Jeannie Chin, PhD

Contact Dr. Chin

900 Walnut St.
Suite 444
Philadelphia, PA 19107

(215)-503-4294
(215)-955-4949 fax

Research and Clinical Interests
The focus of my research is to understand the cellular and network mechanisms underlying cognitive impairments in Alzheimer's disease (AD), and to identify therapeutic entry points for the treatment of this devastating disease. The amyloid precursor protein (APP) and the amyloid-β (Aβ) peptides derived from it play a central role in AD, although the precise mechanisms by which they impair neuronal function and lead to cognitive deficits remain to be fully defined. Transgenic mouse models of AD produce high levels of Aβ and develop neuropathology and memory deficits similar to those observed in patients with AD, and are thus extremely useful for interrogating the role of Aβ in memory impairments.

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Publications

Most recent Peer-reviewed Publications

1. Sodium channel cleavage is associated with aberrant neuronal activity and cognitive deficits in a mouse model of alzheimer's disease
2. Shared cognitive and behavioral impairments in epilepsy and Alzheimer's disease and potential underlying mechanisms
3. Early cerebrovascular inflammation in a transgenic mouse model of Alzheimer's disease
4. Altered intrinsic neuronal excitability and reduced Na + currents in a mouse model of Alzheimer's disease
5. Selecting a mouse model of Alzheimer's disease.
6. Amyloid-β/fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of alzheimer's disease
7. Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease
8. β-amyloid modulation of synaptic transmission and plasticity
9. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease
10. Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease
11. A network dysfunction perspective on neurodegenerative diseases
12. AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
13. TGF-β1-induced long-term changes in neuronal excitability in Aplysia sensory neurons depend on MAPK
14. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease
15. Vulnerability of dentate granule cells to disruption of Arc expression in human amyloid precursor protein transgenic mice
16. Coregulation of glutamate uptake and long-term sensitization in Aplysia
17. Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice
18. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits
19. Inhibitor of glutamate transport alters synaptic transmission at sensorimotor synapses in Aplysia
20. Serotonin stimulates phosphorylation of Aplysia synapsin and alters its subcellular distribution in sensory neurons

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