Presenilin-1 but not amyloid precursor protein mutations present in mouse models of Alzheimer's disease attenuate the response of cultured cells to Î³-secretase modulators regardless of their potency and structure.

Hahn, Stefanie; Brüning, Tanja; Ness, Julia; Czirr, Eva; Baches, Sandra; Gijsen, Harrie; Korth, Carsten; Pietrzik, Claus U; Bulic, Bruno; Weggen, Sascha

Hahn, Stefanie; Brüning, Tanja; Ness, Julia; Czirr, Eva; Baches, Sandra; Gijsen, Harrie; Korth, Carsten; Pietrzik, Claus U; Bulic, Bruno; Weggen, Sascha.

Affiliation

Hahn S; Department of Neuropathology, Heinrich Heine University, Düsseldorf, Germany.

J Neurochem ; 116(3): 385-95, 2011 Feb.

Article in En | MEDLINE | ID: mdl-21091478

Subject(s)

Alzheimer Disease/enzymology; Alzheimer Disease/genetics; Amyloid Precursor Protein Secretases/metabolism; Amyloid beta-Protein Precursor/genetics; Mutation/genetics; Presenilin-1/genetics; Protease Inhibitors/chemistry; Protease Inhibitors/pharmacology; Alzheimer Disease/metabolism; Amyloid beta-Protein Precursor/physiology; Animals; CHO Cells; Cricetinae; Cricetulus; Disease Models, Animal; Humans; Mice; Mice, Transgenic; Neuroprotective Agents/chemistry; Neuroprotective Agents/pharmacology; Presenilin-1/physiology; Structure-Activity Relationship

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Full text: 1 Database: MEDLINE Main subject: Protease Inhibitors / Amyloid beta-Protein Precursor / Amyloid Precursor Protein Secretases / Presenilin-1 / Alzheimer Disease / Mutation Type of study: Prognostic_studies Limits: Animals / Humans Language: En Year: 2011 Type: Article

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