We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Elizabeth M. Rodrigues is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2006 — 2009 |
Rodrigues, Elizabeth M |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Axonal Transport and Alzheimer's Disease Pathogenesis @ University of California San Diego
[unreadable] DESCRIPTION (provided by applicant): Several Alzheimer's Disease (AD)-related proteins, such as amyloid precursor protein (APP) and presenilin (PS1), have been shown to be involved in axonal transport. Mouse models of both intracellular transport defects and AD, as well as preliminary data on early AD human brain cholinergic neurons, all exhibit axonal swellings typical of vesicle and organelle accumulation and disrupted axonal transport. Reducing axonal transport in AD models exacerbates this phenotype, as well as plaque formation. This research proposal aims to test the hypothesis that defects in axonal transport contribute to the early neurodegeneration associated with AD. Human AD cholinergic axonal pathology will be correlated with AD progression, synaptic failures, and cognitive deficits. Study of a mouse wildtype APP overexpression model will test if motor protein receptor overexpression causes axonal pathology. Mutant human APP and PS1 will reveal if altered motor receptor processing is sufficient to cause the same axonal. pathology. The relative timing of neuronal pathology, synapse loss, and their correlation with cognitive deficits and plaque deposition will be crucial in understanding the order and likely cause-effect relationships of pathological events. [unreadable] [unreadable] [unreadable]
|
1 |