{"id":270794,"date":"2026-01-06T19:17:14","date_gmt":"2026-01-06T19:17:14","guid":{"rendered":"https:\/\/www.europesays.com\/ie\/270794\/"},"modified":"2026-01-06T19:17:14","modified_gmt":"2026-01-06T19:17:14","slug":"how-the-brain-protects-itself-from-alzheimers-disease-study","status":"publish","type":"post","link":"https:\/\/www.europesays.com\/ie\/270794\/","title":{"rendered":"How the brain protects itself from Alzheimer\u2019s disease: study"},"content":{"rendered":"

High levels of calcium are toxic to cells and contribute to loss of neurons in Alzheimer\u2019s disease<\/a>.<\/p>\n

A new JCI Insight study identifies a mechanism through which the young brain protects itself against high calcium levels, and it could help scientists learn how to protect the brain from this devastating neurodegenerative condition.<\/p>\n

Glyoxalase 1 (GLO1) is a protein that plays an essential role in getting rid of toxic byproducts in cells. In the study, Yale School of Medicine<\/a>, or YSM, researchers discovered elevated GLO1 levels in the brains of animals with excessive levels of cellular calcium, finding that the brain increased GLO1 expression as a protective mechanism to mitigate the effects of the calcium dysregulation.<\/p>\n

However, with advancing age, GLO1 activity declined, the researchers found, which may make the brain less resilient to neurodegeneration. The study could inform the development of therapeutics that target GLO1 and prevent neurodegeneration.<\/p>\n

\u201cWe discovered how the brain itself deals with calcium leak and uses a resilience factor that erodes with age,\u201d says Amy Arnsten, PhD, Albert E. Kent Professor of Neuroscience and the study\u2019s co-principal investigator.<\/p>\n

\u201cIf we could keep this mechanism going, we\u2019d be protecting the brain in a way that the brain itself has devised.\u201d<\/p>\n

The study was a collaboration between Arnsten\u2019s laboratory and the laboratory of Lauren Hachmann Sansing, MD, professor of neurology at YSM.<\/p>\n

How calcium dysregulation impacts the brain<\/p>\n

Arnsten\u2019s laboratory focuses on calcium dysregulation at a channel known as ryanodine receptor 2 (RyR2), which releases calcium from storage within a cell\u2019s smooth endoplasmic reticulum.<\/p>\n

\u201cThis channel is like a faucet that you can turn on and off,\u201d says\u00a0Elizabeth Woo, an MD-PhD student at YSM and the study\u2019s first author. \u201cIt can cause calcium to come out into the neuron, which has many downstream effects.\u201d<\/p>\n

\n

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Previous research has shown that RyR2 can become altered with age so that the faucet is constantly \u201con,\u201d and that these changes are associated with Alzheimer\u2019s disease and even Long COVID.<\/p>\n

In their new study, the researchers explored how the brain responds to this unregulated influx of calcium.<\/p>\n

The team used an animal model in which RyR2 was genetically altered to always be \u201con,\u201d causing chronic calcium leakage in the brain. They observed elevated GLO1 expression and activity in both the prefrontal cortex and hippocampus, two regions that are important for cognition and memory. GLO1 expression initially increased with age, peaking at 12 months in mice, but then declined in older animals.<\/p>\n

Then, the researchers introduced the older animals to a T-shaped maze designed to test their memory. They found that those with genetically modified RyR2 receptors who no longer had elevated GLO1 had worse memory compared to their healthy counterparts.<\/p>\n

The findings confirmed that calcium dysfunction is associated with worsened cognition.<\/p>\n

\n

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The study points to GLO1 expression as a potential mechanism in the brain to compensate for chronic calcium dysregulation. \u201cCalcium is a very powerful mediator in the brain,\u201d says Woo. \u201cGLO1 has detoxifying properties that can help the brain counter the changes in calcium over time.\u201d<\/p>\n

The researchers are hopeful that uncovering the processes preceding Alzheimer\u2019s disease could one day lead to new therapies.<\/p>\n

\n

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\u201cThere\u2019s a lot of important parallel research looking into how to treat Alzheimer\u2019s disease once it\u2019s developed,\u201d Woo says. \u201cBut as the upstream biology becomes clearer, we can also develop preventative therapeutics to target the disease before it becomes an issue.\u201d<\/p>\n

Isabella Backman is a senior science writer and editor at Yale School of Medicine. This story is shared by Yale School of Medicine.<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"High levels of calcium are toxic to cells and contribute to loss of neurons in Alzheimer\u2019s disease. A…\n","protected":false},"author":2,"featured_media":270795,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[275],"tags":[869,138042,31234,141,138043,10401,50978,38395,2597,18,135,475,474,19,17,81105,66249,72543,13360,138044,138045,172,133,20581,57653],"class_list":{"0":"post-270794","1":"post","2":"type-post","3":"status-publish","4":"format-standard","5":"has-post-thumbnail","7":"category-healthcare","8":"tag-alzheimers-disease","9":"tag-brain-degeneration","10":"tag-brains","11":"tag-calcium","12":"tag-calcium-dysfunction","13":"tag-cognition","14":"tag-connecticut-news","15":"tag-ct-news","16":"tag-education","17":"tag-eire","18":"tag-health","19":"tag-health-care","20":"tag-healthcare","21":"tag-ie","22":"tag-ireland","23":"tag-leaks","24":"tag-long-covid","25":"tag-mice","26":"tag-neurodegeneration","27":"tag-preventative-therapeutics","28":"tag-professor-of-neuroscience","29":"tag-research","30":"tag-science","31":"tag-yale-school-of-medicine","32":"tag-yale-university"},"share_on_mastodon":{"url":"https:\/\/pubeurope.com\/@ie\/115849766040749547","error":""},"_links":{"self":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts\/270794","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/comments?post=270794"}],"version-history":[{"count":0,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/posts\/270794\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/media\/270795"}],"wp:attachment":[{"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/media?parent=270794"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/categories?post=270794"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.europesays.com\/ie\/wp-json\/wp\/v2\/tags?post=270794"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}