response, increasing studies suggest that the T cell immune response may be involved in the inflammation process of AD (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26). In vitro data showed a cross-talking between microglia and T cells; microglia can serve as APCs for A␤-reactive T cells and, in turn, T cells themselves can influence microglial differentiation (12)(13)(14)(15).…”

mentioning

confidence: 99%

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

Shang²,

Zhao³

et al. 2009

The Journal of Immunology

104

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How circulating T cells infiltrate into the brain in Alzheimer disease (AD) remains unclear. We previously reported that amyloid β (Aβ)-dependent CCR5 expression in brain endothelial cells is involved in T cell transendothelial migration. In this study, we explored the signaling pathway of CCR5 up-regulation by Aβ. We showed that inhibitors of JNK, ERK, and PI3K significantly decreased Aβ-induced CCR5 expression in human brain microvascular endothelial cells (HBMECs). Chromatin immunoprecipitation assay revealed that Aβ-activated JNK, ERK, and PI3K promoted brain endothelial CCR5 expression via transcription factor Egr-1. Furthermore, neutralization Ab of receptor for advanced glycation end products (RAGE; an Aβ receptor) effectively blocked Aβ-induced JNK, ERK, and PI3K activation, contributing to CCR5 expression in HBMECs. Aβ fails to induce CCR5 expression when truncated RAGE was overexpressed in HBMECs. Transendothelial migration assay showed that the migration of MIP-1α (a CCR5 ligand)-expressing AD patients’ T cells through in vitro blood-brain barrier model was effectively blocked by anti-RAGE Ab, overexpression of truncated RAGE, and dominant-negative PI3K, JNK/ERK, or Egr-1 RNA interference in HBMECs, respectively. Importantly, blockage of intracerebral RAGE abolished the up-regulation of CCR5 on brain endothelial cells and the increased T cell infiltration in the brain induced by Aβ injection in rat hippocampus. Our results suggest that intracerebral Aβ interaction with RAGE at BBB up-regulates endothelial CCR5 expression and causes circulating T cell infiltration in the brain in AD. This study may provide a new insight into the understanding of inflammation in the progress of AD.

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Immunophenotypes in the circulation of patients with mild cognitive impairment

Cited by 21 publications

References 42 publications

Premature Immunosenescence Is Associated with Memory Dysfunction in Rheumatoid Arthritis

Premature Immunosenescence Is Associated with Memory Dysfunction in Rheumatoid Arthritis

Mild Cognitive Impairment: A Systematic Review

Amyloid β Interaction with Receptor for Advanced Glycation End Products Up-Regulates Brain Endothelial CCR5 Expression and Promotes T Cells Crossing the Blood-Brain Barrier

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