We are analyzing https://link.springer.com/article/10.1007/bf02740836.

Title:
A potential role for apoptosis in neurodegeneration and Alzheimer's disease | Molecular Neurobiology
Description:
Previous studies have shown that β-amyloid (Aβ) peptides are neurotoxic. Recent data suggest that neurons undergoing Aβ-induced cell death exhibit characteristics that correspond to the classical features of apoptosis, suggesting that these cells may initiate a program of cell death. This chapter explores the criteria and precautions that must be applied to evaluate mechanisms of cell death in vitro and in vivo, discusses the evidence supporting an apoptotic mechanism of cell death in response to Aβ in cultured neurons, and describes potential correlations for these findings in the Alzheimer
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Keywords {🔍}

google, scholar, cas, pubmed, cell, alzheimers, death, apoptosis, protein, amyloid, disease, res, sci, acad, cotman, usa, natl, gene, neuronal, dna, human, neurons, brain, alzheimer, biol, expression, programmed, role, beta, induced, rat, cells, fragmentation, induction, peptide, aging, article, cultured, growth, betaamyloid, βamyloid, biophys, apolipoprotein, anderson, evidence, neurol, plaque, orrenius, molecular, pike,

Topics {✒️}

c-fos protein immuno-reactivity inducible proto-oncogenesfos andjun month download article/chapter calcium-dependent cell death gamma-aminobutyric acid concentration il-1 beta-converting enzyme intracerebrally injected beta-amyloid β-amyloid protein increases �calcium set-point hypothesis” prolonged expression ofc-jun large early-onset pedigrees regulatesc-jun gene transcription transforming growth factor-β1 fibroblasts byc-myc protein concanavalin a-induced proliferation sequence-specifictrans-activator similar aggregated β-amyloid peptide synthetic β-amyloid protein t-cell hybrid require p53-mediated cell death ca2+-mediated endonuclease activation c-myc-induced apoptosis n-acetylcysteine inhibits apoptosis aβ-induced network dysfunction cascade induction ofc-fos apoptosis—programmed cell death β-amyloid-induced apoptosis jun dna-binding activity hypoxic-ischaemic brain injury cultured gaba-immunoreactive neurons familial early-onset alzheimer' high oxygen atmosphere cytosolic calcium concentration high-avidity binding bcl-2 inhibits death nerve growth factor late-onset alzheimer disease programmed cell death β-amyloid peptides bfgf immunopositive plaques dna fragmentation induced induced neuronal death c-fos protein privacy choices/manage cookies disease amyloid-β neurotoxicity nerve cell death early gene expression growth factor deprivation inducible transcription factor apoptotic cell death

Questions {❓}

(1988) Glucose metabolism as the site of the primary abnormality in early-onset dementia of Alzheimer type?
(1991) Are the neuroprotective effects of the protein synthesis inhibitor cycloheximide due to prevention of apoptosis?
(1992) Apoptosis—programmed cell death: a role in the aging process?
(1993) Do deficits in mitochondrial energy metabolism underlie the pathology of neurodegenerative diseases?
(1993) Is c-Jun involved in nerve cell death following status epilepticus and hypoxic-ischaemic brain injury?

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         description:Previous studies have shown that β-amyloid (Aβ) peptides are neurotoxic. Recent data suggest that neurons undergoing Aβ-induced cell death exhibit characteristics that correspond to the classical features of apoptosis, suggesting that these cells may initiate a program of cell death. This chapter explores the criteria and precautions that must be applied to evaluate mechanisms of cell death in vitro and in vivo, discusses the evidence supporting an apoptotic mechanism of cell death in response to Aβ in cultured neurons, and describes potential correlations for these findings in the Alzheimer's disease brain. In addition, cellular signaling pathways that may be associated with apoptosis in response to Aβ are examined, and support for apoptosis as a mechanism of cell death for other neurodegeneration-inducing stimuli (e.g., oxidative injury) is described. The connection of multiple stimuli that induce neuronal cell death to an apoptotic mechanism suggests that apoptosis could play a central role in neurodegeneration in the brain.
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