TY - JOUR
T1 - Expression of metallothionein-I, -II, and -III in Alzheimer disease and animal models of neuroinflammation
AU - Hidalgo, Juan
AU - Penkowa, Milena
AU - Espejo, Carmen
AU - Martínez-Cáceres, Eva M
AU - Carrasco, Javier
AU - Quintana, Albert
AU - Molinero, Amalia
AU - Florit, Sergi
AU - Giralt, Mercedes
AU - Ortega-Aznar, Arantxa
N1 - Keywords: Alzheimer Disease; Animals; Brain; Humans; In Situ Hybridization; Inflammation; Male; Metallothionein; Mice; Models, Animal; Oxidative Stress; RNA, Messenger
PY - 2006
Y1 - 2006
N2 - In recent years it has become increasingly clear that the metallothionein (MT) family of proteins is important in neurobiology. MT-I and MT-II are normally dramatically up-regulated by neuroinflammation. Results for MT-III are less clear. MTs could also be relevant in human neuropathology. In Alzheimer disease (AD), a major neurodegenerative disease, clear signs of inflammation and oxidative stress were detected associated with amyloid plaques. Furthermore, the number of cells expressing apoptotic markers was also significantly increased in these plaques. As expected, MT-I and MT-II immunostaining was dramatically increased in cells surrounding the plaques, consistent with astrocytosis and microgliosis, as well as the increased oxidative stress elicited by the amyloid deposits. MT-III, in contrast, remained essentially unaltered, which agrees with some but not all studies, of AD. In situ hybridization results in a transgenic mouse model of AD amyloid deposits, the Tg2576 mouse, which expresses human Abeta precursor protein harboring the Swedish K670N/M671L mutations, are in accordance with results in human brains. Overall, these and other studies strongly suggest specific roles for MT-I, MT-II, and MT-III in brain physiology.
AB - In recent years it has become increasingly clear that the metallothionein (MT) family of proteins is important in neurobiology. MT-I and MT-II are normally dramatically up-regulated by neuroinflammation. Results for MT-III are less clear. MTs could also be relevant in human neuropathology. In Alzheimer disease (AD), a major neurodegenerative disease, clear signs of inflammation and oxidative stress were detected associated with amyloid plaques. Furthermore, the number of cells expressing apoptotic markers was also significantly increased in these plaques. As expected, MT-I and MT-II immunostaining was dramatically increased in cells surrounding the plaques, consistent with astrocytosis and microgliosis, as well as the increased oxidative stress elicited by the amyloid deposits. MT-III, in contrast, remained essentially unaltered, which agrees with some but not all studies, of AD. In situ hybridization results in a transgenic mouse model of AD amyloid deposits, the Tg2576 mouse, which expresses human Abeta precursor protein harboring the Swedish K670N/M671L mutations, are in accordance with results in human brains. Overall, these and other studies strongly suggest specific roles for MT-I, MT-II, and MT-III in brain physiology.
M3 - Journal article
C2 - 17018866
SN - 1535-3702
VL - 231
SP - 1450
EP - 1458
JO - Experimental Biology and Medicine
JF - Experimental Biology and Medicine
IS - 9
ER -
