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Title:
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The Revitalized Tau Hypothesison Alzheimer's Disease |
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Author:
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Maccioni, Ricardo B.; Farías, Gonzalo; Morales, Inelia; Navarrete, Leonardo
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Abstract:
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Many hypotheseshavebeenraisedregardingthepathophysiologyofAlzheimer’sdisease
(AD).Becauseamyloidbetapeptide(Ab) depositioninsenileplaquesappearsasalate,
nonspecificevent,recentevidencepointstotauphosphorylationandaggregationasthe
finalcommonpathwayinthismultifactorialdisease.Currentapproachesthatprovide
evidenceinfavorofneuroimmunomodulationinADandtherolesoftaupathological
modificationsandaggregationintooligomersandfilamentousformsarepresented.We
proposeanintegrativemodelonthepathogenesisofADthatincludesseveraldamage
signalssuchasAb oligomers,oxygenfreeradicals,ironoverload,homocysteine,
cholesterolandLDLspecies.Theseactivatemicrogliacells,releasingproinflammatory
cytokines andproducingneuronaldegenerationandtaupathologicalmodifications.
Alteredandaggregatedformsoftauappeartoactasatoxicstimulicontributingto
neurodegeneration.Recentfindingsprovidefurthersupporttothecentralroleoftauin
the pathogenesisofAD,sothisproteinhasturnedintoadiagnosticandtherapeutictarget
for thisdisease. |
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URI:
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http://www.captura.uchile.cl/handle/2250/14708
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Date:
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2010-03-01 |
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dc.identifier.citation:
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Archives of Medical Research, 41, 226-231, 2010. |