Dr Ben Bahr

  • William C. Friday Chair and Professor of Molecular Biology and Biochemistry
  • Chemistry and Physics , UNCP
  • bahr@uncp.edu
  • 910-775-4383
  • 1 University Dr.
  • Pembroke NC 28372

There are 16 included publications by Dr Ben Bahr :

TitleDateViewsBrief Description
Aß42-mediated proteasome inhibition and associated tau pathology in hippocampus are governed by a lysosomal response involving cathepsin B: Evidence for protective crosstalk between protein clearance pathways 2017 27 Impaired protein clearance likely increases the risk of protein accumulation disorders including Alzheimer’s disease (AD). Protein degradation through the proteasome pathway decreases with age and in AD brains, and the Aß42 peptide has been shown to ...
Cleavage of the Vesicular Glutamate Transporters Under Excitotoxic Conditions 2011 393 Glutamate is loaded into synaptic vesicles by vesicular glutamate transporters (VGLUTs), and alterations in the transporters expression directly regulate neurotransmitter release. We investigated changes in VGLUT1 and VGLUT2 protein levels after isch...
Endo-lysosomal dysfunction: a converging mechanism in neurodegenerative diseases 2017 53 Endo-lysosomal pathways are essential in maintaining protein homeostasis in the cell. Numerous genes in the endo-lysosomal pathways have been found to associate with neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease ...
Glutamate-induced and NMDA receptor-mediated neurodegeneration entails P2Y1 receptor activation 2018 14 Despite the characteristic etiologies and phenotypes, different brain disorders rely on common pathogenic events. Glutamate-induced neurotoxicity is a pathogenic event shared by different brain disorders. Another event occurring in different brain pa...
Guidelines for the use and interpretation of assays for monitoring autophagy 2012 31 In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies...
Inhibitor of Endocannabinoid Deactivation Protects Against In Vitro and In Vivo Neurotoxic Effects of Paraoxon 2017 43 The anticholinesterase paraoxon (Pxn) is related to military nerve agents that increase acetylcholine levels, trigger seizures, and cause excitotoxic damage in the brain. In rat hippocampal slice cultures, high-dose Pxn was applied resulting in a pre...
A New Generation Fatty Acid Amide Hydrolase Inhibitor Protects Against Kainate-Induced Excitotoxicity 2010 24 Endocannabinoids, including anandamide (AEA), have been implicated in neuroprotective on-demand responses. Related to such a response to injury, an excitotoxic kainic acid (KA) injection (i.p.) was found to increase AEA levels in the brain. To modula...
Nuclear Translocation and Calpain-Dependent Reduction of Bcl-2 After Neonatal Cerebral Hypoxia–Ischemia 2009 343 Apoptosis-related mechanisms are important in the pathophysiology of hypoxic–ischemic injury in the neonatal brain. Caspases are the major executioners of apoptosis, but there are a number of upstream players that influence the cell death pathways. T...
Paraoxon: An Anticholinesterase That Triggers an Excitotoxic Cascade of Oxidative Stress, Adhesion Responses, and Synaptic Compromise 2017 41 The anticholinesterase paraoxon (Pxn) is an organophosphate (OP) and the active metabolite of the insecticide parathion. It potently inhibits the enzyme acetylcholinesterase and leads to enhanced glutamate release, diminished GABA uptake, oxidative d...
Poor cognitive ageing: Vulnerabilities, mechanisms and the impact of nutritional interventions 2017 51 Ageing is a highly complex process marked by a temporal cascade of events, which promote alterations in the normal functioning of an individual organism. The triggers of normal brain ageing are not well understood, even less so the factors which init...
Positive Lysosomal Modulation As a Unique Strategy to Treat Age-Related Protein Accumulation Diseases 2012 27 Lysosomes are involved in degrading and recycling cellular ingredients, and their disruption with age may contribute to amyloidogenesis, paired helical filaments (PHFs), and a-synuclein and mutant huntingtin aggregation. Lysosomal cathepsins are upre...
Potential Alzheimer’s Disease Therapeutics Among Weak Cysteine Protease Inhibitors Exhibit Mechanistic Differences Regarding Extent of Cathepsin B Up-Regulation and Ability to Block Calpain 2017 32 Cysteine protease inhibitors have long been part of drug discovery programs for Alzheimer's disease (AD), traumatic brain injury (TBI), and other disorders. Select inhibitors reduce accumulating proteins and AD pathology in mouse models. One such com...
Protective Effects of Positive Lysosomal Modulation in Alzheimer's Disease Transgenic Mouse Models 2011 21 Alzheimer's disease (AD) is an age-related neurodegenerative pathology in which defects in proteolytic clearance of amyloid ß peptide (Aß) likely contribute to the progressive nature of the disorder. Lysosomal proteases of the cathepsin family exhibi...
Purkinje Neuron Ca2+ Influx Reduction Rescues Ataxia in SCA28 Model 2015 0 Spinocerebellar ataxia type 28 (SCA28) is a neurodegenerative disease caused by mutations of the mitochondrial proteaseAFG3L2. The SCA28 mouse model, which is haploinsufficient for Afg3l2, exhibits a progressive decline in motor functionand displays ...
A Single Pathway Targets Several Health Challenges of the Elderly 2014 194 New avenues to modulate the autophagy–lysosomal route of protein clearance have the potential to help treat several disease states to which the elderly are particularly vulnerable. Two recent papers identi?ed distinct ways to tap into the lysosomal d...
Submicromolar Aß42 Reduces Hippocampal Glutamate Receptors and Presynaptic Markers in an Aggregation-Dependent Manner 2011 417 Synaptic pathology in Alzheimer's disease brains is thought to involve soluble Aß42 peptide. Here, sterile in-cubation in PBS caused small Aß42 oligomer formation as well as heterogeneous, 6E10-immunopositive ag-gregates of 80–100 kDa. The high molec...