Previous studies have shown that the chemical hormone corticosteroid, which is released into the body\u2019s blood as a stress response, is found at levels two to three times higher in Alzheimer\u2019s patients<\/strong> than non-Alzheimer\u2019s patients.<\/p>\n \u201cStress is an environmental factor that looks like it may play a very important role in the onset of Alzheimer\u2019s disease,\u201d said Domenico Pratic\u00f2, professor of pharmacology and microbiology and immunology in Temple\u2019s School of Medicine, who led the study. \u201cWhen the levels of corticosteroid are too high for too long, they can damage or cause the death of neuronal cells, which are very important for learning and memory<\/strong>.\u201d<\/p>\n In their study, \u201cKnockout of 5-lipoxygenase prevents dexamethasone-induced tau pathology in 3xTg mice,\u201d published in the journal Aging Cell<\/em>, the Temple researchers set up a series of experiments to examine the mechanisms by which stress can be responsible for the Alzheimer\u2019s pathology in the brain.<\/p>\n Using triple transgenic mice, which develop amyloid beta and the tau protein, two major brain lesion signatures for Alzheimer\u2019s, the Temple researchers injected one group with high levels of corticosteroid each day for a week in order to mimic stress.<\/p>\n While they found no significant difference in the mice\u2019s memory ability at the end of the week, they did find that the tau protein was significantly increased in the group that received the corticosteroid<\/strong>. In addition, they found that the synapses, which allow neuronal cells to communicate and play a key role in learning and memory, were either damaged or destroyed.<\/p>\n \u201cThis was surprising because we didn\u2019t see any significant memory impairment, but the pathology for memory and learning impairment was definitely visible,\u201d said Pratico. \u201cSo we believe we have identified the earliest type of damage that precedes memory deficit in Alzheimer\u2019s patients.\u201d<\/p>\n Pratico said another surprising outcome was that a third group of mice that were genetically altered to be devoid of the brain enzyme 5-lipoxygenase appeared to be immune and showed no neuronal damage from the corticosteroid.<\/p>\n In previous studies, Pratico and his team have shown that elevated levels of 5-lipoxygenase cause an increase in tau protein levels in regions of the brain controlling memory and cognition, disrupting neuronal communications and contributing to Alzheimer\u2019s disease<\/strong>. It also increases the levels of amyloid beta, which is thought to be the cause for neuronal death and forms plaques in the brain.<\/p>\n Pratico said the corticosteroid causes the 5-lipoxygenase to over-express and increase its levels, which in turn increases the levels of the tau protein and amyloid beta.<\/p>\n \u201cThe question has always been what up-regulates or increases 5-lipoxygenase, and now we have evidence that it is the stress hormone,\u201d he said. \u201cWe have identified a mechanism by which the risk factor \u2014 having high levels of corticosteroid \u2014 could put you at risk for the disease<\/strong>.<\/p>\n \u201cCorticosteroid uses the 5-lipoxygenase as a mechanism to damage the synapse, which results in memory and learning impairment, both key symptoms for Alzheimer\u2019s,\u201d said Pratico. \u201cSo that is strong support for the hypothesis that if you block 5-lipoxygenase, you can probably block the negative effects of corticosteroid in the brain.\u201d<\/span><\/p>\n The research was supported by National Institutes of Health and the Alzheimer Art Quilt Initiative.<\/p><\/blockquote>\n","protected":false},"excerpt":{"rendered":" From the Temple University press release via HealthCanal: A chemical hormone released in the body as a reaction to stress could be a key trigger of the mechanism for the… Read more »<\/a><\/p>\n","protected":false},"author":5,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[5,10,4,6],"tags":[195,42,18,194,62],"_links":{"self":[{"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/posts\/14265"}],"collection":[{"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/users\/5"}],"replies":[{"embeddable":true,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/comments?post=14265"}],"version-history":[{"count":5,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/posts\/14265\/revisions"}],"predecessor-version":[{"id":14301,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/posts\/14265\/revisions\/14301"}],"wp:attachment":[{"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/media?parent=14265"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/categories?post=14265"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/therapytoronto.ca\/news\/wp-json\/wp\/v2\/tags?post=14265"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}![\"senior_medication\"](\"http:\/\/therapytoronto.ca\/news\/wp-content\/uploads\/2012\/12\/senior_medication1.jpg\")
A chemical hormone released in the body as a reaction to stress could be a key trigger of the mechanism for the late onset of Alzheimer\u2019s disease<\/strong>, according to a study by researchers at Temple University.<\/p>\n