Transthyretin amyloid deposition in the ligamentum flavum of an Italian cohort of patients with lumbar spinal stenosis.

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Title: Transthyretin amyloid deposition in the ligamentum flavum of an Italian cohort of patients with lumbar spinal stenosis.
Authors: Vitali, Francesca (AUTHOR), Fenu, Silvia (AUTHOR), Izzo, Alessandro (AUTHOR), Montano, Nicola (AUTHOR), Polli, Filippo Maria (AUTHOR), Rapisarda, Alessandro (AUTHOR), Costa, Francesco (AUTHOR), Schiariti, Marco Paolo (AUTHOR), Gessi, Marco (AUTHOR), Marucci, Gianluca (AUTHOR), Giaccone, Giorgio (AUTHOR), Sciarrone, Maria Ausilia (AUTHOR), Guglielmino, Valeria (AUTHOR), Romano, Angela (AUTHOR), Pareyson, Davide (AUTHOR), Luigetti, Marco (AUTHOR)
Source: Neurological Sciences. Jul2025, Vol. 46 Issue 7, p3295-3298. 4p.
Subjects: Spinal stenosis, Amyloid plaque, Spinal canal, DNA analysis, Amyloid
Abstract: Transthyretin amyloidosis (ATTR amyloidosis) is a rare systemic disorder characterized by the extracellular deposition of amyloid fibrils, which can affect multiple tissues. Lumbar spinal stenosis (LSS), a condition involving narrowing of the lumbar spinal canal, has been frequently associated with amyloid deposition in the ligamentum flavum (LF). This study aimed to evaluate the prevalence of ATTR deposits in LF samples obtained from patients undergoing LSS surgery at two Italian centers. A total of 37 patients were included, with LF thickness measured via pre-operative MRI scans. Amyloid deposits were detected in 27% of patients, all confirmed as ATTR by immunohistochemistry. DNA analysis revealed no pathogenic mutations in the TTR gene, suggesting that the detected amyloid fibrils originated from the wild-type protein. LF thickness values were consistent with those reported in literature, supporting LF thickening as a potential marker of amyloid deposition. These findings contribute to the understanding of ATTR involvement in LSS and highlight the need for further research to explore the pathophysiological mechanisms and clinical significance of amyloid deposits in the LF. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Transthyretin amyloid deposition in the ligamentum flavum of an Italian cohort of patients with lumbar spinal stenosis.
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  Data: <searchLink fieldCode="AR" term="%22Vitali%2C+Francesca%22">Vitali, Francesca</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Fenu%2C+Silvia%22">Fenu, Silvia</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Izzo%2C+Alessandro%22">Izzo, Alessandro</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Montano%2C+Nicola%22">Montano, Nicola</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Polli%2C+Filippo+Maria%22">Polli, Filippo Maria</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Rapisarda%2C+Alessandro%22">Rapisarda, Alessandro</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Costa%2C+Francesco%22">Costa, Francesco</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Schiariti%2C+Marco+Paolo%22">Schiariti, Marco Paolo</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Gessi%2C+Marco%22">Gessi, Marco</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Marucci%2C+Gianluca%22">Marucci, Gianluca</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Giaccone%2C+Giorgio%22">Giaccone, Giorgio</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sciarrone%2C+Maria+Ausilia%22">Sciarrone, Maria Ausilia</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Guglielmino%2C+Valeria%22">Guglielmino, Valeria</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Romano%2C+Angela%22">Romano, Angela</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Pareyson%2C+Davide%22">Pareyson, Davide</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Luigetti%2C+Marco%22">Luigetti, Marco</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Neurological+Sciences%22">Neurological Sciences</searchLink>. Jul2025, Vol. 46 Issue 7, p3295-3298. 4p.
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  Data: <searchLink fieldCode="DE" term="%22Spinal+stenosis%22">Spinal stenosis</searchLink><br /><searchLink fieldCode="DE" term="%22Amyloid+plaque%22">Amyloid plaque</searchLink><br /><searchLink fieldCode="DE" term="%22Spinal+canal%22">Spinal canal</searchLink><br /><searchLink fieldCode="DE" term="%22DNA+analysis%22">DNA analysis</searchLink><br /><searchLink fieldCode="DE" term="%22Amyloid%22">Amyloid</searchLink>
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  Label: Abstract
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  Data: Transthyretin amyloidosis (ATTR amyloidosis) is a rare systemic disorder characterized by the extracellular deposition of amyloid fibrils, which can affect multiple tissues. Lumbar spinal stenosis (LSS), a condition involving narrowing of the lumbar spinal canal, has been frequently associated with amyloid deposition in the ligamentum flavum (LF). This study aimed to evaluate the prevalence of ATTR deposits in LF samples obtained from patients undergoing LSS surgery at two Italian centers. A total of 37 patients were included, with LF thickness measured via pre-operative MRI scans. Amyloid deposits were detected in 27% of patients, all confirmed as ATTR by immunohistochemistry. DNA analysis revealed no pathogenic mutations in the TTR gene, suggesting that the detected amyloid fibrils originated from the wild-type protein. LF thickness values were consistent with those reported in literature, supporting LF thickening as a potential marker of amyloid deposition. These findings contribute to the understanding of ATTR involvement in LSS and highlight the need for further research to explore the pathophysiological mechanisms and clinical significance of amyloid deposits in the LF. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10072-025-08101-1
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        Text: English
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        Type: general
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