Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable

Lewy Body Disease (LBD) and Multiple System Atrophy (MSA) are synucleinopathies with distinct prognoses and neuropathologies, however, with overlapping clinical symptoms. Different disease characteristics are proposed to be determined by distinct conformations of alpha-synuclein (α-Syn) aggregates,...

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Main Authors: Rabab Al-Lahham, Mark E. Corkins, Mohd Ishtikhar, Prakruti Rabadia, Santiago Ramirez, Victor Banerjee, Mohammad Shahnawaz
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Cells
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Online Access:https://www.mdpi.com/2073-4409/14/10/684
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author Rabab Al-Lahham
Mark E. Corkins
Mohd Ishtikhar
Prakruti Rabadia
Santiago Ramirez
Victor Banerjee
Mohammad Shahnawaz
author_facet Rabab Al-Lahham
Mark E. Corkins
Mohd Ishtikhar
Prakruti Rabadia
Santiago Ramirez
Victor Banerjee
Mohammad Shahnawaz
author_sort Rabab Al-Lahham
collection DOAJ
description Lewy Body Disease (LBD) and Multiple System Atrophy (MSA) are synucleinopathies with distinct prognoses and neuropathologies, however, with overlapping clinical symptoms. Different disease characteristics are proposed to be determined by distinct conformations of alpha-synuclein (α-Syn) aggregates, which can self-propagate and spread between cells via a prion-like mechanism. The goal of this study is to investigate whether α-syn aggregates amplified from brain and CSF samples of LBD and MSA patients using the Seed Amplification Assay (SAA) maintain α-Syn seeding properties similar to those of α-syn aggregates derived from patients’ brains. To address this, SAA-amplified and un-amplified α-Syn aggregates from LBD and MSA patients’ brains, as well as SAA-amplified α-Syn aggregates from LBD and MSA patients’ CSF samples, were used to treat synuclein biosensor cells, and induced intracellular α-Syn inclusions were analyzed by confocal microscopy. Our data indicate that induced α-Syn aggregates from LBD and MSA patients’ brains have similar seeding properties and morphological characteristics in the α-Syn biosensor cells as those amplified from LBD and MSA patients’ brains, as well as those amplified from LBD and MSA patients’ CSF samples. In this study, we demonstrated that, regardless of the source of aggregates, the seeds from LBD and MSA produce cellular accumulation of α-Syn with distinct morphologies, confirming the presence of different conformational strains of α-Syn in LBD and MSA and allowing us to differentiate synucleinopathies based on the morphology of aggregates and seeding properties.
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spelling doaj-art-21b30c9ca36c41d8bc36cf50c9d6ff6f2025-08-20T01:56:17ZengMDPI AGCells2073-44092025-05-01141068410.3390/cells14100684Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically IndistinguishableRabab Al-Lahham0Mark E. Corkins1Mohd Ishtikhar2Prakruti Rabadia3Santiago Ramirez4Victor Banerjee5Mohammad Shahnawaz6Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USADepartment of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USAMitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USAMitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USAMitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USAMitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USAMitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USALewy Body Disease (LBD) and Multiple System Atrophy (MSA) are synucleinopathies with distinct prognoses and neuropathologies, however, with overlapping clinical symptoms. Different disease characteristics are proposed to be determined by distinct conformations of alpha-synuclein (α-Syn) aggregates, which can self-propagate and spread between cells via a prion-like mechanism. The goal of this study is to investigate whether α-syn aggregates amplified from brain and CSF samples of LBD and MSA patients using the Seed Amplification Assay (SAA) maintain α-Syn seeding properties similar to those of α-syn aggregates derived from patients’ brains. To address this, SAA-amplified and un-amplified α-Syn aggregates from LBD and MSA patients’ brains, as well as SAA-amplified α-Syn aggregates from LBD and MSA patients’ CSF samples, were used to treat synuclein biosensor cells, and induced intracellular α-Syn inclusions were analyzed by confocal microscopy. Our data indicate that induced α-Syn aggregates from LBD and MSA patients’ brains have similar seeding properties and morphological characteristics in the α-Syn biosensor cells as those amplified from LBD and MSA patients’ brains, as well as those amplified from LBD and MSA patients’ CSF samples. In this study, we demonstrated that, regardless of the source of aggregates, the seeds from LBD and MSA produce cellular accumulation of α-Syn with distinct morphologies, confirming the presence of different conformational strains of α-Syn in LBD and MSA and allowing us to differentiate synucleinopathies based on the morphology of aggregates and seeding properties.https://www.mdpi.com/2073-4409/14/10/684Parkinson’s diseasemultiple system atrophyα-synucleinaggregationSAAbiosensor cells
spellingShingle Rabab Al-Lahham
Mark E. Corkins
Mohd Ishtikhar
Prakruti Rabadia
Santiago Ramirez
Victor Banerjee
Mohammad Shahnawaz
Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
Cells
Parkinson’s disease
multiple system atrophy
α-synuclein
aggregation
SAA
biosensor cells
title Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
title_full Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
title_fullStr Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
title_full_unstemmed Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
title_short Intracellular Inclusions Induced by Patient-Derived and Amplified α-Synuclein Aggregates Are Morphologically Indistinguishable
title_sort intracellular inclusions induced by patient derived and amplified α synuclein aggregates are morphologically indistinguishable
topic Parkinson’s disease
multiple system atrophy
α-synuclein
aggregation
SAA
biosensor cells
url https://www.mdpi.com/2073-4409/14/10/684
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AT markecorkins intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable
AT mohdishtikhar intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable
AT prakrutirabadia intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable
AT santiagoramirez intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable
AT victorbanerjee intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable
AT mohammadshahnawaz intracellularinclusionsinducedbypatientderivedandamplifiedasynucleinaggregatesaremorphologicallyindistinguishable