Dr. Schneider Jay S. Schneider, PhD

Contact Dr. Schneider

1020 Locust Street.
Suite 521
Philadelphia, PA 19107

(215) 503-0370
fax

How Can We Improve the Lives of Parkinson's Disease Patients?

The primary research focus of my laboratory is Parkinson's disease (PD). Parkinson's disease is a progressive neurodegenerative disorder in which the main pathology is death of dopamine-producing neurons in the substantia nigra. This leads to a variety of motor and non-motor symptoms that can be controlled to some extent with current drug treatments, but the efficacy of these treatments decreases over time. There is no cure for PD and its symptoms worsen over time leading to significant disability. Our basic, clinical and translational research programs are aimed at improving the quality of life for PD patients.

The multi-disciplinary research program in my laboratory is attacking the problem of PD in a way we hope will benefit patients at all stages of the disease. Part of our research is aimed at understanding the molecular/neurochemical factors contributing to dopamine neuron death in PD. We are assessing potential neuroprotective and neurorestorative therapies that we hope will stop or slow the death of dopamine neurons and restore function to damaged cells. Our neuroprotection/neurorestoration program encompasses both basic pre-clinical studies as well as clinical trials of putative neuroprotective/neurorestorative agents in PD patients. Other pre-clinical and clinical studies are examining ways to improve and prolong the therapeutic response to standard anti-parkinson medications. We are developing molecular-based therapies that would reverse major physiological imbalances in the brains of PD patients and provide more effective symptom relief for late stage patients. Relief of non-motor symptoms of PD is a major unmet medical need. Ongoing research in our lab is examining the neurochemical basis of cognitive impairments associated with PD with the goal of developing therapies that will improve motor and cognitive impairments in PD patients.

We use a variety of techniques in our basic research including state of the art techniques of molecular and cellular biology, neurochemistry, neuroanatomy and behavior. Our clinical research employs standard techniques to assess human motor and cognitive functioning.

In addition to our PD research program, the lab is also involved in studies of heavy metal neurotoxicity. Recent studies have examined the effects of developmental lead exposure on the functional maturation of the brain and neuroplasticity and have assessed the effects of chronic low level manganese exposure on brain neurochemistry and cognitive and motor functioning.

Publications

Most recent Peer-reviewed Publications

  1. Effects of memantine and galantamine on cognitive performance in aged rhesus macaques
  2. Manganese exposure induces α-synuclein aggregation in the frontal cortex of non-human primates
  3. Rearing environment, sex and developmental lead exposure modify gene expression in the hippocampus of behaviorally naïve animals
  4. Influence of developmental lead exposure on expression of DNA methyltransferases and methyl cytosine-binding proteins in hippocampus
  5. A randomized, controlled, delayed start trial of GM1 ganglioside in treated Parkinson's disease patients
  6. Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model
  7. Sex and rearing condition modify the effects of perinatal lead exposure on learning and memory
  8. Effects of developmental lead exposure on the hippocampal transcriptome: Influences of sex, developmental period, and lead exposure level
  9. Impaired spatial working memory learning and performance in normal aged rhesus monkeys
  10. Differential effect of postnatal lead exposure on gene expression in the hippocampus and frontal cortex
  11. Behavioral toxicology of cognition: Extrapolation from experimental animal models to humans. Behavioral toxicology symposium overview
  12. Protective effects of valproic acid on the nigrostriatal dopamine system in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease
  13. Sex-based differences in gene expression in hippocampus following postnatal lead exposure
  14. Effects of the alpha-2 adrenoceptor agonist guanfacine on attention and working memory in aged non-human primates
  15. Functional significance of aldehyde dehydrogenase ALDH1A1 to the nigrostriatal dopamine system
  16. Attention, executive functioning and memory in normal aged rhesus monkeys
  17. Manganese exposure induces microglia activation and dystrophy in the substantia nigra of non-human primates
  18. Protection of dopaminergic cells from MPP+-mediated toxicity by histone deacetylase inhibition
  19. The dopamine D3 receptor antagonist, S33138, counters cognitive impairment in a range of rodent and primate procedures
  20. Predictors of cognitive outcomes in early Parkinson disease patients: The National Institutes of Health Exploratory Trials in Parkinson Disease (NET-PD) experience

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