{"id":15006,"date":"2025-04-17T13:38:48","date_gmt":"2025-04-17T17:38:48","guid":{"rendered":"https:\/\/www.med.unc.edu\/cellbiophysio\/?p=15006"},"modified":"2025-04-17T13:42:05","modified_gmt":"2025-04-17T17:42:05","slug":"pathogen-sensing-immune-protein-in-the-brain","status":"publish","type":"post","link":"https:\/\/www.med.unc.edu\/cellbiophysio\/pathogen-sensing-immune-protein-in-the-brain\/","title":{"rendered":"The unexpected role of a pathogen-sensing immune protein in the brain"},"content":{"rendered":"

Trimming neuronal axons involves a distinct pathway and a rare pathogen-sensing immune protein that could have implications for Alzheimer\u2019s disease.<\/em><\/p>\n

\n

Neurons have the remarkable ability to kill parts of themselves without dying in a phenomenon known as axon pruning. During axon pruning, neurons trim unnecessary axons, long, threadlike projections from nerve cells that transmit electrical signals to other cells.<\/p>\n

\u201cAxon pruning fine tunes the connectivity and communications between neurons. Just think about the preciseness with which this system must consolidate one axon but not the other,\u201d said Mohanish Deshmukh<\/a>, a professor in the Department of Cell Biology and Physiology and the Neuroscience Center at the University of North Carolina at Chapel Hill.<\/p>\n

In an article published in EMBO Reports<\/em><\/a>, Selena Romero, a scientist in Deshmukh\u2019s lab who recently defended her PhD, found that axon pruning shares much of the same molecular degeneration machinery as apoptosis, a programmed mechanism by which cells die. However, Romero found that there are distinct differences. In particular, axon pruning requires the unexpected use of an immune molecule called NLRP1 typically activated during pathogen infection.<\/p>\n

\u201cIt didn\u2019t make sense for the neuron to express this because our axon pruning model doesn\u2019t use viruses or any inflammatory stimulus,\u201d said Romero. Unlike apoptosis, axon pruning does not require the apoptosome complex to initiate degeneration. This suggested to Romero and Deshmukh, that axon pruning may occur through a different pathway.<\/p>\n

\u201cWe started looking for other mechanisms cells use to activate caspases [the enzymes needed for degeneration] that are independent of the apoptosome,\u201d said Romero. They came across the inflammasome complex, which typically activates during immune responses.<\/p>\n

She systematically knocked out the expression of the essential components involved in the inflammasome complex one at a time until finally, she found the lynchpin protein. When she removed NLRP1 expression, axon pruning did not occur.<\/p>\n

\"A
Romero found that when she removed NLRP1 expression from neurons the infrapyramidal bundle (IPB) of axons, which is typically trimmed during development grew to almost the same length as the suprapyramidal bundle (SPB) of axons in mouse brains, indicating that NLRP1 stopped developmental axon pruning. IMAGE CREDIT: Selena Romero, PhD<\/figcaption><\/figure>\n

How an immune protein got a new job in the brain<\/strong><\/p>\n

\u201cNLRP1 belongs to a family of pathogen sensing proteins. This one is an outlier and very few pathogens can activate it. It\u2019s not the most well studied,\u201d said Deshmukh. NLRP1 activates in response to infections with anthrax and several viruses. It is also not a neuroimmune protein that typically interacts with the developing nervous system. \u201cFrom our perspective, that is even more unexpected in that it is a bonafide immune molecule. What the heck is it doing in neurons in a nonpathogenic or diseased setting,\u201d said Deshmukh.<\/p>\n

Romero reasoned that one advantage of utilizing the pathogen-sensing molecule NLRP1 for physiological axon pruning is that it may have evolved to quarantine potentially problematic axons to protect the body. If a virus infects distal axons in someone\u2019s fingertips, for example, the virus could retroactively travel through the spine and affect the central nervous system. Thus, NLRP1 may not only regulate physiological axon pruning but could also halt the spread of pathogens in the nervous system.<\/p>\n

\u201cThe other thing is that we have far fewer proteins in our genome than we thought we did,\u201d said Deshmukh. When researchers started sequencing the human genome, they thought humans had 50,000 to 100,000 genes. Now, they know humans have only 20,000 protein-coding genes, just 1,000 more than the roundworm C. elegans<\/em>. \u201cWe\u2019re going to use the same proteins for multiple functions. NLRP1 has one ability to detect a pathogen and cause degradation. Why not engage the same protein under physiological conditions,\u201d said Deshmukh.<\/p>\n

A potential therapeutic role in disease<\/strong><\/p>\n

NLRP1 may also have an unexpected role in Alzheimer\u2019s disease. Another group noted that loss of NLRP1 expression in neurons improved Alzheimer\u2019s disease outcomes in animal models. \u201cNow that we\u2019ve discovered the axon pruning function of NLRP1, it could very well be the case that there is unexpected hyperactivation of NLRP1 in Alzheimer\u2019s disease, and inhibiting it could be a good therapeutic target,\u201d said Deshmukh.<\/p>\n

Romero and Deshmukh\u2019s findings show unequivocally that although apoptosis and axon pruning share many of the same molecular degradation events, they are two distinct pathways. Now they are on the quest to better understand those pathways and their roles in human health and disease.<\/p>\n

\n

Reference\u00a0<\/strong><\/p>\n

Romero, SE., Geden, MJ., Basundra, R., et al. The NLRP1 inflammasome is an essential and selective mediator of axon pruning in neurons<\/a>. EMBO Reports<\/em> 26<\/strong>(7), 1724-1736 (2025).<\/p>\n

Written by Tiffany Garbutt, PhD<\/em><\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

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During axon pruning, neurons trim unnecessary axons, long, threadlike projections from nerve cells that transmit electrical … Read more<\/a><\/p>\n","protected":false},"author":77299,"featured_media":15007,"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":[52,2],"tags":[121,122,123,84,75],"featured-item":[],"class_list":["post-15006","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-featured-news","category-news","tag-alzheimers-disease","tag-axons","tag-brain","tag-neurons","tag-neuroscience","odd"],"acf":[],"yoast_head":"\nThe unexpected role of a pathogen-sensing immune protein in the brain - Department of Cell Biology and Physiology<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.med.unc.edu\/cellbiophysio\/pathogen-sensing-immune-protein-in-the-brain\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"The unexpected role of a pathogen-sensing immune protein in the brain - Department of Cell Biology and Physiology\" \/>\n<meta property=\"og:description\" content=\"Trimming neuronal axons involves a distinct pathway and a rare pathogen-sensing immune protein that could have implications for Alzheimer\u2019s disease. 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