Area:
Alzheimer's Disease
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, Santiago Viveros Salazar is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 2017 |
Salazar, Santiago Viveros |
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.). |
Investigating the Role of Pyk2 in Alzheimer's Disease Pathophysiology
PROJECT SUMMARY Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects millions of people worldwide. In spite of millions of patients with this disease it remains unclear why only a subset of elderly patients develop senile plaques and neurofibrillary tangles that are hallmarks of AD. Understanding the basic biological mechanisms that govern those differences is crucial in developing effective therapeutics to stave off disease progression. AD acutely affects synapse formation and loss of synapses is highly correlated with disease progression. The amyloid hypothesis suggests amyloid-beta (A?) as the primary component of senile plaques leads to synaptotoxicity, the loss of synapses and eventually neuronal cell death. Specifically, it is hypothesized that high-molecular weight A? oligomers (A?o) produced in the brains of AD patients are the trigger in AD pathophysiology. Previous studies show A?o derived from AD patients can bind the cellular-Prion protein (PrPC) with high affinity and initiate a signaling cascade that leads to synapse loss, cognitive decline, and even cell death, all symptoms of synaptotoxicity. Our preliminary data suggests a novel component of the A?o-PrPC signaling pathway, Proline-rich Tyrosine Kinase II (Pyk2, CAK?, PTK2B), that potentially mediates synaptotoxicity in AD. Here we propose elucidating the role of Pyk2 in AD using a genetic and pharmacological approach. Aim 1 will investigate Pyk2 function in mediating biochemical and anatomical deficits in AD. Experiment 1a will test the hypothesis that deletion and inhibition of Pyk2 will rescue activation of A?o-PrPC signaling pathway. Experiment 1b will test the hypothesis that deletion and inhibition of Pyk2 will rescue synapse density. Aim 2 will Investigate Pyk2 function in mediating learning and memory phenotypes in AD mouse model. Experiment 2a will test the hypothesis that deletion and inhibition of Pyk2 will rescue A??-dependent deficits in long-term potentiation (LTP). Experiment 2b will test the hypothesis that deletion and inhibition of Pyk2 will rescue Morris Water Maze (MWM) deficit in AD mouse model. Evidence suggests A?o-PrPC is important for mediating synaptotoxicity in murine models of familial-AD. Nevertheless, it remains unclear exactly how this signaling mediates the synapse loss and neuronal dysfunction observed in AD and whether Pyk2 plays a role. Our proposed research will help elucidate the biological mechanisms that mediate neuronal dysfunction and potentially identify a new therapeutic target for the treatment of Alzheimer's disease.
|
1.009 |