{"id":3182,"date":"2017-08-29T16:00:00","date_gmt":"2017-08-29T20:00:00","guid":{"rendered":"https:\/\/www.med.unc.edu\/neurology\/unraveling-alzheimer2019s-new-study-documents-how-brain-cells-go-bad-1\/"},"modified":"2022-12-05T14:23:47","modified_gmt":"2022-12-05T19:23:47","slug":"unraveling-alzheimer2019s-new-study-documents-how-brain-cells-go-bad-1","status":"publish","type":"post","link":"https:\/\/www.med.unc.edu\/neurology\/unraveling-alzheimer2019s-new-study-documents-how-brain-cells-go-bad-1\/","title":{"rendered":"Unraveling Alzheimer\u2019s: New Study Documents How Brain Cells Go Bad"},"content":{"rendered":"

<\/p>\n

In a first-of-its-kind study, UNC researchers show how a damaging cascade of events inside brain cells \u2013 and related to Alzheimer\u2019s disease \u2013 can be stopped or reversed.<\/p>\n

\n
\"image2\"
Todd Cohen, PhD<\/figcaption><\/figure>\n<\/div>\n
\n

August 29, 2017<\/p>\n

\"Figure
Neurons treated with Alzheimer’s-associated proteins exhibit drastic calcium increases (blue, green, yellow, red to white), and the cells form tau-filled beaded structures (shown with arrows) identical to neurons seen in Alzheimer’s patients.<\/figcaption><\/figure>\n

CHAPEL HILL, NC \u2013 In the brains of people with Alzheimer\u2019s disease, there are abnormal deposits of amyloid beta protein and tau protein, and swarms of activated immune cells. But scientists do not fully understand how these three major factors combine to drive the disease. Now, UNC School of Medicine and National Institutes of Health researchers have untangled the mystery in lab experiments to reveal why one Alzheimer\u2019s drug currently in development shows promise and how other therapies might reverse the disease process.<\/p>\n

Led by Todd Cohen, PhD, assistant professor of neurology, UNC scientists used human cell cultures to show how amyloid beta can trigger a dramatic inflammatory response in immune cells and how that interaction damages neurons. Then they showed how that kind of neuron damage leads to the formation of bead-like structures filled with abnormal tau protein. Similar bead-like structures are known to form in the brain cells of people with Alzheimer\u2019s disease.<\/p>\n

The UNC researchers also identified two proteins \u2013 MMP-9 and HDAC6 \u2013 that help promote this harmful, amyloid-to-inflammation-to-tau cascade. These proteins and others associated with them could become drug targets to treat or prevent Alzheimer\u2019s.<\/p>\n

\u201cIt\u2019s exciting that we were able to observe tau \u2013 the major Alzheimer\u2019s protein \u2013 inside these beaded structures,\u201d said Cohen, who is also a member of the UNC Neuroscience Center. \u201cWe think that preventing these structures from forming would leave people with healthier neurons that are more resistant to Alzheimer\u2019s.\u201d<\/p>\n

The findings, published today in the journal Cell Reports, <\/i>were made possible through a collaboration of three UNC labs led by Rick Meeker, PhD, Xian Chen, PhD, and Cohen, as well as the NIH lab of Jau-Shyong Hong, PhD.<\/p>\n

To begin the study, Cohen, Meeker, and colleagues exposed immune cells normally found in an activated, inflammatory state in Alzheimer\u2019s brains to tiny clusters of amyloid beta \u2013 or oligomers, which are believed to be the most harmful forms of the protein.<\/p>\n

\u201cOur thinking was that the amyloid beta oligomers would activate an inflammatory response in these immune cells, as prior research from Meeker suggested, and we wanted to see if this would induce pathological forms of tau when given to neurons,\u201d Cohen said.<\/p>\n

The researchers then focused on the fluid in which the immune cells had been growing. This fluid, which was filled with inflammatory factors \u2013 or proteins \u2013 resembled the fluid in which these cells typically live inside human brains. Cohen\u2019s team added this fluid to cultures of human cortical neurons. The neurons soon developed abnormal, bead-like swellings along their axons and dendrites that were well-studied previously in Meeker\u2019s laboratory.<\/p>\n

This \u201cneuritic beading\u201d on axons and dendrites has been seen in Alzheimer\u2019s patients and has been considered an early sign of neuronal damage, although it hasn\u2019t been clear how beading was connected to abnormal tau or if the beading led to Alzheimer\u2019s disease.<\/p>\n

Cohen\u2019s team then looked for tau in the beads and found a striking accumulation of it, though it was in an abnormal form and undetectable with the usual tools scientists use to detect the type of tau typically seen in Alzheimer\u2019s patients. Instead, the beaded tau was modified in a different way than previously thought. This modification is what Cohen said causes tau to become aggregated.<\/p>\n

Tau proteins normally provide structural support for long, railway-like structures called microtubules, which are used to transport key molecules along axons. For reasons that have never been clear, tau proteins in Alzheimer\u2019s-affected neurons have a different pattern. They are detached from microtubules, bear abnormal chemical modifications, and clump into long, tangled, and thread-like aggregates. Whether these tau aggregates actively harm neurons isn\u2019t clear, but prior studies suggested that the loss of tau from microtubules and resulting disruption of axonal transport might cause serious damage.<\/p>\n

The finding of abnormal tau in the neuritic beads indicated that these beads could mark tau\u2019s entry into the Alzheimer\u2019s disease process. Within the beads, Cohen\u2019s lab also found high calcium levels, which are known to harm neurons and are considered an important feature of neurons in people with Alzheimer\u2019s.<\/p>\n

\u201cWe think these neuroinflammatory factors trigger this cascade,\u201d Cohen said. \u201cThey flood the neuron with calcium. And we think that once the calcium accumulates, it causes tau to become abnormally modified. This probably leads to a snowball effect: tau detaches from microtubules and is trafficked throughout the neuron, ending up in these beads. One possibility is that these tau-filled beads are the sites where the classic tangle-like aggregates of tau will eventually emerge, which is the hallmark of Alzheimer\u2019s disease.\u201d<\/p>\n

A team led by collaborating researcher Xian Chen, PhD, associate professor of biochemistry and biophysics at UNC, used mass spectrometry to sort out the amyloid beta-induced neuroinflammatory molecules that had triggered the calcium influx and neuritic beading. They were able to show that one protein in particular, MMP-9, was responsible for some of these adverse effects.<\/p>\n

\u201cMMP-9 is an inflammatory protein shown to be elevated in the brains of Alzheimer\u2019s patients,\u201d Cohen said. \u201cIn our study, we show that MMP-9 alone can trigger a calcium influx that floods the neuron.\u201d<\/span><\/p>\n

The researchers also identified the protein HDAC6, which originates from within neurons and concentrates in the neuritic beads. Normally, HDAC6 is thought to detect unwanted protein aggregates within neurons and transport them away for disposal. However, blocking HDAC6 stopped nearly all beads from forming in Cohen\u2019s lab experiments.<\/p>\n

Both of these proteins have been found to be elevated in affected areas of Alzheimer\u2019s brains. Drug companies are now developing and testing HDAC6 inhibitors, which have performed surprisingly well in early studies, although it has not been fully understood how these inhibitors work.<\/p>\n

\u201cOur work might explain why HDAC6 inhibitors have shown such early promise,\u201d Cohen said. \u201cAnd we think our work can help inform the development of other kinds of inhibitors that affect this cascade, particularly those that might impact cognitive processes.\u201d<\/p>\n

A therapeutic strategy to block HDAC6 \u2013 and\/or MMP-9 \u2013 might have applications beyond Alzheimer\u2019s. Neuritic beading is seen in several other neurodegenerative diseases as well as after head injury. Scientists have even observed beading to small extents in seemingly healthy elderly brains. Beading might be a general mechanism underlying cognitive decline, Cohen said.<\/p>\n

In their study, Cohen and colleagues found some tau-filled neuritic beads in the brains of aged mice. And they discovered that chronic neuroinflammation could induce the beads to form in younger mice.<\/span><\/p>\n

The researchers are now focused on creating a mouse model to confirm and further investigate the amyloid-to-inflammation-to tau process seen in this Cell Reports<\/i> study.<\/p>\n

\u201cIf we can demonstrate this cascade in a wild-type mouse, then we\u2019ll be able to study Alzheimer\u2019s and test therapies in ordinary lab mice without the need for artificial genetic engineering used in traditional Alzheimer\u2019s mouse models,\u201d Cohen said.<\/p>\n

The lead author of the study was UNC postdoctoral researcher Jui-Heng Tseng, PhD. Other co-authors were Ling Xie, Youmei Xie,<\/i> Lauren Allen, Deepa Ajit, Meeker, Chen, and Hong.<\/i><\/p>\n

Xian Chen is an associate professor of biochemistry and biophysics, Faculty Director of the Quantitative Proteomics Center for Disease Marker Discovery, and member of the UNC Lineberger Comprehensive Cancer Center. Rick Meeker is a professor of neurology at UNC. Jau-Shyong Hong heads the Neuropharmacology Group within the Laboratory of Toxicology and Pharmacology.<\/i><\/p>\n

The National Institutes of Health, the Alzheimer\u2019s Association, the National Center for Advancing Translational Sciences, and the American Federation for Aging Research funded this work.<\/i><\/p>\n

Media Contact: Mark Derewicz, 919-923-0959, <\/span>mark.derewicz@unchealth.unc.edu<\/a>
\n<\/span><\/i><\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

<\/p>\n

In a first-of-its-kind study, UNC researchers show how a damaging cascade of events inside brain cells \u2013 and related to Alzheimer\u2019s disease \u2013 can be stopped or reversed.<\/p>\n","protected":false},"author":58435,"featured_media":3183,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"layout":"","cellInformation":"","apiCallInformation":"","footnotes":"","_links_to":"","_links_to_target":""},"categories":[2],"tags":[3],"class_list":["post-3182","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-news","tag-home-page-news","odd"],"acf":[],"yoast_head":"\nUnraveling Alzheimer\u2019s: New Study Documents How Brain Cells Go Bad | Department of Neurology<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" 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