said Macauley<\/a>. \u201cMicroglia are immune cells that, when they respond to plaques, kick off this elaborate cascade of inflammation, as if the microglia are partying all night, and keeping the brain awake.\u201d<\/p>\nSeeing inside<\/p>\n
To isolate the effects of Alzheimer\u2019s from the natural changes of aging, the team compared two groups of mice: those with a genetic predisposition to develop amyloid plaques and \u201cwild-type\u201d mice that aged normally. They studied these mice at six months, when plaques first emerge, and at 18 months, representing late-stage disease.<\/p>\n
The researchers employed several sophisticated technologies to track these changes and monitor exactly when the mice were in deep, restorative sleep, dreaming sleep, or awake.<\/p>\n
To prove that microglia were the cause of sleep loss, the team used a drug called Pexidartinib (PLX3397). This medication, originally used in cancer research, works by blocking a signal that microglia need to survive. By feeding the mice this drug for 14 days, they were able to temporarily remove 87% of the brain\u2019s immune cells to see if sleep would return.<\/p>\n
The team used a mathematical algorithm to separate the brain\u2019s electrical activity into different parts: periodic activity (the rhythmic waves we usually think of as brain waves) and aperiodic activity (the background electrical noise).<\/p>\n
To use a car metaphor, they were checking to see if the brain\u2019s engine was revving too high, even during rest.<\/p>\n
A new view is \u2018mind-blowing\u2019<\/p>\n
Macauley described the findings as \u201cmind-blowing and unexpected.\u201d The research revealed that the relationship between plaque buildup and sleep loss is not a simple downward slide.<\/p>\n
\u201cI expected that as plaque burden became more severe, sleep disruption would also worsen,\u201d said Constantino. \u201cThe disruptions in sleep and cortical EEG activity that occur at six months, when plaques first emerge, did not worsen by 18 months, despite more than double the amount of plaque burden.\u201d<\/p>\n
The researchers described this as a ceiling effect: even when plaque levels more than doubled, the sleep deficit remained stable. This suggests that the initial immune storm triggered by early plaques is what causes the damage, regardless of how many plaques follow.<\/p>\n
The study also clarified how the brain changes during normal aging compared to disease. Normal aging selectively reduces rapid eye movement (REM) sleep \u2014 the stage where we dream and consolidate memories. Amyloid pathology present in Alzheimer\u2019s selectively targets nonrapid eye movement (NREM) sleep or restorative sleep.<\/p>\n
\u201cThat restorative sleep is super important for physical repair, learning and memory and washing out the toxins of the day,\u201d Macauley said. \u201cWhen Alzheimer\u2019s patients lose this stage, they lose their brain\u2019s primary cleaning cycle, creating a feed-forward loop that may drive further damage.\u201d<\/p>\n
2 hours of sleep restored per night<\/p>\n
The most impactful finding was the result of the microglial depletion. When the immune cells were removed, the mice with Alzheimer\u2019s gained more than two hours of sleep per night. Their restorative NREM sleep bouts became longer, allowing them more opportunities to transition into healthy dreaming sleep important for making new memories.<\/p>\n
Crucially, this sleep was restored without changing the amount of amyloid plaques in the brain. This suggests that the body\u2019s inflammatory response is a reversible cause of sleep loss that can be treated independently of the plaques themselves.<\/p>\n
Answering the question of whether this vital sleep can be restored for humans, is the ultimate goal of this research\u2014to create affordable, noninvasive tools for people facing Alzheimer\u2019s disease that allow their brains to break the \u201cfeed-forward loop\u201d.<\/p>\n
This study, which was partly funded by grants from NIH, the Cure Alzheimer\u2019s Fund and The CART Fund, accomplished several things that can be built upon in future research.<\/p>\n
The team identified specific electrical signatures in the brain that distinguish Alzheimer\u2019s from normal aging, and they believe EEG could be used as a \u201creadily accessible, affordable and longitudinal biomarker of Alzheimer\u2019s disease.\u201d<\/p>\n
\u201cPortable EEG systems could allow us to monitor people in their home environments and potentially screen for changes associated with an Alzheimer\u2019s disease, without the initial need for expensive or invasive tests,\u201d Macauley said.<\/p>\n
This could allow doctors at local clinics across Kentucky to potentially screen those at risk before requiring individuals to travel hours for more specialized tests at major hospitals.<\/p>\n
Macauley\u2019s lab is now investigating how to calm down these immune cells without removing them entirely. They are exploring the use of safe, existing medications \u2014 such as the diabetes drug Metformin or anti-seizure drug Stiripentol \u2014 to reset the way microglia use fuel and change how overactive these cells become. By stopping the immune cells from revving the brain\u2019s engine, they hope to restore sleep and improve quality of life years before memory loss begins.<\/p>\n
\u201cIf we can target that process, it might help with quality of life, attention, cognition and confusion,\u201d Macauley said.<\/p>\n
SHARE THE SLEEP TIPS By Sharing This on Social Media\u2026<\/p>\n","protected":false},"excerpt":{"rendered":"Credit: A. C. for Unsplash+ [By Christian Honce | UK College of Medicine] Picture this: You find a…\n","protected":false},"author":2,"featured_media":740548,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[11355,854,59,102,1906,547,370,56,54,55],"class_list":["post-740547","post","type-post","status-publish","format-standard","has-post-thumbnail","category-health","tag-breakthroughs","tag-dementia","tag-gb","tag-health","tag-mental-health","tag-research","tag-sleep","tag-uk","tag-united-kingdom","tag-unitedkingdom"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts\/740547","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/comments?post=740547"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/posts\/740547\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/media\/740548"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/media?parent=740547"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/categories?post=740547"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/uk\/wp-json\/wp\/v2\/tags?post=740547"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
![\"\"](\"https:\/\/www.newsbeep.com\/uk\/wp-content\/uploads\/2026\/08\/Senior-sleeping-old-aging-eye-mask-sick-in-bed-by-A-C-For-Unsplash-pZVOgkmBM0Y.jpeg\")
Credit: A. C. for Unsplash+<\/p>\n