Genetic absence of ALOX5 protects from homocysteine-induced memory impairment, tau phosphorylation and synaptic pathology

• Published in: Human molecular genetics Vol. 26; no. 10; pp. 1855 - 1862
• Main Authors: Li, Jian-Guo, Barrero, Carlos, Merali, Salim, Praticò, Domenico
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 15.05.2017
• Subjects: Animals; Arachidonate 5-Lipoxygenase - deficiency; Arachidonate 5-Lipoxygenase - genetics; Arachidonate 5-Lipoxygenase - metabolism; Brain - enzymology; Brain - metabolism; Disease Models, Animal; Female; Homocysteine - genetics; Homocysteine - metabolism; Humans; Male; Memory - physiology; Memory Disorders - metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurodegenerative Diseases - enzymology; Neurodegenerative Diseases - genetics; Neurodegenerative Diseases - metabolism; Phosphorylation; Synapses - metabolism

Elevated level of homocysteine (Hcy) is considered a risk factor for neurodegenerative diseases, but the mechanisms remain to be established. Because high Hcy is associated with an up-regulation of the ALOX5 gene product, the 5Lipoxygenase (5LO), herein we investigated whether this activation is res...