Sequential activation of individual caspases, and of alterations in Bcl-2 proapoptotic signals in a mouse model of Huntington’s disease
Caspases play an important role in neurodegeneration in Huntington’s disease (HD). Members of the Bcl-2 family are critical modulators of terminal cell death pathways. However, alterations of Bcl-2 family members and their functional role in an in vivo model of HD have not been documented.
Melatonin Deficits Result in Pathologic Metabolic Reprogramming in Differentiated Neurons
Differentiation from neural progenitor to mature neuron requires a metabolic switch, whereby mature neurons become almost entirely dependent upon oxidative phosphorylation (OXPHOS) for ATP production.
Increased stem cell proliferation in the spinal cord of adult amyotrophic lateral sclerosis transgenic mice
Harnessing the regenerative potential of the central nervous system to repopulate depleted cellular populations from endogenous stem cells would be a novel approach for the treatment of neurological diseases resulting from cell death.
Dysregulation of Receptor Interacting Protein-2 and Caspase Recruitment Domain Only Protein Mediates Aberrant Caspase-1 Activation in Huntington’s Disease
Caspase-1 plays a role in the pathogenesis of a variety of neurological diseases. Caspase-1 activation is an early event in models of Huntington’s disease (HD). However, mechanisms regulating the activation of this apical caspase in cell death are not known. Receptor interacting protein-2 (Rip2) and caspase recruitment domain (CARD) only protein (Cop) are two CARD proteins with significant homology to the caspase-1 CARD and modulate caspase-1 activation in inflammation.
Minocycline Inhibits Cytochrome C Release and Delays Progression (Mayo/Elsevier)
Minocycline mediates neuroprotection in experimental models of neurodegeneration. It inhibits the activity of caspase-1, caspase-3, inducible form of nitric oxide synthetase (iNOS) and p38 mitogen-activated protein kinase (MAPK). Although minocycline does not directly inhibit these enzymes, the effects may result from interference with upstream mechanisms resulting in their secondary activation.
Role of Caspase 1 in Neurologic Disease, JAMA Neurology 2000
In recent years substantial advances have taken place in understanding the mechanistic pathways mediating neuronal cell death in a variety of neurologic diseases. Since the central nervous system (CNS) has little, if any, power of functional neuronal regeneration, prevention of neuronal cell death is an important target of modern neurotherapeutics.
Apoptosis and Caspasesin Neurodegenerative Diseases
Acute and chronic neurodegenerative diseases are illnesses
associated with high morbidity and mortality, and few or no effective options
are available for their treatment.