Dr. Chin Jeannie Chin, Ph.D.

Contact Dr. Chin

900 Walnut St.
Suite 444
Philadelphia, PA 19107

(215)-955-4949 fax

Graduate School
University of Texas Graduate School of Biomedical Sciences, Houston, Texas

Gladstone Institute of Neurological Disease and University of California San Francisco, San Francisco, California

University Appointment
Assistant Professor, 2010

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.

Notably, Aβ disrupts synaptic transmission and impairs learning and memory before frank neurodegeneration is observed. This suggests that elucidating the mechanisms by which Aβ perturbs neuronal function will pave the way for development of treatments that improve cognitive function and delay or prevent the progression of the disease.

To this end, we use a multi-disciplinary approach that combines biochemistry, immunohistochemistry, in vivo physiology, and behavioral paradigms to link cellular alterations to memory deficits in transgenic mouse models of AD. We use video-recorded EEG measurements to characterize patterns of (aberrant) brain activity in individual mice and correlate this activity with performance in various behavioral paradigms designed to test different aspects of memory and cognitive function. Finally, we use biochemical, molecular, and immunohistochemical techniques to examine the links between alterations in particular proteins or pathways and dysfunction of cognitive processes on a mouse-by-mouse basis. This integrated approach allows us to investigate the molecular basis of memory impairments observed in AD and to identify therapeutic entry points for the treatment of this neurodegenerative disease.


Most recent Peer-reviewed Publications

  1. Delayed thalamic astrocytosis and disrupted sleep-wake patterns in a preclinical model of traumatic brain injury
  2. Chronic at-level thermal hyperalgesia following rat cervical contusion spinal cord injury is accompanied by neuronal and astrocyte activation and loss of the astrocyte glutamate transporter, GLT1, in superficial dorsal horn
  3. Impairments in neurogenesis are not tightly linked to depressive behavior in a transgenic mouse model of Alzheimer's disease
  4. Expression of c-fos in hilar mossy cells of the dentate gyrus in vivo
  5. Sodium channel cleavage is associated with aberrant neuronal activity and cognitive deficits in a mouse model of alzheimer's disease
  6. Shared cognitive and behavioral impairments in epilepsy and Alzheimer's disease and potential underlying mechanisms
  7. Early cerebrovascular inflammation in a transgenic mouse model of Alzheimer's disease
  8. Selecting a mouse model of Alzheimer's disease
  9. Altered intrinsic neuronal excitability and reduced Na + currents in a mouse model of Alzheimer's disease
  10. Amyloid-β/fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of alzheimer's disease
  11. Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease
  12. β-amyloid modulation of synaptic transmission and plasticity
  13. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease
  14. Reelin depletion in the entorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease
  15. A network dysfunction perspective on neurodegenerative diseases
  16. AMPA receptors regulate transcription of the plasticity-related immediate-early gene Arc
  17. TGF-β1-induced long-term changes in neuronal excitability in Aplysia sensory neurons depend on MAPK
  18. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease
  19. Vulnerability of dentate granule cells to disruption of Arc expression in human amyloid precursor protein transgenic mice
  20. Coregulation of glutamate uptake and long-term sensitization in Aplysia

View All Publications