Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1219367 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hippocampal pathways in cognitive impairment
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Project description:Plasma EV proteomic profiling from patients with typical PD combined with different degrees of cognitive impairments (PD with Dementia, PD with mild cognitive impairment, and PD with normal cognition), atypical Parkinsonism represented by Multiple System Atrophy, and healthy individuals
2024-04-27 | PXD051421 | JPOST Repository
Project description:The experiment is for demonstrating the miRNA profiles in plasma exosomes derived from mild cognitive impairment and Alzheimer's disease patients and healthy donors.
2022-01-30 | E-MTAB-11222 | biostudies-arrayexpress
Project description:It is important to maintain cognitive integrity during underwater operations, which may also trigger cognitive alterations. Cognitive effect of underwater operations and the underlying mechanism remain elusive. Here, we found a single underwater operation affects cognition in a time-dependent model. Prolonged exposure elicits significant cognitive impairment and hippocampal dysfunction, which was accompanied by activation of microglia and upregulation of pro-inflammatory cytokines. RNA-sequencing supported the involvement of neuroinflammation and indicated the critical role of CCR3. Knockdown of CCR3 significantly rescued cognitive impairment and hippocampal dysfunction. Furthermore, the upregulation of pro-inflammatory cytokines was also reversed. Mechanistically, CCR3 knockdown switched the activated microglia from a pro-inflammatory to neuroprotective phenotype. Taken together, these results highlighted the time-dependent effects of a single underwater operation on cognitive function. Knocking down CCR3 can attenuate neuroinflammation by regulating polarization of activated microglia, thereby alleviating prolonged underwater operation-induced cognitive impairment.
2024-05-20 | GSE247651 | GEO
Project description:Unravel the mechanisms underlying brain aging and Alzheimer´s disease (AD) has been difficult because of complexity of the networks that drive these aging-related changes. Analysis of the gene expression in the brain is a valuable tool to study the function of the brain under normal and pathological conditions. Gene microarray technology allows massively parallel analysis of most genes expressed in a tissue, and therefore is an important research tool that potentially can provide the investigative power needed to address the complexity of brain aging and neurodegenerative processes. One of the reasons that account for the resistance of AD pathogenesis to analysis is that clinically normal subjects may exhibit considerable AD pathology, blurring criteria for distinguishing subjects with normal aging or AD. Here, we analyzed hippocampal and cortex frontal gene expression from 32 subjects separated in individuals presenting, 1) both pathologic and clinical AD (definitive AD); 2) AD pathology and normal clinic (pathologic AD); 3) cognitive impairment, without AD pathology (others dementias); and 4) no cognitive impairment, without AD pathology (normal individuals). Our results show that based on gene expression profile these individuals we could verify similarity between the definitive AD group and the group that only had AD-type pathology (pathologic AD). Specimens of hippocampus and cortex frontal used in this study were obtained at autopsy from 32 subjects. Neuropathology, specifically NFT and NP, was assessed in accordance to the Braak staging and CERAD scores, respectively. Based on pathologic and clinic criteria, subjects were categorized into four groups: 1) nine subjects with AD neuropathologic (Braak = IV / V / VI and CERAD ≠ 0) presenting cognitive impairment (CDR ≥ 1), termed “definitive AD” (dAD); 2) five subjects with AD neuropathologic (Braak = IV / V / VI and CERAD ≠ 0) and without cognitive impairment (CDR = 0), termed “pathologic AD” (pAD); 3) nine subjects without AD neuropathologic (Braak = 0 / I / II and CERAD ≠ C) presenting cognitive impairment (CDR ≥ 1), termed “other dementias” (OD); 4) - nine subjects without AD neuropathologic (Braak = 0 / I / II and CERAD ≠ C) and without cognitive impairment (CDR = 0), termed “normal” (N). RNA isolation and Amplification. From total RNA, a two-round linear amplification procedure (T7-based protocol) was carried out for all samples and for a pool of RNAs obtained from 15 distinct human cell lines used as reference. Labeled cDNA was generated in a reverse transcriptase reaction using amplified RNA (aRNA). Equal amounts of test and reference cDNA reverse color Cy-labeled aRNA targets were competitively hybridized against the cDNA probes in a customized cDNA platform with 4,608 ORESTES representing human genes. Dye-swap was performed for each sample as control for dye bias and used as replicate.
2013-01-11 | E-GEOD-13214 | biostudies-arrayexpress
Project description:Cognitive impairment due to cancer and its therapy is a major concern among cancer survivors. Extracellular vesicles (EVs) composition altered by cancer and chemotherapy may affect neurological processes such as neuroplasticity, potentially impacting the cognitive abilities of cancer survivors. We investigated the EV proteome of breast cancer patients with and without cognitive impairment following anthracycline-based chemotherapy from longitudinally collected plasma. EVs were cup-shaped and positive for Flotillin-1 and TSG-101. We identified 517 differentially expressed EV proteins between the cognitive impaired and non-impaired groups during and post-chemotherapy. The observed decreased expression of p2X purinoceptor, cofilin-1, ADAM 10, and dynamin-1 in the plasma EVs of cognitive impaired group may suggest alterations in mechanisms underlying synaptic plasticity. The reduced expression of tight junction proteins among cognitive-impaired patients may imply weakening of the blood-brain barrier. These EV protein signatures may serve as a fingerprint that underscore the mechanisms underlying cognitive impairment in cancer survivors.
2021-05-27 | PXD021395 | Pride
Project description:To explore the potential mechanism linking circRNAs in Obesity-associated cognitive impairment induced by a longtime high-fat diet. The male mouse was treated by HFD up to16 weeks . Then the hippocaum tissues was isloated and circRNA Microarray analysis was applied. The expression profiles of hippocaum from mouse treated with HFD changed and 2 circRNA (mmu-circRNA-004797,mmu-circRNA-21040) from this signature was quantified by real-time PCR, confirming high-fat diet can change the profiles of circRNAs of hippocaum from mouse and may participated in the obesity associated cognitive impairment.
2022-09-07 | GSE208344 | GEO
Project description:Neural imaging, genetics, and circulating biomarkers are being developed to differentiate normal aging from diseases that affect cognition. The blood based biomarkers, such as plasma exosome could provide a simple and relatively inexpensive means for tracking the progression of cognitive decline and effectiveness of treatments, as well as providing information on mechanism for cognitive impairment.
2017-10-11 | GSE97644 | GEO