Inflammatory Markers in Mild Cognitive Impairment and Anxiety disorders in Middle Aged Subjects with Metabolic Syndrome

Anxiety disorders are increasingly being associated with metabolic and cardiovascular burden, in contrast with depression; the role of inflammation in anxiety has sparsely been discussed. A number of reports of elevated inflammatory markers in mild cognitive impairment (MCI) suggest that inflammation may be a potential early marker of the pathological cascade associated with dementia. The aim of this study was to evaluate a possible association between peripheral blood concentrations of inflammatory factors in patients with MCI and mental processes such as, cognitive impairment and anxiety in obesity.Methods and resultsThe data collected from 271 patients with MetS according IDF criteria, (aged 30–60 years) have been analyzed. Lifetime diagnoses of depression (D), anxiety (A) was self-reported. Current D and A were confirmed by psychodiagnostic interview according to the criteria of ICD-10. All patients passed through: MMSE test, Wechsler memory scale, symbol coding and category Fluency test, scales HADS, HAM-A. Inflammatory markers included CRP, IL-6, IL-1 and TNF-α. Subjects were divided into group A–with D and/or A (139) and group B–without affective disorders (132). Using Mann–Whitney test significant connection between presence of MCI and high levels of inflammation is associated with simultaneous presence affective disorders. High correlations in subjects with A/D were between IL-6, IL-1 and MCI. In-group B, there was no significant correlations between inflammatory markers and MCI.ConclusionThere is link between affective disorders and levels of inflammatory markers. Increased levels of IL-6 and IL-1 provoke co-morbidity of MCI and depression or anxiety.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Mutual associations among diseases causing disability, such as musculoskeletal diseases, metabolic syndrome components, and mild cognitive impairment: a 3-year follow-up of the ROAD study

Bone Abstracts ◽

10.1530/boneabs.3.pp1 ◽

2014 ◽

Author(s):

Noriko Yoshimura ◽

Shigeyuki Muraki ◽

Hiroyuki Oka ◽

Sakae Tanaka ◽

Hiroshi Kawaguchi ◽

...

Keyword(s):

Metabolic Syndrome ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Musculoskeletal Diseases ◽

The Road ◽

Road Study ◽

Metabolic Syndrome Components

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Elevated Inflammatory Markers and Arterial Stiffening Exacerbate Tau but Not Amyloid Pathology in Older Adults with Mild Cognitive Impairment

Journal of Alzheimer s Disease ◽

10.3233/jad-201382 ◽

2021 ◽

pp. 1-13

Author(s):

Alexandra L. Clark ◽

Alexandra J. Weigand ◽

Kelsey R. Thomas ◽

Seraphina K. Solders ◽

Lisa Delano-Wood ◽

...

Keyword(s):

Older Adults ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Inflammatory Markers ◽

Memory Performance ◽

Cognitive Testing ◽

Interactive Effects ◽

Protein Biomarkers ◽

Age Related ◽

T Tau

Background: Age-related cerebrovascular and neuroinflammatory processes have been independently identified as key mechanisms of Alzheimer’s disease (AD), although their interactive effects have yet to be fully examined. Objective: The current study examined 1) the influence of pulse pressure (PP) and inflammatory markers on AD protein levels and 2) links between protein biomarkers and cognitive function in older adults with and without mild cognitive impairment (MCI). Methods: This study included 218 ADNI (81 cognitively normal [CN], 137 MCI) participants who underwent lumbar punctures, apolipoprotein E (APOE) genotyping, and cognitive testing. Cerebrospinal (CSF) levels of eight pro-inflammatory markers were used to create an inflammation composite, and amyloid-beta 1–42 (Aβ 42), phosphorylated tau (p-tau), and total tau (t-tau) were quantified. Results: Multiple regression analyses controlling for age, education, and APOE ɛ4 genotype revealed significant PP x inflammation interactions for t-tau (B = 0.88, p = 0.01) and p-tau (B = 0.84, p = 0.02); higher inflammation was associated with higher levels of tau within the MCI group. However, within the CN group, analyses revealed a significant PP x inflammation interaction for Aβ 42 (B = –1.01, p = 0.02); greater inflammation was associated with higher levels of Aβ 42 (indicative of lower cerebral amyloid burden) in those with lower PP. Finally, higher levels of tau were associated with poorer memory performance within the MCI group only (p s < 0.05). Conclusion: PP and inflammation exert differential effects on AD CSF proteins and provide evidence that vascular risk is associated with greater AD pathology across our sample of CN and MCI older adults.

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