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Low neural exosomal levels of cellular survival factors in Alzheimer's disease.

ABSTRACT: Transcription factors that mediate neuronal defenses against diverse stresses were quantified in plasma neural-derived exosomes of Alzheimer's disease or frontotemporal dementia patients and matched controls. Exosomal levels of low-density lipoprotein receptor-related protein 6, heat-shock factor-1, and repressor element 1-silencing transcription factor all were significantly lower in Alzheimer's disease patients than controls (P < 0.0001). In frontotemporal dementia, the only significant difference was higher levels of repressor element 1-silencing transcription factor than in controls. Exosomal transcription factors were diminished 2-10 years before clinical diagnosis of Alzheimer's disease. Low exosomal levels of survival proteins may explain decreased neuronal resistance to Alzheimer's disease neurotoxic proteins.

SUBMITTER: Goetzl EJ

PROVIDER: S-EPMC4531059 | biostudies-literature | 2015 Jul

REPOSITORIES: biostudies-literature

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Low neural exosomal levels of cellular survival factors in Alzheimer's disease.

Goetzl Edward J EJ Boxer Adam A Schwartz Janice B JB Abner Erin L EL Petersen Ronald C RC Miller Bruce L BL Carlson Olga D OD Mustapic Maja M Kapogiannis Dimitrios D

Annals of clinical and translational neurology 20150513 7

Transcription factors that mediate neuronal defenses against diverse stresses were quantified in plasma neural-derived exosomes of Alzheimer's disease or frontotemporal dementia patients and matched controls. Exosomal levels of low-density lipoprotein receptor-related protein 6, heat-shock factor-1, and repressor element 1-silencing transcription factor all were significantly lower in Alzheimer's disease patients than controls (P < 0.0001). In frontotemporal dementia, the only significant differ ...[more]

PMID: 26273689

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Project description:Background and aimsInflammatory bowel diseases (IBD) are considered to be dysregulated, immune-mediated disorders; and immunosuppressive medications are the mainstay of their treatment. Clinically, we have often observed low serum immunoglobulin (Ig) levels in these patients. The aim of this study was to assess the frequency and risk factors of secondary humoral immunodeficiency in IBD patients.MethodsWe conducted a cross-sectional study of eligible IBD patients with Crohn's disease (CD), ulcerative colitis (UC), indeterminate colitis (IC) or restorative proctocolectomy with ileal pouch, who having serum Ig measured. Demographic and clinical variables were measured. Univariate and multivariate analyses were performed.ResultsA total of 324 patients was included, with a mean age of 38.8 years and 158 (48.8%) being male. Low IgG, IgG1, IgA, and IgM were found in 22.7%, 23.4%, 7.9%, and 10.9% of patients, respectively. The shared risk factors for a low IgG or IgM level were increasing age [odds ratio (OR)?=?1.13; 95% confidence interval (CI) 1.03-1.23 for low IgG level and OR?=?1.33; 95% CI 1.15-1.56 for low IgM level] and hypoalbuminemia (OR?=?1.83; 95% CI 1.01-3.33 for low IgG level and OR?=?3.17; 95% CI 1.23-8.15 for low IgM level). In addition, thioprine use was associated with low IgA level (OR?=?2.76; 95% CI 1.03-7.39). IBD disease duration was a risk factor for low IgG1 level (OR?=?1.40; 95% CI 1.12-1.76). The presence of concurrent primary sclerosing cholangitis (OR?=?0.064; 95% CI 0.007-0.60) and the use of biologics (OR?=?0.16; 95% CI 0.033-0.79) were associated with normal IgG1 level. IgG level was lower in CD patients than that in UC/IC and ileal pouch patients (P?=?0.042). IgG and IgA levels were elevated in patients with inflammatory conditions of the pouch (P?=?0.01; P?=?0.003, respectively).ConclusionsLow Ig level appears to be common in IBD patients. Increasing age, disease duration and hypoalbuminemia appeared to be risk factors. The findings may provide rationale for targeted therapy to boost humoral immunity in selected patients with IBD.

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Low neural exosomal levels of cellular survival factors in Alzheimer's disease.

Publications

Low neural exosomal levels of cellular survival factors in Alzheimer's disease.

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