ABSTRACT
Objective To conduct an in-depth analysis on the correlation of miRNA and Alzheimer disease (AD) pathogenesis and provide an experimental basis for AD potential biomarkers by analysis of serum miRNA expression profiles in AD patients. Methods The miRNA expression profiles were exmined in 7 severe AD patients and 5 normal controls using high-throughput sequencing and bioinformatic analysis. Results Compared with the normal controls, there were serum differential expression of 112 miRNAs (DEmiRNAs) including 57 being up-regulated and 55 being down-regulated in patients with severe AD (P<0.05). GO-term function enrichment analysis showed that DEmiRNAs participated in the protein binding, ion binding, transcription metal binding, and biological metabolism and regulation process of organelle and cell membrane, etc. KEGG pathway enrichment analysis found that PI3K-Akt signal pathway was an important pathway of target genes. Conclusion The differential expression of serum miRNAs may be potential biomarkers of AD and the target genes of DEmiRNAs are related to the pathological changes of AD.
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Objective We aimed to use 1H-MRS to characterize metabolite concentrations in the bilateral hippo?campus in GPI patient. Methods Metabolite ratios in the bilateral hippocampus were compared between patients with GPI (n=52) and Normal Control (NC) (n=38). Clinical neurological tests were measured in all subjects and were correlat?ed to the metabolite concentrations. Results The GPI patients showed significantly lower concentrations of N-acetylas?partate(NAA)/creatine(Cr) ratios in the bilateral hippocampus region compared to the NC subjects. There was significant?ly difference in the NAA/Cr ratios between the mild GPI dementia and the severe GPI dementia groups on the left hippo?campus region. We found that the NAA/Cr ratios concentrations were positively correlated with Mini Mental state Exami?nation (MMSE) and Montreal Cognitive Assessment scale (MoCA) scores in the left hippocampus region and the mI/Cr ra?tios concentrations were positively correlated. Conclusions GPI Patients have neuronal dysfunction in the bilateral hippo?campus. The severity of cognitive impairments is associated with the severity of the damage in the left side.
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Objective To investigate the cognitive characteristics and vascular risk factor between early onset de?pression and late onset depression in late life depression and provide a clue to elucidate the cause of cognitive impairment in late life depression. Method Fifty-six late life depression patients were recruited in our hospital, including 29 early on?set depression patients and 27 late onset depression patients. 25 controls were recruited from Guangzhou community. Cog?nitive evaluation were conducted in all the patients and controls, including MMSE, memory, attention, language, visuospa?tial abilities,executive function and Framingham vascular risk assessment, and analyze the cognitive and vascular risk be?tween the patients. Result There were statistically significant differences in overall cognitive assessment MMSE(24.8 ± 2.9,22.8±3.5,P=0.030), symbol digit modalities test(SDMT)(29.8±10.5, 22.9±11.8, P=0.028), clock drawing test(CDT) (3.6 ± 0.8, 2.9 ± 1.3, P=0.006) and trail making test(TMT) (60.4 ± 20.6, 74.7 ± 28.8, P=0.027) between late onset depression and early onset depression. In addition, the score of vascular risk assessment was significant between late onset depression and early onset depression(14.6±2.7,12.3±2.2,P=0.001). Conclusion Compare with early onset depression, late onset de?pression has much severe cognitive impairments and increased vascular risk factors.
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Objective To explore the plasma levels of soluble CD40 (sCD40) and soluble CD40 ligand (sCD40L) in the patients with Alzheimer’s disease (AD) and those with amnestic mild cognitive impairment (aMCI). Methods The levels of plasma sCD40 and sCD40L were measured in 20 patients with AD, 35 patients with aMCI, and 32 cognitively normal controls (NC) using commercially available ELISAs. The cognitive function of AD and aMCI patients was mea?sured by mini-mental state examination (MMSE). Results There were significant differences in plasma sCD40 among AD, aMCI and NC groups (P<0.05) as the medians (the upper and lower quartiles) of plasma levels were 123.3 (97.4, 149.5) pg/mL, 102.9 (63.6, 124.0) pg/mL and 70.66 (51.0, 90.8) pg/mL, respectively. There were significant differences in plasma sCD40L among AD, aMCI and NC groups (P<0.05) as plasma levels were 537.0 (316.0, 1134.0) pg/mL, 316.0 (190.0,546.0) pg/mL and 167.0 (107.5,478.0) pg/mL. A negative correlation between the plasma concentrations of sCD40L and the MMSE scores was found in aMCI patients (r=-0.736, P<0.001). Conclusions There are relevant chang?es of plasma sCD40 and sCD40L levels in patients with AD and aMCI. The present results suggest that plasma levels of sCD40 and sCD40L may be appropriate biomarkers for AD patients and indicate that CD40-CD40L signaling may be in?volved in AD pathophysiology.