Relation of <scp>CDC42</scp>, Th1, Th2, and Th17 cells with cognitive function decline in Alzheimer's disease

Zhang, Yi; Niu, Chenglin

doi:10.1002/acn3.51643

Cited by 13 publications

(10 citation statements)

References 38 publications

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“…The links between AD pathophysiology and neuroinflammation seem to be primarily mediated by the innate immune system and the activation of microglia - a brain-specific monocyte [ 15 ] . Microglia generally exhibit either a proinflammatory (M1) or anti-inflammatory phenotype (M2), each of which is positively or negatively correlated with AD, respectively [ 16 , 17 ] . The microglial-related neuroinflammatory pathways associated with AD pathogenesis are depicted in Figure 1 .…”

Section: Neuroinflammation - a Trigger For Admentioning

confidence: 99%

Pathways linking microbiota-gut-brain axis with neuroinflammatory mechanisms in Alzheimer’s pathophysiology

Hochuli,

Kadyan,

Park

et al. 2023

Microbiome Res Rep

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Disturbances in the local and peripheral immune systems are closely linked to a wide range of diseases. In the context of neurodegenerative disorders such as Alzheimer’s disease (AD), inflammation plays a crucial role, often appearing as a common manifestation despite the variability in the occurrence of other pathophysiological hallmarks. Thus, combating neuroinflammation holds promise in treating complex pathophysiological diseases like AD. Growing evidence suggests the gut microbiome’s crucial role in shaping the pathogenesis of AD by influencing inflammatory mediators. Gut dysbiosis can potentially activate neuroinflammatory pathways through bidirectional signaling of the gut-brain axis; however, the precise mechanisms of this complex interweaved network remain largely unclear. In these milieus, this review attempts to summarize the contributing role of gut microbiome-mediated neuroinflammatory signals in AD pathophysiology, while also pondering potential mechanisms through which commensal and pathogenic gut microbes affect neuroinflammation. While certain taxa such as Roseburia and Escherichia have been strongly correlated with AD, other clades such as Bacteroides and Faecalibacterium exhibit variations at the species and strain levels. In order to disentangle the inflammatory aspects of neurodegeneration attributed to the gut microbiome, it is imperative that future mechanistic studies investigate the species/strain-level dependency of commensals, opportunistic, and pathogenic gut microbes that consistently show correlations with AD patients across multiple associative studies.

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Section: Neuroinflammation - a Trigger For Admentioning

confidence: 99%

Pathways linking microbiota-gut-brain axis with neuroinflammatory mechanisms in Alzheimer’s pathophysiology

Hochuli,

Kadyan,

Park

et al. 2023

Microbiome Res Rep

View full text Add to dashboard Cite

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“…However, the detailed mechanisms remain unclear. Th2 cell levels are reduced in patients with AD [ 78 ]. Further investigation of the underlying mechanisms of AD mediated by atopic skin inflammation is necessary.…”

Section: Dementiamentioning

confidence: 99%

Involvement of Atopic Dermatitis in the Development of Systemic Inflammatory Diseases

Itamura

Sawada

2022

IJMS

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The skin is recognized as a peripheral lymphoid organ that plays an essential defensive action against external environmental stimuli. However, continuous stimulation of these factors causes chronic inflammation at the local site and occasionally causes tissue damage. Chronic inflammation is recognized as a trigger for systemic organ inflammation. Atopic dermatitis (AD) is a chronic inflammatory skin disease that is influenced by various external environmental factors, such as dry conditions, chemical exposure, and microorganisms. The pathogenesis of AD involves various Th2 and proinflammatory cytokines. Recently updated studies have shown that atopic skin-derived cytokines influence systemic organ function and oncogenesis. In this review, we focus on AD’s influence on the development of systemic inflammatory diseases and malignancies.

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“…A previous report found that overexpression of CDC42 alleviates cognitive impairment in mice ( 13 ). Another recent study reports that CDC42 is positively correlated with the MMSE score in Alzheimer's disease patients ( 21 ). Similarly, our study revealed that CDC42 was positively associated with MMSE score, and low CDC42 was related to the occurrence of cognitive impairment in stroke patients.…”

Section: Discussionmentioning

confidence: 99%

“…Another study reported that CDC42 aggravated the Th1/Th2 cell imbalance and inhibited Th17 cell differentiation ( 19 ). Regarding clinical practices, a study found that CDC42 is positively correlated with Th2 cells and inversely correlated with Th17 cells in Alzheimer's disease patients ( 21 ). Another study also found a positive association of CDC42 with Th2 cells and a negative association of CDC42 with Th17 cells in acute ischemic stroke patients ( 12 ).…”

Section: Discussionmentioning

confidence: 99%

Linkage of blood cell division cycle 42 with T helper cells, and their correlation with anxiety, depression, and cognitive impairment in stroke patients

Ma,

Chang,

Jia

et al. 2023

Braz J Med Biol Res

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Cell division cycle 42 (CDC42) regulates T helper (Th) cell differentiation and is related to psychological disorders. This study aimed to assess the correlation between blood CDC42 and Th cells, and their association with mental issues in stroke patients. Peripheral blood samples were obtained from 264 stroke patients and 50 controls. Then, serum CDC42 was measured by enzyme-linked immunosorbent assay, and Th1, Th2, and Th17 cells were detected by flow cytometry. Hospital Anxiety and Depression Scale (HADS) and Mini Mental State Examination (MMSE) were applied to patients. CDC42 was decreased (P<0.001), Th1 (P=0.013) and Th17 (P<0.001) cells were elevated, while Th2 cells (P=0.108) showed no difference in stroke patients compared to controls. In addition, CDC42 was negatively associated to Th1 (P=0.013) and Th17 (P<0.001) cells in stroke patients but were not associated with Th2 cells (P=0.223). Interestingly, CDC42 was negatively associated with HADS-anxiety (P<0.001) and HADS-depression scores (P=0.034) and positively associated with MMSE score (P<0.001) in stroke patients. Lower CDC42 was associated to lower occurrence of anxiety (P=0.002), depression (P=0.001), and cognitive impairment (P=0.036) in stroke patients. Furthermore, increased Th17 cells were positively correlated with HADS-anxiety and HADS-depression scores and inversely correlated with MMSE score, which were also associated with higher occurrence of anxiety, depression, and cognitive impairment in stroke patients (all P<0.05). Blood CDC42 and Th17 cells were correlated, and both of them were linked to the risk of anxiety, depression, and cognitive impairment. However, the findings need further large-scale validation, and the implicated mechanism needs more investigation.

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Relation of CDC42, Th1, Th2, and Th17 cells with cognitive function decline in Alzheimer's disease

Cited by 13 publications

References 38 publications

Pathways linking microbiota-gut-brain axis with neuroinflammatory mechanisms in Alzheimer’s pathophysiology

Pathways linking microbiota-gut-brain axis with neuroinflammatory mechanisms in Alzheimer’s pathophysiology

Involvement of Atopic Dermatitis in the Development of Systemic Inflammatory Diseases

Linkage of blood cell division cycle 42 with T helper cells, and their correlation with anxiety, depression, and cognitive impairment in stroke patients

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