Dataset Information

Alzheimer’s Disease (AD) and Lewy Body Dementia (LBD): Detection of S-Nitrosylation in Key Proteins in Human, Post-mortem Brain Samples

ABSTRACT: FAD and Lewy Body Dementia (LBD): Detection of S-Nitrosylation in Key Proteins in Human, Post-mortem Brain Samples

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain

SUBMITTER: Hongmei Yang

LAB HEAD: Steven. R. Tannenbaum

PROVIDER: PXD020945 | Pride | 2023-03-10

REPOSITORIES: Pride

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Publications

Mechanistic insight into female predominance in Alzheimer's disease based on aberrant protein S-nitrosylation of C3.

Yang Hongmei H Oh Chang-Ki CK Amal Haitham H Wishnok John S JS Lewis Sarah S Schahrer Emily E Trudler Dorit D Nakamura Tomohiro T Tannenbaum Steven R SR Lipton Stuart A SA

Science advances 20221214 50

Protein S-nitros(yl)ation (SNO) is a posttranslational modification involved in diverse processes in health and disease and can contribute to synaptic damage in Alzheimer's disease (AD). To identify SNO proteins in AD brains, we used triaryl phosphine (<i>SNO</i>TRAP) combined with mass spectrometry (MS). We detected 1449 SNO proteins with 2809 SNO sites, representing a wide range of S-nitrosylated proteins in 40 postmortem AD and non-AD human brains from patients of both sexes. Integrative prot ...[more]

PMID: 36516243

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Project description:Aging is often characterized by a progressive loss of cognitive abilities due to the onset of different forms of dementia. Among these, Alzheimer’s Disease (AD) and dementia with Lewy bodies (LBD) are the most widespread ones. However, little is known about the common aspects between these conditions and how these aspects can be linked to aging itself. With this work, we aim to identify a molecular fil rouge that could link aging and different dementias in order to possibly highlight strategic targets for novel therapeutical approaches. A whole transcriptome analysis and a Gene Set Enrichment Analysis (GSEA) have been carried out on brain samples from hippocampus (HI), temporal and parietal cortex (TC, PC), cingulate cortex (CG), and substantia nigra (SN) from the Abbiategrasso Brain Bank (ABB) of subjects with a neuropathological diagnosis of AD and LBD (6 per pathology) and 3 age-matched controls with no dementia (CTRLs). Clinical and neuropsychological profile were obtained through serial evaluations, made at the baseline and in the following years. According to the ABB protocol, the neuropathological diagnosis was based on a complete histological characterization, including all the main proteinopathies and vascular scoring. Transcriptomic results showed some major differences in the number of differentially expressed genes (DEGs) between the two pathologies and in particular that AD brains gene expression is more affected compared to LBD’s one (DEGsAD=3156; DEGsLBD=278). Furthermore, the GSEA showed that in AD it is possible to cluster the analysed regions by biological processes (HI and TC: DEGs primarily related to synaptic transmission; PC, CG and SN: DEGs primarily related to proper protein folding and inflammation) while in LBD there is only a strong and peculiar involvement of SN (DEGs primarily related to proper protein folding and inflammation) and PC (DEGs primarily related to myelination and glial system activation). AD and LBD are different forms of dementia characterized by a definite time and severity-related pattern. Therefore, it is possible to draw a molecular map of pathology spreading in the brain that could unveil unexplored roads and possible shortcuts leading to a better understanding of AD and LBD pathogenesis. This could help to discover novel biological targets in order to develop effective and well-timed therapeutical approaches.

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