Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

de la Monte, Suzanne M.; Tong, Ming; Hapel, Andrew J.

doi:10.3390/biomedicines11092394

Cited by 3 publications

(1 citation statement)

References 156 publications

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“…These biomarkers include TNFα, IL-1β, IL-4, IL-5, IL-9, IL-13, YKL-40 (also known as chitinase-3-like protein-1 (CHI3L1)), and glial fibrillary acidic protein (GFAP). Additionally, two chemokines, MCP-1, and eotaxin-1, have previously been associated with more significant memory impairment in individuals with Mild Cognitive Impairment (MCI) and AD [8,13,14].…”

Section: Discussionmentioning

confidence: 99%

The INFLUENCE OF THE APOEε4 ALLELE ON PRO-INFLAMMATORY CYTOKINE LEVELS IN THE CEREBROSPINAL FLUID OF PATIENTS WITH ALZHEIMER’S DISEASE

Bašić,

Milošević,

Đorđević

et al. 2024

FU Med Biol

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Single nucleotide polymorphisms (SNPs) rs429358 and rs7412, the most commonly investigated variants in the apolipoprotein E gene (APOE) are crucial for APOEε4 carrier status determination. However, their association with inflammatory cytokine levels in patients with dementia due to Alzheimer’s disease (AD) remains unclear. This study aimed to investigate the influence of the APOEε4 allele on pro-inflammatory cytokine levels in the cerebrospinal fluid of patients with AD dementia. The research was conducted on 36 patients with probable dementia due to AD. APOE rs429358 and rs7412 were analyzed using the Real-Time PCR method with allele-specific TaqMan assays, followed by the analysis of APOEε4 allele carrier status. Patients carrying at least one APOEε4 allele were assigned as APOEε4+. Core biomarkers (Aβ42/40 ratio, t-Tau, p-Tau levels), as well as pro-inflammatory cytokine (Tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b)) levels, were determined in the patient’s cerebrospinal fluid (CSF) using Enzyme-linked Immunosorbent Assay (ELISA). Seventeen patients (47.22%) were assigned as APOEε4+. CSF TNF-α levels were significantly higher in APOEε4+ AD dementia patients in comparison to APOEε4- patients (p<0.001), while no significant differences in IL-1b levels between these two groups were obtained. Correlation analysis showed that TNF-α negatively correlated with the Aβ42/40 ratio (p=0.033), while positive correlation with t-Tau and p-Tau was observed (p=0.001, p=0.015, respectively). These findings highlight the potential significance of TNF-α in the context of APOEε4 positivity and its implications in AD pathology.

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Section: Discussionmentioning

confidence: 99%

The INFLUENCE OF THE APOEε4 ALLELE ON PRO-INFLAMMATORY CYTOKINE LEVELS IN THE CEREBROSPINAL FLUID OF PATIENTS WITH ALZHEIMER’S DISEASE

Bašić,

Milošević,

Đorđević

et al. 2024

FU Med Biol

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Differentiation and regulation of CD4+ T cell subsets in Parkinson’s disease

Sun,

Gu,

Bai

2024

Cell. Mol. Life Sci.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease, and its hallmark pathological features are the loss of dopaminergic (DA) neurons in the midbrain substantia nigra pars compacta (SNpc) and the accumulation of alpha-synuclein (α-syn). It has been shown that the integrity of the blood-brain barrier (BBB) is damaged in PD patients, and a large number of infiltrating T cells and inflammatory cytokines have been detected in the cerebrospinal fluid (CSF) and brain parenchyma of PD patients and PD animal models, including significant change in the number and proportion of different CD4 + T cell subsets. This suggests that the neuroinflammatory response caused by CD4 + T cells is an important risk factor for the development of PD. Here, we systematically review the differentiation of CD4 + T cell subsets, and focus on describing the functions and mechanisms of different CD4 + T cell subsets and their secreted cytokines in PD. We also summarize the current immunotherapy targeting CD4 + T cells with a view to providing assistance in the diagnosis and treatment of PD.

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Maf1 loss regulates spinogenesis and attenuates cognitive impairment in Alzheimer’s disease

Han,

Chen,

et al. 2024

Brain

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Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive impairment. Synaptic dysfunction has appeared in the early stage of AD and is significantly correlated with cognitive impairment. However, the specific regulatory mechanism remains unclear. Here we found upregulated Maf1 transcription factor in AD, and Maf1 conditional knockout in AD transgenic mice restored learning and memory function. Downregulation of Maf1 reduced intraneuronal Ca2+ concentration and restored neuronal synaptic morphology. We also demonstrated that Maf1 regulates the expression of NMDAR1 by binding to the promoter region of Grin1, further regulating calcium homeostasis and synaptic remodeling in neurons. Therefore, our results clarified the important role and mechanism of the Maf1-NMDAR1 signaling pathway in the stability of the synaptic structure, neuronal function, and behavior during the pathogenesis of AD, serving as a potential diagnostic and therapeutic target for the early onset of AD.

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Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer’s Disease

Cited by 3 publications

References 156 publications

The INFLUENCE OF THE APOEε4 ALLELE ON PRO-INFLAMMATORY CYTOKINE LEVELS IN THE CEREBROSPINAL FLUID OF PATIENTS WITH ALZHEIMER’S DISEASE

The INFLUENCE OF THE APOEε4 ALLELE ON PRO-INFLAMMATORY CYTOKINE LEVELS IN THE CEREBROSPINAL FLUID OF PATIENTS WITH ALZHEIMER’S DISEASE

Differentiation and regulation of CD4+ T cell subsets in Parkinson’s disease

Maf1 loss regulates spinogenesis and attenuates cognitive impairment in Alzheimer’s disease

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