The enemy of our enemy could very well become our friend. Scientists have possibly uncovered a new approach to treating Alzheimer\u2019s disease\u2014one tied to the development of cancer.<\/p>\n
Researchers at the Huazhong University of Science and Technology in China studied mice given human cancers. These mice were protected from Alzheimer\u2019s, they found, likely due to a protein produced by tumor cells known as cystatin-C, or cyst-C. The research could lead to novel treatments for the currently incurable form of dementia, the researchers say.<\/p>\n
\u201cThese findings provide significant conceptual advances into cancer neuroscience and establish therapeutic avenues that are distinct from present amyloid-lowering strategies, the authors wrote in their paper, published<\/a> this month in the journal Cell.<\/p>\n A strange heated rivalry <\/p>\n With their work, the team was hoping to unravel a peculiar phenomenon documented<\/a> by past studies: People diagnosed with cancer are less likely to later develop Alzheimer\u2019s. Even stranger, this pattern goes both ways<\/a>, since people with Alzheimer\u2019s also seem less likely to catch cancer.<\/p>\n<\/p>\n They experimented with mice predisposed to develop Alzheimer\u2019s. They gave the mice (via transplantation) various cancers taken from people: lung, colon, and prostate cancer. Compared to the control group, the cancer-bearing mice didn\u2019t develop a high level of amyloid plaques in their brains, a key biomarker of Alzheimer\u2019s.<\/p>\n The researchers then went looking for a specific cause behind this protection. They ultimately found the tumor cells in these mice were producing noticeable amounts of cyst-C, and that the protein was able to travel through the bloodstream, bypass the blood-brain barrier, and reach the brain.<\/p>\n In subsequent mice experiments, they found evidence that cyst-C could bind to amyloid oligomers, the toxic clumps of amyloid that are a precursor to plaques. The cyst-C also seemed to activate microglia, the specialized immune cells of the brain, via a receptor called TREM2. Furthermore, it appeared that\u00a0these activated microglia were better at clearing out amyloid plaques.<\/p>\n And when they gave their Alzheimer\u2019s mice added amounts of cyst-C, the mice became better at solving mazes, indicating their cognition and memory had improved.<\/p>\n What does it all mean? <\/p>\n This research, impressive as it is, is still in its early days. More studies will be needed to know whether cyst-C\u2019s effects against Alzheimer\u2019s can actually be seen in people as opposed to mice, for instance. Even if this work does bear fruit, no one\u2019s suggesting that we should try to get cancer as a way to avoid Alzheimer\u2019s down the road.<\/p>\n<\/p>\n That said, the findings certainly do provide more places for scientists to start looking for the next Alzheimer\u2019s treatment, whether it\u2019s in cyst-C, TREM2 activation, or other compounds produced by cancer cells. That\u2019s more help we urgently need. It\u2019s estimated<\/a> at least 7 million Americans currently have Alzheimer\u2019s, a number that could nearly double within the next few decades. And even the best medications today only modestly slow the progression of the disease, which is still currently 100% fatal.<\/p>\n","protected":false},"excerpt":{"rendered":"The enemy of our enemy could very well become our friend. Scientists have possibly uncovered a new approach…\n","protected":false},"author":3,"featured_media":545672,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":"","_share_on_mastodon":"0"},"categories":[11],"tags":[10263,235,240069,210,67,132,68],"class_list":["post-545671","post","type-post","status-publish","format-standard","has-post-thumbnail","category-health","tag-alzheimers-disease","tag-cancer","tag-experimental-research","tag-health","tag-united-states","tag-unitedstates","tag-us"],"share_on_mastodon":{"url":"https:\/\/pubeurope.com\/@us\/115964364978805916","error":""},"_links":{"self":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/545671","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/users\/3"}],"replies":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/comments?post=545671"}],"version-history":[{"count":0,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/posts\/545671\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media\/545672"}],"wp:attachment":[{"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/media?parent=545671"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/categories?post=545671"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.europesays.com\/us\/wp-json\/wp\/v2\/tags?post=545671"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}