Phospholipases A2 Mediate Amyloid-beta Peptide-Induced Mitochondrial Dysfunction
نویسندگان
چکیده
منابع مشابه
Neurobiology of Disease Phospholipases A2 Mediate Amyloid- Peptide-Induced Mitochondrial Dysfunction
Mitochondrial dysfunction has been implicated in the pathophysiology of Alzheimer’s disease (AD) brains. To unravel the mechanism(s) underlying this dysfunction, we demonstrate that phospholipases A2 (PLA2s), namely the cytosolic and the calcium-independent PLA2s (cPLA2 and iPLA2 ), are key enzymes mediating oligomeric amyloidpeptide (A 1– 42)-induced loss of mitochondrial membrane potential an...
متن کاملSynaptic memory mechanisms: Alzheimer's disease amyloid beta-peptide-induced dysfunction.
There is growing evidence that mild cognitive impairment in early AD (Alzheimer's disease) may be due to synaptic dysfunction caused by the accumulation of non-fibrillar, oligomeric Abeta (amyloid beta-peptide), long before widespread synaptic loss and neurodegeneration occurs. Soluble Abeta oligomers can rapidly disrupt synaptic memory mechanisms at extremely low concentrations via stress-acti...
متن کاملMitochondrial amyloid-beta peptide: pathogenesis or late-phase development?
Mitochondrial and metabolic dysfunction have been linked to Alzheimer's disease for some time. Key questions regarding this association concern the nature and mechanisms of mitochondrial dysfunction, and whether such changes in metabolic properties are pathogenic or secondary, with respect to neuronal degeneration. In terms of mitochondria and Alzheimer's, altered function could reflect intrins...
متن کاملNicotinic Acetylcholine Receptors Mediate -Amyloid Peptide-induced Tau Protein Phosphorylation*
The Alzheimer’s disease pathogenic peptide, -amyloid42 (A 42), induces tau protein phosphorylation. Because hyperphosphorylated tau is a consistent component of neurofibrillary tangles, a pathological hallmark of Alzheimer’s disease, we investigated the signaling molecules involved in A 42-induced tau phosphorylation. We show that A 42 elicited rapid and reversible tau protein phosphorylation o...
متن کاملInhibition of Alzheimer's amyloid-beta peptide-induced reduction of mitochondrial membrane potential and neurotoxicity by gelsolin.
Amyloid-beta (A beta) peptides play a central role in the development of Alzheimer's disease. They are known to induce mitochondrial dysfunction and caspase activation, resulting in apoptosis of neuronal cells. Here we show that human cytoplasmic gelsolin inhibits A beta peptide-induced cell death of neuronally differentiated rat pheochromocytoma (PC-12) cells. We also show that the segment 5 b...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Neuroscience
سال: 2006
ISSN: 0270-6474,1529-2401
DOI: 10.1523/jneurosci.3505-06.2006