Homo sapiens isolate:H4
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA294025 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2191008_1.fastq.gz | Fastqsanger.gz | |||
| SRR2191008_2.fastq.gz | Fastqsanger.gz | |||
| SRR2213985_1.fastq.gz | Fastqsanger.gz | |||
| SRR2213985_2.fastq.gz | Fastqsanger.gz | |||
| SRR2214068_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
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Project description:Gene expression changes in mice overexpressing amyloid precursor protein with the Swedish mutation (Tg2576; APPSw). The gene expression levels in male 12 month-old APPSw mice (GSM26708, GSM26709) were compared to those in male nontransgenic littermate control mice (GSM26706, GSM26707). Data were analyzed with MAS 5.0 and scaled to 2500.
2004-07-30 | GSE1556 | GEO
Project description:Gene expression changes in mice overexpressing amyloid precursor protein with the Swedish mutation (Tg2576; APPSw). The gene expression levels in male 12 month-old APPSw mice (GSM26708, GSM26709) were compared to those in male nontransgenic littermate control mice (GSM26706, GSM26707). Data were analyzed with MAS 5.0 and scaled to 2500. See Stein, TD, Anders, NJ, DeCarli, C, Chan, SL, Mattson, MP, and Johnson JA. Neutralization of transthyretin reverses the neuroprotective effects of secreted APP in APPSw mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis. J Neurosci. in press.
2008-06-11 | E-GEOD-1556 | biostudies-arrayexpress
Project description:Olfaction is often deregulated in Alzheimer's disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from Tg2576 mice (2, and 6 months of age) respect to age-matched wild-type (WT) littermates.
2019-07-01 | GSE106643 | GEO
Project description:To investigate transcriptomic changes in human brain parymary endohtelial cells in response to conditioned media obtained from BNMN (unconditioned media), hiPSC-CN harboring swedish mutation (Swe22) and hiPSC-CN harboring isogneic control background (CVIA2). Overall, we are tyring to understand how EC transcriptome changes in reponse to Alzheimer's disease mimicking condition.
2022-08-31 | GSE205496 | GEO
Project description:Kyrtsos2011 - A systems biology model for
Alzheimer's disease (Cholesterol in AD)
Encoded non-curated model. Issues:
- Confusing HmgCoA differential equation
- Confusing d2 and t1 parameters
- Lack of initial values for several key species
This model is described in the article:
Of Mice and Math: A Systems
Biology Model for Alzheimer's disease
Kyrtsos, Christina Rose
UMD Theses and Dissertations
Abstract:
Alzheimer's disease (AD) is the most prevalent
neurodegenerative disorder in the US, affecting over 1 in 8
people over the age of 65. There are several well-known
pathological changes in the brains of AD patients, namely: the
presence of diffuse beta amyloid plaques derived from the
amyloid precursor protein (APP), hyper-phosphorylated tau
protein, neuroinflammation and mitochondrial dysfunction.
Recent studies have shown that cholesterol levels in both the
plasma and the brain may play a role in disease pathogenesis,
however, this exact role is not well understood. Additional
proteins of interest have also been identified (ApoE, LRP-1,
IL-1) as possible contributors to AD pathogenesis. To help
understand these roles better, a systems biology mathematical
model was developed. Basic principles from graph theory and
control analysis were used to study the effect of altered
cholesterol, ApoE, LRP and APP on the system as a whole.
Negative feedback regulation and the rate of cholesterol
transfer between astrocytes and neurons were identified as key
modulators in the level of beta amyloid. Experiments were run
concurrently to test whether decreasing plasma and brain
cholesterol levels with simvastatin altered the expression
levels of beta amyloid, ApoE, and LRP-1, to ascertain the edge
directions in the network model and to better understand
whether statin treatment served as a viable treatment option
for AD patients. The work completed herein represents the first
attempt to create a systems-level mathematical model to study
AD that looks at intercellular interactions, as well as
interactions between metabolic and inflammatory pathways.
This model is hosted on
BioModels Database
and identified by:
MODEL1504240000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2016-05-09 | MODEL1504240000 | BioModels
Project description:Oligomeric forms of amyloid-beta peptide (Abeta) are presumed to play a pivotal role in the pathogenesis of Alzheimer’s disease (AD). However, it is still unclear how Abeta oligomers contribute to AD pathogenesis in patient neural cells. We generated induced pluripotent stem cells (iPSCs) from a familial AD patient and differentiated them into neural cells. Abeta oligomers were accumulated in neural cells of AD bearing amyloid precursor protein (APP)-E693delta mutation. To uncover Abeta oligomers in AD(APP-E693delta) neural cells, we analyzed gene expression profiles of control and the AD neural cells
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Project description:STING deletion protects against amyloid beta-induced Alzheimer's disease pathogenesis
| PRJNA1218462 | ENA
Project description:STING deletion protects against amyloid beta-induced Alzheimer's disease pathogenesis
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Project description:Plaques consisting of amyloid-β (Aβ) in the brain are characteristic for patients with Alzheimer´s disease. Aβ is enzymatically generated of the amyloid precursor protein (APP). During the disease, Aβ starts to aggregate forming soluble oligomers, soluble protofibrils and eventually insoluble fibrils. Aβ pathology starts mainly at the hippocampus and the surrounding cortical area. Mice overexpressing the A�-precursor protein with the Swedish mutation (APPswe) are one of the most commonly used animal models in Alzheimer’s field. These mice overexpress APP with the Swedish mutation (KM670/671NL), which is adjacent to the β-secretase cleavage site on APP. This results in increased production of Aβ. The aim of this study was to study the proteome of APPswe brain at the early stages (7-8 months old) of the disease, before plaque onset, which starts at around 11-12 months of age in this mouse model. Homogenates of the hippocampus and the rest of the cerebrum from 7-8 months-old APPswe and wild-type (WT) controls were lysed. Afterwards, filter aided tryptic digestion was performed. The resulting peptides were analyzed using LC-UDMSE. The data was searched against a randomized mouse database and label-free quantification analysis was done. In total 2487 proteins were found. In the hippocampus of APPswe mice, the levels of 1283 proteins were significantly altered compared to WT controls. While 1379 proteins were significantly altered in the rest of the cerebrum of APPswe mice compared to WT controls. Among these, mitochondrial proteins and proteins involved in neuron's development were significantly downregulated, suggesting mitochondrial dysfunction and dysregulation of neuron’s growth in the brain of APPswe mice at already this stage of the disease.
2021-06-28 | PXD026566 | Pride
Project description:Puri2010 - Mathematical Modeling for the
Pathogenesis of Alzheimer's Disease
Puri2010 - Mathematical Modeling for the Pathogenesis of
Alzheimer's Disease
Encoded non-curated model. Issues:
- Confusing replacement of
α16
when t = 3 years
- Confusing 4th rate equation
This model is described in the article:
Mathematical modeling for
the pathogenesis of Alzheimer's disease.
Puri IK, Li L.
PLoS ONE 2010; 5(12): e15176
Abstract:
Despite extensive research, the pathogenesis of
neurodegenerative Alzheimer's disease (AD) still eludes our
comprehension. This is largely due to complex and dynamic
cross-talks that occur among multiple cell types throughout the
aging process. We present a mathematical model that helps
define critical components of AD pathogenesis based on
differential rate equations that represent the known
cross-talks involving microglia, astroglia, neurons, and
amyloid-? (A?). We demonstrate that the inflammatory activation
of microglia serves as a key node for progressive
neurodegeneration. Our analysis reveals that targeting
microglia may hold potential promise in the prevention and
treatment of AD.
This model is hosted on
BioModels Database
and identified by:
MODEL1409240001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-04-15 | MODEL1409240001 | BioModels