Summary of project PR000355
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000355. The data can be accessed directly via it's Project DOI: 10.21228/M85C88 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR000355 |
| Project DOI: | doi: 10.21228/M85C88 |
| Project Title: | CNS and peripheral metabolomics of calorie restriction in a mouse model of Alzheimer’s disease |
| Project Summary: | Alzheimer’s disease (AD) is a devastating neurodegenerative disorder that robs people of their memory and cognitive function. Currently, no successful treatment or preventative measure exists for AD. Calorie restriction (CR) is a dietary regimen posited to suppress genetic programs of aging and reduce AD-related pathology. CR is known to enhance longevity and mitigate aging phenotypes in multiple model species. Mechanisms underlying the benefits of CR remain unknown, particularly in areas of the brain selectively vulnerable to age-related AD pathology such as the hippocampus, a region crucial for learning and memory. Moreover, AD pathology can be influenced by changes in diet, metabolism, and immunity, indicating that factors distant from the brain may play a role in pathogenesis. The intestinal microbiota, composed of trillions of microbial cells, influences host metabolism, immunity, and cognitive function, and is posited to be linked mechanistically to AD pathobiology, but a specific role remains to be adequately tested. We hypothesize that mechanisms underlying the benefits of CR are cell-type and organ specific, involving the gut-brain microbiome throughout the lifespan, this requiring subregional analysis in the brain as well as coordinated assessments of key peripheral targets including the liver, fecal pellets , and plasma. Thus, CR is proposed to be a viable treatment option that may ameliorate the development of AD-related pathology, and importantly, reveal mechanisms that attenuate age-related expression changes in vulnerable cells. |
| Institute: | New York University |
| Department: | Langone Medical Center |
| Last Name: | Ginsberg |
| First Name: | Stephen |
| Address: | 140 Old Orangeburg Road, Orangeburg, NY 10962 |
| Email: | stephen.ginsberg@nyumc.org |
| Phone: | 845-398-2170 |
Summary of all studies in project PR000355
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST000462 | CNS and peripheral metabolomics of calorie restriction in a mouse model of Alzheimer’s disease (part I) | Mus musculus | University of North Carolina | NMR | 2017-10-03 | 1 | 78 | Uploaded data (39.8M)* |
| ST000463 | CNS and peripheral metabolomics of calorie restriction in a mouse model of Alzheimer’s disease (part II) | Mus musculus | University of North Carolina | NMR | 2017-10-03 | 1 | 77 | Uploaded data (131.5M)* |
