Aβ(1–42)-induced JNK and ERK activation in rabbit hippocampus is differentially regulated by lithium but is not involved in the phosphorylation of tau

• Published in: Brain research. Molecular brain research. Vol. 119; no. 2; pp. 201 - 206
• Main Authors: Ghribi, Othman, Prammonjago, Patcharin, Herman, Mary M., Spaulding, Natalie K., Savory, John
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 26-11-2003; Elsevier
• Subjects: Biological and medical sciences; Caspase-3; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; ERK; JNK; Lithium; Medical sciences; Neurology; tau; Disorders of the nervous system; Aβ; JNK; Lithium; tau; Caspase-3; ERK; Phosphorylation; Alzheimer disease; Central nervous system; Rabbit; Encephalon; Degenerative disease; Nervous system diseases; Enzyme; Caspase; Lagomorpha; Cerebral disorder; Peptidases; Vertebrata; Mammalia; Tau protein; β Amyloid protein; Animal; Central nervous system disease; Hydrolases; Hippocampus; Apoptosis
• ISSN: 0169-328X; 1872-6941
• DOI: 10.1016/j.molbrainres.2003.09.001

Administration of Aβ(1–42) into the rabbit brain induces apoptosis and phosphorylation of tau. These Aβ effects correlate with the activation of JNK and ERK, but not of p38. Treatment with 7 mM lithium inhibits apoptosis, modulates JNK and ERK and does not affect the phosphorylation of tau. Our results demonstrate that lithium, at this dose, effectively inhibits the Aβ-induced apoptosis but has no effect on tau phosphorylation, and that MAP kinases are not involved in the phosphorylation of tau.