Project description:Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:Human brain tissue was obtained from the New Zealand Brain Bank from donors with Alzheimer's disease (AD) or age-matched controls (n=9/group). Mean post mortem delays were ~12h. Six distinct brain regions were dissected, Hippocampus, Cingulate Gyrus, Entorhinal Cortex (severely affected), Motor and Sensory Cortex (less affected) and Cerebellum (spared). Protein was extracted from each sample and, each region was analysed independently. For each region, samples were divided into 3 sets of 3 cases and 3 controls and assigned to an iTRAQ 8 plex, alongside two aliquots of a pooled QC sample. Samples were digested, iTRAQ labelled and analysed. For each region, between 3000 and 4200 proteins were compared between AD and control, identifying a series of known and novel protein expression changes associated with the progression of AD.
Project description:We quantified genome-wide levels of H3K27ac in post-mortem entorhinal cortex tissue samples, identifying widespread Alzheimer's disease (AD)-associated acetylomic variation. Differentially acetylated peaks were identified in the vicinity genes implicated in both tau and amyloid neuropathology (MAPT, APP, PSEN1, PSEN2), as well as genomic regions containing variants associated with sporadic late-onset AD (CR1, TOMM40). Both MAPT and PSEN2 are characterized by an extended hyperacetylated region upstream of the TSS mapping to enhancers in the brain. We show that genes annotated to AD-associated hyper- and hypoacetylated peaks are enriched for brain- and neuropathology-related functions.
Project description:This dataset contains microarray data from normal controls (aged 20-99 yrs) and Alzheimer's disease cases, from 4 brain regions: hippocampus, entorhinal cortex, superior frontal cortex, post-central gyrus. Changes in expression of synaptic and immune related genes were analyzed, investigating age-related changes and AD-related changes, and region-specific patterns of change. These AD cases were processed simultaneously with the control cases (young and aged) included in GSE11882 (GSE11882 dataset contains data exclusively from normal control brains).
Project description:Using highly-parallel RNA-sequencing on samples from rTg4510 and J20 mice (n = 121 mice), collected at four different time points, we profiled transcriptional changes in the entorhinal cortex paralleling the progression of Alzheimer's disease-associated pathology.
