A characteristic N-glycopeptide signature associated with diabetic cognitive impairment (Unenriched total peptides)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens (human)
SUBMITTER: Yuri Miura
PROVIDER: PXD039936 | JPOST Repository | Thu Feb 08 00:00:00 GMT 2024
REPOSITORIES: jPOST
Dataset's files
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Project description:Adverse effects in diabetic mothers offspring (DMO) are a major concern of increasing incidence. Among these, chronic central complications in DMO remain poorly understood, and in extreme cases, diabetes can essentially function as a gestational brain insult. Nevertheless, therapeutic alternatives for DMO are limited.Therefore, we have analyzed the central long-term complications in the offspring from CD1 diabetic mothers treated with streptozotozin, as well as the possible reversion of these alterations by insulin administration to neonates. Brain atrophy, neuronal morphology, tau phosphorylation, proliferation and neurogenesis were assessed in the short term (P7) and in the early adulthood (10 weeks) and cognitive function was also analyzed in the long-term.Central complications in DMO were still detected in the adulthood, including cortical and hippocampal thinning due to synaptic loss and neuronal simplification, increased tau hyperphosphorylation, and diminished cell proliferation and neurogenesis. Additionally, maternal diabetes increased the long-term susceptibility to spontaneous central bleeding, inflammation and cognition impairment in the offspring. On the other hand, intracerebroventricular insulin administration to neonates significantly reduced observed alterations. Moreover, non-invasive intranasal insulin reversed central atrophy and tau hyperphosphorylation, and rescued central proliferation and neurogenesis. Vascular damage, inflammation and cognitive alterations were also comparable to their counterparts born to nondiabetic mice, supporting the utility of this pathway to access the central nervous system.Our data underlie the long-term effects of central complications in DMO. Moreover, observed improvement after insulin treatment opens the door to therapeutic alternatives for children who are exposed to poorly controlled gestational diabetes, and who may benefit from more individualized treatments.
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Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.
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Project description:Alzheimer's disease (AD) is a neurodegenerative disease and is the most common form of dementia, cognitive dysfunction is a pre-AD manifestation, followed by progressive deterioration in behavior and mood, CK has good pharmacological activity, inhibit neuronal damage associated with Aβ and improve learning memory in mice through its antioxidative properties. We used microarrays to detail the regulation of brain tissue genes in cognitively impaired mice by ginsenoside CK.
2023-02-10 | GSE221791 | GEO
Project description:BackgroundAnatomic total shoulder arthroplasty (ATSA) and reverse total shoulder arthroplasty (RTSA) reliably alleviate pain and restore shoulder function for a variety of indications. However, these procedures are not well-studied in patients with neurocognitive impairment. Therefore, the purpose of this study was to investigate whether patients with dementia or mild cognitive impairment (MCI) have increased odds of surgical or medical complications following arthroplasty.MethodsThe PearlDiver database was queried from 2010 through October 2021 to identify a cohort of patients who underwent either ATSA or RTSA and had a minimum 2-year follow-up. Current Procedural Terminology and International Classification of Diseases codes were used to stratify this cohort into three groups: (1) patients with dementia, (2) patients with MCI, and (3) patients with neither condition. Surgical and medical complication rates were compared among these three groups.ResultsThe overall prevalence of neurocognitive impairment among patients undergoing total shoulder arthroplasty was 3.0% in a cohort of 92,022 patients. Patients with dementia had increased odds of sustaining a periprosthetic humerus fracture (odds ratio [OR] = 1.46, P < .001), developing prosthesis instability (OR = 1.72, P < .001), and undergoing revision arthroplasty (OR = 1.55, P = .003) after RTSA compared to patients with normal cognition. ATSA patients with dementia did not have an elevated risk of surgical complications or revision. Conversely, RTSA patients with MCI did not have an elevated risk of complications or revision, although ATSA patients with MCI had greater odds of prosthesis instability (OR = 2.51, P = .008). Additionally, patients with neurocognitive impairment had elevated odds of medical complications compared to patients with normal cognition, including acute myocardial infarction and cerebrovascular accident.ConclusionCompared to patients with normal cognition, RTSA patients with preoperative dementia and ATSA patients with preoperative MCI are at increased risk for surgical complications. Moreover, both ATSA and RTSA patients with either preoperative MCI or dementia are at increased risk for medical complications. As the mean age in the U.S. continues to rise, special attention should be directed towards patients with neurocognitive impairment to minimize postoperative complications aftertotal shoulder arthroplasty, and the risks of this surgery more carefully discussed with patients and their families and caretakers.
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