Amyloid plaques and symptoms of Alzheimer's
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The relationship between amyloid plaques and symptoms of Alzheimer's disease is controversial, but it has been widely accepted that the mature amyloid- (A) fibrils that form the plaques are stable and cannot revert to a soluble, intermediary form. Now, however, Martins et al. have shown that lipids normally present in the brain can destabilize the fibrils and resolubilize them into protofibrils, which have neurotoxic effects in vitro and in vivo.
Inert amyloid fibrils of the Alzheimer's A-peptide 1–42 (A42) were incubated overnight with liposomes and various lipids including cholesterol, sphingolipids, gangliosides and brain extract. Whereas neither the lipids nor the fibrils alone were neurotoxic when incubated with primary hippocampal mouse neurons, the fibril–lipid mixture induced apoptotic cell death. Furthermore, injection of the supernatant of the fibril–lipid mixture into the brains of adult mice led to tau phosphorylation and impairments in memory, effects not observed following injection of fibrils or lipids alone. Biophysical assays revealed that the liquid, toxic phase of the lipid–fibril emulsion contained protofibrillar oligomers of various molecular sizes, which were demonstrated to have the same morphology, biochemical properties and toxicity as protofibrils formed by A aggregation. Immunostaining revealed that the fibril-derived protofibrils diffused rapidly through the brain into areas associated with Alzheimer's disease.
The authors concluded that changes in the balance of natural lipids in the brain, which could be affected by environmental conditions or genetic make-up, could revert stable, inert amyloid plaques into toxic protofibrils. Nature Clinical Practice Neurology (2008) 4, 123
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Inert amyloid fibrils of the Alzheimer's A-peptide 1–42 (A42) were incubated overnight with liposomes and various lipids including cholesterol, sphingolipids, gangliosides and brain extract. Whereas neither the lipids nor the fibrils alone were neurotoxic when incubated with primary hippocampal mouse neurons, the fibril–lipid mixture induced apoptotic cell death. Furthermore, injection of the supernatant of the fibril–lipid mixture into the brains of adult mice led to tau phosphorylation and impairments in memory, effects not observed following injection of fibrils or lipids alone. Biophysical assays revealed that the liquid, toxic phase of the lipid–fibril emulsion contained protofibrillar oligomers of various molecular sizes, which were demonstrated to have the same morphology, biochemical properties and toxicity as protofibrils formed by A aggregation. Immunostaining revealed that the fibril-derived protofibrils diffused rapidly through the brain into areas associated with Alzheimer's disease.
The authors concluded that changes in the balance of natural lipids in the brain, which could be affected by environmental conditions or genetic make-up, could revert stable, inert amyloid plaques into toxic protofibrils. Nature Clinical Practice Neurology (2008) 4, 123
A compound found in broccoli, previously linked to anti-cancer benefits, may also counter the decline in the body's immune system associated with age, says a new study from UCLA. http://www.nutraingredients.com
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