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BACKGROUND AND PURPOSE Mild cognitive deficit in early Parkinson's disease (PD) has been widely studied. Here we have examined the effects of memantine in preventing memory deficit in experimental PD models and elucidated some of the underlying mechanisms. EXPERIMENTAL APPROACHES I.p. injection of 1-methyl-4- phenyl-1,2,3,6-tetrahydro pyridine (MPTP) in(More)
RESP18 (Regulated endocrine-specific protein, 18 kDa) was first identified as a dopaminergic drugs-regulated intermediate pituitary transcript. RESP18 protein is a unique endoplasmic reticulum (ER) resident protein. Its functions in the brain especially in the nervous system disorders remain unknown. ER stress (ERS) has been proved to be one of the(More)
Mutations in the parkin gene are currently thought to be the most common cause of recessive familial Parkinsonism. Parkin functions as an E3 ligase to regulate protein turnover, and its function in mitochondrial quality control has been reported recently. Overexpression of parkin has been found to prevent neuronal degeneration under various conditions both(More)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a severe decline of memory performance. A widely studied AD mouse model is the APPswe/PSEN1ΔE9 (APP/PS1) strain, as mice exhibit amyloid plaques as well as impaired memory capacities. To test whether restoring synaptic plasticity and decreasing β-amyloid load by Parkin(More)
Epidemiological and clinico-pathological studies indicate a causal relationship between heart disease and Alzheimer's disease (AD). To learn whether heart disease causes an onset of AD, mice with myocardial infarction (MI) and congestive heart failure (HF) were used to test neuropsychiatric and cognitive behaviors as well as for measurements of AD related(More)
SAP97 is directly involved in exporting NMDA receptors with a specific subunit composition from the endoplasmic reticulum (ER). Characterization of the interactions between SAP97 and an NMDA receptor splice variant, GluN1-3, and of the effects on forward trafficking revealed that an ER-level interaction blocked the RXR ER-retention motif in the GluN1-3(More)
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