Abstract Glioblastomas (GBMs) are the most aggressive brain tumors. GBM cells form extensive tumoral networks to communicate with each other and surrounding neurons. Neuronal activity promotes cell proliferation by secreting protumorigenic factors triggering neuronal-activity-dependent Ca2+ transients, which persisted transmitted via tumor promote overall growth therapy resistance. While how th...

AIM Presentation of a prenatally diagnosed case of Werdnig-Hoffmann disease, the most severe type of spinal muscular atrophy. METHODS DNA obtained from cultivated amniocytes was analyzed for deletions in the survival motor neuron gene and neuronal apoptosis inhibitory protein gene. RESULTS The fetus was diagnosed as an affected homozygote for deletions in exon 7 and exon 8 of the survival m...

Alzheimer's disease (AD) is the most common neurodegenerative disorder of late life characterized by insidious, chronic, and progressive memory impairment in association with the accumulation of senile plaques, neurofibrillary tangles, and massive loss of neurons. Apoptosis is believed to be an important contributor to progression and pathology of neurodegeneration in AD. There is considerable ...

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca2+ and Na+ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Ap...

Caspase-9 is critical for cytochrome c (cyto-c)-dependent apoptosis and normal brain development. We determined that this apical protease in the cyto-c pathway for apoptosis resides inside mitochondria in several types of cells, including cardiomyocytes and many neurons. Caspase-9 is released from isolated mitochondria on treatment with Ca2+ or Bax, stimuli implicated in ischemic neuronal cell ...

Apoptosis is a fundamental process required for normal development of the nervous system and is triggered during neurodegenerative disease. To dissect the molecular events leading to neuronal cell death, we have developed a cell-free model of neuronal apoptosis. The model faithfully reproduces key elements of apoptosis, including chromatin condensation, DNA fragmentation, caspase activation/pro...

Platinum nanoparticles (nPts) have neuroprotective/antioxidant properties, but the mechanisms of their action in cerebrovascular disease remain unclear. We investigated brain bioavailability nPts and effects on damage, cerebral blood flow (CBF), development systemic oxidative stress (OS) a model ischemia (hemorrhage + temporary bilateral common carotid artery occlusion, tBCAO) rats. The (0.04 g...

The proapoptotic BH3-only protein Bim is a crucial regulator of neuronal apoptosis. Previous studies have indicated the involvement of the c-Jun, FOXO1/3a, and B/C-Myb transcription factors in the regulation of Bim during neuronal apoptosis. However, the mechanism underlying the transcriptional regulation of Bim in activity deprivation-induced neuronal apoptosis has remained unclear. The presen...

Active cellular suicide, apoptosis, plays an important role in the correct formation of the nervous system during development. Furthermore, during neurodegenerative conditions, such as Alzheimer’s disease, apoptosis may have a major impact on the outcome. In neuronal cells, the constant interaction between pro-apoptotic and prosurvival molecules and signaling pathways is considered to determine...

Programmed cell death is critical for normal nervous system development and is regulated by Bcl-2 and Caspase family members. Targeted disruption of bcl-x(L), an antiapoptotic bcl-2 gene family member, causes massive death of immature neurons in the developing nervous system whereas disruption of caspase-9, a proapoptotic caspase gene family member, leads to decreased neuronal apoptosis and neu...