Neuronal damage / vitamin E supplementation

ironjustice@aol.com · medicine forum Guru Joined: 28 Apr 2005 Posts: 1522

Appearance of amyloid beta-like substances and delayed-type apoptosis
in rat hippocampus CA1 region through aging and oxidative stress.

J Alzheimers Dis. 2005; 8(3):299-309 (ISSN: 1387-2877)
Fukui K; Takatsu H; Shinkai T; Suzuki S; Abe K; Urano S
Division of Biological Chemistry, Shibaura Institute of Technology,
3-9-14 Shibaura, Minato-ku, Tokyo 108-8548, Japan.

To elucidate whether oxidative stress induces cognitive deficit, and
whether nerve cells in the hippocampus, which modulates learning and
memory functions in the brain, are damaged by oxidative stress and
during aging, the influence of hyperoxia as oxidative stress on either
the cognitive function of rats or the oxidative damage of nerve cells
was investigated. Young rats showed better learning ability than both
old rats and vitamin E-deficient young rats. Vitamin E- supplemented
young rats showed similar ability to young control rats. After they
learned the location of the platform in the Morris water maze test, the
young rats and vitamin E-supplemented young rats were subjected to
oxidative stress for 48 h, and the old rats and vitamin E-deficient
young rats were kept in normal atmosphere. The memory function of the
old rats and vitamin E-deficient young rats declined even when they
were not subjected to oxidative stress for 48 h. In contrast, the young
rats maintained their memory function for 4 days after the oxidative
stress. However, their learning abilities suddenly declined toward that
of the normal old rats after 5 days. At this point, nerve cell loss and
apoptosis were observed in the hippocampal CA 1 region of young rats.
Vitamin E-supplementation in the young rats prevented either memory
deficit or the induction of delayed-type apoptosis. The old rats and
vitamin E-deficient young rats kept in normal atmosphere for 48 h also
showed apoptosis in the hippocampus. Also, 10 days after oxidative
stress, amyloid beta-like substances appeared in the CA-1 region of
control young rats; these substances were also observed in the CA-1
region of the old rats and vitamin E- deficient young rats. These
results suggest that reactive oxygen species (ROS) generated by
oxidative stress induced amyloid beta-like substances and delayed-type
apoptosis in the rat hippocampus, resulting in cognitive deficit. Since
amyloid beta in Alzheimer's disease characterized by cognitive deficit
induces neuronal cell death, it is reasonable to consider that amyloid
beta deposition in the brain may be associated with memory dysfunction.
The results of this study imply that age-related hippocampal neuronal
damage is prevented by vitamin E supplementation due to the antioxidant
effect of vitamin E.

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk

Google