Fibrillar Amyloid-β Accumulation Triggers an Inflammatory Mechanism Leading to Hyperphosphorylation of the Carboxyl-Terminal End of Tau Polypeptide in the Hippocampal Formation of the 3×Tg-AD Transgenic Mouse.

scientific article published on 22 March 2016

Fibrillar Amyloid-β Accumulation Triggers an Inflammatory Mechanism Leading to Hyperphosphorylation of the Carboxyl-Terminal End of Tau Polypeptide in the Hippocampal Formation of the 3×Tg-AD Transgenic Mouse. is …
instance of (P31):
scholarly articleQ13442814

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P356DOI10.3233/JAD-150837
P8608Fatcat IDrelease_ghwjyefd4bcnlcphv2my6tzowy
P698PubMed publication ID27031470

P50authorGeorge PerryQ5543353
P2093author name stringJuan Pedro Luna-Arias
María Luisa Labra-Barrios
Raúl Mena
Sofía Díaz-Cintra
Claudia Luna-Herrera
José Luna-Muñoz
Samadhi Moreno-Campuzano
Azucena Ruth Aguilar-Vázquez
Paola Flores-Rodríguez
Benjamín Florán-Garduño
Miguel Ángel Ontiveros-Torres
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P433issue1
P304page(s)243-269
P577publication date2016-03-22
P1433published inJournal of Alzheimer's DiseaseQ6294755
P1476titleFibrillar Amyloid-β Accumulation Triggers an Inflammatory Mechanism Leading to Hyperphosphorylation of the Carboxyl-Terminal End of Tau Polypeptide in the Hippocampal Formation of the 3×Tg-AD Transgenic Mouse.
P478volume52

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cites work (P2860)
Q93061586Chronic low dose of AM404 ameliorates the cognitive impairment and pathological features in hyperglycemic 3xTg-AD mice
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Q97536272Peroxisome Proliferator-activated Receptor (PPAR)-γ Modifies Aβ Neurotoxin-induced Electrophysiological Alterations in Rat Primary Cultured Hippocampal Neurons