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The transcription factor combination MEF2 and KLF7 promotes axonal sprouting in the injured spinal cord with functional improvement and regeneration-associated gene expression Mol. Neurodegener. (IF 14.9) Pub Date : 2025-02-08 Callan L. Attwell, Inés Maldonado-Lasunción, Ruben Eggers, Bastiaan A. Bijleveld, Ward M. Ellenbroek, Natascha Siersema, Lotte Razenberg, Dédé Lamme, Nitish D. Fagoe, Ronald E. van Kesteren, August B. Smit, Joost Verhaagen, Matthew R. J. Mason
Axon regeneration after injury to the central nervous system (CNS) is limited by an inhibitory environment but also because injured neurons fail to initiate expression of regeneration associated genes (RAGs). The potential of strong RAG expression to promote regeneration in the CNS is exemplified by the conditioning lesion model, whereby peripheral nerve injury promotes regeneration of centrally projecting
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Disparate and shared transcriptomic signatures associated with cortical atrophy in genetic behavioral variant frontotemporal degeneration Mol. Neurodegener. (IF 14.9) Pub Date : 2025-02-07 Ting Shen, Jacob W. Vogel, Vivianna M. Van Deerlin, EunRan Suh, Laynie Dratch, Jeffrey S. Phillips, Lauren Massimo, Edward B. Lee, David J. Irwin, Corey T. McMillan
Cortical atrophy is a common manifestation in behavioral variant frontotemporal degeneration (bvFTD), exhibiting spatial heterogeneity across various genetic subgroups, which may be driven by distinct biological mechanisms. We employed an integrative imaging transcriptomics approach to identify both disparate and shared transcriptomic signatures associated with cortical thickness in bvFTD with C9orf72
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Loss of MEF2C function by enhancer mutation leads to neuronal mitochondria dysfunction and motor deficits in mice Mol. Neurodegener. (IF 14.9) Pub Date : 2025-02-07 Ali Yousefian-Jazi, Suhyun Kim, Jiyeon Chu, Seung-Hye Choi, Phuong Thi Thanh Nguyen, Uiyeol Park, Min-gyeong Kim, Hongik Hwang, Kyungeun Lee, Yeyun Kim, Seung Jae Hyeon, Hyewhon Rhim, Hannah L. Ryu, Grewo Lim, Thor D. Stein, Kayeong Lim, Hoon Ryu, Junghee Lee
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the loss of both upper and lower motor neurons, leading to progressive paralysis. Both genetic alterations and epigenetic modifications contribute to neuronal dysfunction in the pathogenesis of ALS. However, the mechanism behind genetic mutations in the non-coding region of genes that affect epigenetic modifications
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Cellular senescence induced by cholesterol accumulation is mediated by lysosomal ABCA1 in APOE4 and AD Mol. Neurodegener. (IF 14.9) Pub Date : 2025-02-04 Shaowei Wang, Boyang Li, Jie Li, Zhiheng Cai, Cristelle Hugo, Yi Sun, Lu Qian, Julia TCW, Helena C. Chui, Dante Dikeman, Isaac Asante, Stan G. Louie, David A. Bennett, Zoe Arvanitakis, Alan T. Remaley, Bilal E. Kerman, Hussein N. Yassine
Cellular senescence, a hallmark of aging, has been implicated in Alzheimer’s disease (AD) pathogenesis. Cholesterol accumulation is known to drive cellular senescence; however, its underlying mechanisms are not fully understood. ATP-binding cassette transporter A1 (ABCA1) plays an important role in cholesterol homeostasis, and its expression and trafficking are altered in APOE4 and AD models. However
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Lewy body diseases and the gut Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-30 Timothy R. Sampson, Malú Gámez Tansey, Andrew B. West, Rodger A. Liddle
Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson. Recent experimental and human observational studies raise the possibility that pathogenic alpha-synuclein (⍺-syn) might develop in the GI tract and subsequently spread to susceptible brain regions. The cellular and mechanistic origins of ⍺-syn propagation in
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Molecular and cellular characteristics of cerebrovascular cell types and their contribution to neurodegenerative diseases Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-29 Francisco J. Garcia, Myriam Heiman
Many diseases and disorders of the nervous system suffer from a lack of adequate therapeutics to halt or slow disease progression, and to this day, no cure exists for any of the fatal neurodegenerative diseases. In part this is due to the incredible diversity of cell types that comprise the brain, knowledge gaps in understanding basic mechanisms of disease, as well as a lack of reliable strategies
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Cell-specific transcriptional signatures of vascular cells in Alzheimer’s disease: perspectives, pathways, and therapeutic directions Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-29 Soumilee Chaudhuri, Minyoung Cho, Julia C. Stumpff, Paula J. Bice, Özkan İş, Nilüfer Ertekin-Taner, Andrew J. Saykin, Kwangsik Nho
Alzheimer’s disease (AD) is a debilitating neurodegenerative disease that is marked by profound neurovascular dysfunction and significant cell-specific alterations in the brain vasculature. Recent advances in high throughput single-cell transcriptomics technology have enabled the study of the human brain vasculature at an unprecedented depth. Additionally, the understudied niche of cerebrovascular
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Lipidome disruption in Alzheimer’s disease brain: detection, pathological mechanisms, and therapeutic implications Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-27 Sijia He, Ziying Xu, Xianlin Han
Alzheimer’s disease (AD) is among the most devastating neurodegenerative disorders with limited treatment options. Emerging evidence points to the involvement of lipid dysregulation in the development of AD. Nevertheless, the precise lipidomic landscape and the mechanistic roles of lipids in disease pathology remain poorly understood. This review aims to highlight the significance of lipidomics and
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Emerging targets of α-synuclein spreading in α-synucleinopathies: a review of mechanistic pathways and interventions Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-23 Grace Kuo, Ramhari Kumbhar, William Blair, Valina L. Dawson, Ted M. Dawson, Xiaobo Mao
α-Synucleinopathies constitute a spectrum of neurodegenerative disorders, including Parkinson’s disease (PD), Lewy body dementia (LBD), Multiple System Atrophy (MSA), and Alzheimer’s disease concurrent with LBD (AD-LBD). These disorders are unified by a pathological hallmark: aberrant misfolding and accumulation of α-synuclein (α-syn). This review delves into the pivotal role of α-syn, the key agent
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APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-22 Kristine M. Tran, Nellie E. Kwang, Claire A. Butler, Angela Gomez-Arboledas, Shimako Kawauchi, Cassandra Mar, Donna Chao, Rocio A. Barahona, Celia Da Cunha, Kate I. Tsourmas, Zechuan Shi, Shuling Wang, Sherilyn Collins, Amber Walker, Kai-Xuan Shi, Joshua A. Alcantara, Jonathan Neumann, Duc M. Duong, Nicholas T. Seyfried, Andrea J. Tenner, Frank M. LaFerla, Lindsay A. Hohsfield, Vivek Swarup, Grant
Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer’s Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects. We introduced the R136S variant into mouse
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Genetic context modulates aging and degeneration in the murine retina Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-20 Olivia J. Marola, Michael MacLean, Travis L. Cossette, Cory A. Diemler, Amanda A. Hewes, Alaina M. Reagan, Jonathan Nyandu Kanyinda, Daniel A. Skelly, Gareth R. Howell
Age is the principal risk factor for neurodegeneration in both the retina and brain. The retina and brain share many biological properties; thus, insights into retinal aging and degeneration may shed light onto similar processes in the brain. Genetic makeup strongly influences susceptibility to age-related retinal disease. However, studies investigating retinal aging have not sufficiently accounted
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Chitinase-3-like-1: a multifaceted player in neuroinflammation and degenerative pathologies with therapeutic implications Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-18 Pharaoh Fellow Mwale, Cheng-Ta Hsieh, Ting-Lin Yen, Jing-Shiun Jan, Rajeev Taliyan, Chih-Hao Yang, Wen-Bin Yang
Chitinase-3-like-1 (CHI3L1) is an evolutionarily conserved protein involved in key biological processes, including tissue remodeling, angiogenesis, and neuroinflammation. It has emerged as a significant player in various neurodegenerative diseases and brain disorders. Elevated CHI3L1 levels have been observed in neurological conditions such as traumatic brain injury (TBI), Alzheimer’s disease (AD)
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SIRT2 and ALDH1A1 as critical enzymes for astrocytic GABA production in Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-15 Mridula Bhalla, Jinhyeong Joo, Daeun Kim, Jeong Im Shin, Yongmin Mason Park, Yeon Ha Ju, Uiyeol Park, Seonguk Yoo, Seung Jae Hyeon, Hyunbeom Lee, Junghee Lee, Hoon Ryu, C. Justin Lee
Alzheimer’s Disease (AD) is a neurodegenerative disease with drastically altered astrocytic metabolism. Astrocytic GABA and H2O2 are associated with memory impairment in AD and synthesized through the Monoamine Oxidase B (MAOB)-mediated multi-step degradation of putrescine. However, the enzymes downstream to MAOB in this pathway remain unidentified. Using transcriptomics analysis, we identified two
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Upregulated astrocyte HDAC7 induces Alzheimer-like tau pathologies via deacetylating transcription factor-EB and inhibiting lysosome biogenesis Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-13 Jinwang Ye, Suyue Zhong, Huali Wan, Xing Guo, Xuanbao Yao, Qiong Liu, Liming Chen, Jian-Zhi Wang, Shifeng Xiao
Astrocytes, the most abundant glial cell type in the brain, will convert into the reactive state in response to proteotoxic stress such as tau accumulation, a characteristic feature of Alzheimer's disease (AD) and other tauopathies. The formation of reactive astrocytes is partially attributed to the disruption of autophagy lysosomal signaling, and inhibiting of some histone deacetylases (HDACs) has
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RNA-Targeting CRISPR/CasRx system relieves disease symptoms in Huntington’s disease models Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-13 Yingqi Lin, Caijuan Li, Yizhi Chen, Jiale Gao, Jiawei Li, Chunhui Huang, Zhaoming Liu, Wei Wang, Xiao Zheng, Xichen Song, Jianhao Wu, Jiaxi Wu, Oscar Junhong Luo, Zhuchi Tu, Shihua Li, Xiao-Jiang Li, Liangxue Lai, Sen Yan
HD is a devastating neurodegenerative disorder caused by the expansion of CAG repeats in the HTT. Silencing the expression of mutated proteins is a therapeutic direction to rescue HD patients, and recent advances in gene editing technology such as CRISPR/CasRx have opened up new avenues for therapeutic intervention. The CRISPR/CasRx system was employed to target human HTT exon 1, resulting in an efficient
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Biophysical mapping of TREM2-ligand interactions reveals shared surfaces for engagement of multiple Alzheimer’s disease ligands Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-09 Jessica A. Greven, Joshua R. Wydra, Rory A. Greer, Cynthia Zhi, David A. Price, Jordyn D. Svoboda, Christopher L. M. Camitta, Mya Washington, Daisy W. Leung, Yuhua Song, Jen Alexander-Brett, Tom J. Brett
TREM2 is a signaling receptor expressed on microglia that has emerged as an important drug target for Alzheimer’s disease and other neurodegenerative diseases. While a number of TREM2 ligands have been identified, little is known regarding the structural details of how they engage. To better understand this, we created a protein library of 28 different TREM2 variants that could be used to map interactions
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VCP regulates early tau seed amplification via specific cofactors Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-07 Sushobhna Batra, Jaime Vaquer-Alicea, Clarissa Valdez, Skyler P. Taylor, Victor A. Manon, Anthony R. Vega, Omar M. Kashmer, Sourav Kolay, Andrew Lemoff, Nigel J. Cairns, Charles L. White, Marc I. Diamond
Neurodegenerative tauopathies may progress based on seeding by pathological tau assemblies, whereby an aggregate is released from one cell, gains entry to an adjacent or connected cell, and serves as a specific template for its own replication in the cytoplasm. Seeding into the complex cytoplasmic milieu happens within hours, implying the existence of unknown factors that regulate this process. We
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Positron emission tomography tracers for synucleinopathies Mol. Neurodegener. (IF 14.9) Pub Date : 2025-01-05 Jie Xiang, Zhentao Zhang, Shengxi Wu, Keqiang Ye
Synucleinopathies, such as Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy, are characterized by the aggregation of α-synuclein. Variations in brain distribution allow for differentiation among these diseases and facilitate precise clinical diagnosis. However, distinguishing between synucleinopathies and Parkinsonism with tauopathies poses a challenge, significantly impacting
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Distinct regulation of Tau Monomer and aggregate uptake and intracellular accumulation in human neurons Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-31 Amir T. Marvian, Tabea Strauss, Qilin Tang, Benjamin J. Tuck, Sophie Keeling, Daniel Rüdiger, Negar Mirzazadeh Dizaji, Hossein Mohammad-Beigi, Brigitte Nuscher, Pijush Chakraborty, Duncan S. Sutherland, William A. McEwan, Thomas Köglsperger, Stefan Zahler, Markus Zweckstetter, Stefan F. Lichtenthaler, Wolfgang Wurst, Sigrid Schwarz, Günter Höglinger
The prion-like spreading of Tau pathology is the leading cause of disease progression in various tauopathies. A critical step in propagating pathologic Tau in the brain is the transport from the extracellular environment and accumulation inside naïve neurons. Current research indicates that human neurons internalize both the physiological extracellular Tau (eTau) monomers and the pathological eTau
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Targeted long-read sequencing to quantify methylation of the C9orf72 repeat expansion Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-21 Evan Udine, NiCole A. Finch, Mariely DeJesus-Hernandez, Jazmyne L. Jackson, Matthew C. Baker, Siva Arumugam Saravanaperumal, Eric Wieben, Mark T.W. Ebbert, Jaimin Shah, Leonard Petrucelli, Rosa Rademakers, Björn Oskarsson, Marka van Blitterswijk
The gene C9orf72 harbors a non-coding hexanucleotide repeat expansion known to cause amyotrophic lateral sclerosis and frontotemporal dementia. While previous studies have estimated the length of this repeat expansion in multiple tissues, technological limitations have impeded researchers from exploring additional features, such as methylation levels. We aimed to characterize C9orf72 repeat expansions
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Dementia with lewy bodies patients with high tau levels display unique proteome profiles Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-19 Sinead Greally, Mukesh Kumar, Christoph Schlaffner, Hanne van der Heijden, Elisabeth S. Lawton, Deeptarup Biswas, Sabina Berretta, Hanno Steen, Judith A. Steen
Clinical studies have long observed that neurodegenerative disorders display a range of symptoms and pathological features and, in some cases, overlap, suggesting that these diseases exist on a spectrum. Dementia with Lewy Bodies (DLB), a synucleinopathy, is a prominent example, where symptomatic similarities with tauopathy, Alzheimer’s disease, are observed. Although tau pathology has been observed
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The UFMylation pathway is impaired in Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-18 Tingxiang Yan, Michael G. Heckman, Emily C. Craver, Chia-Chen Liu, Bailey D. Rawlinson, Xue Wang, Melissa E. Murray, Dennis W. Dickson, Nilufer Ertekin-Taner, Zhenkun Lou, Guojun Bu, Wolfdieter Springer, Fabienne C. Fiesel
Alzheimer’s disease (AD) is characterized by the presence of neurofibrillary tangles made of hyperphosphorylated tau and senile plaques composed of beta-amyloid. These pathognomonic deposits have been implicated in the pathogenesis, although the molecular mechanisms and consequences remain undetermined. UFM1 is an important, but understudied ubiquitin-like protein that is covalently attached to substrates
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Mystery of gamma wave stimulation in brain disorders Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-18 Qianting Deng, Chongyun Wu, Emily Parker, Jing Zhu, Timon Cheng-Yi Liu, Rui Duan, Luodan Yang
Neuronal oscillations refer to rhythmic and periodic fluctuations of electrical activity in the central nervous system that arise from the cellular properties of diverse neuronal populations and their interactions. Specifically, gamma oscillations play a crucial role in governing the connectivity between distinct brain regions, which are essential in perception, motor control, memory, and emotions
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Microglial CD2AP deficiency exerts protection in an Alzheimer’s disease model of amyloidosis Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-18 Lingliang Zhang, Lingling Huang, Yuhang Zhou, Jian Meng, Liang Zhang, Yunqiang Zhou, Naizhen Zheng, Tiantian Guo, Shanshan Zhao, Zijie Wang, Yuanhui Huo, Yingjun Zhao, Xiao-fen Chen, Honghua Zheng, David M. Holtzman, Yun-wu Zhang
The CD2-associated protein (CD2AP) was initially identified in peripheral immune cells and regulates cytoskeleton and protein trafficking. Single nucleotide polymorphisms (SNPs) in the CD2AP gene have been associated with Alzheimer’s disease (AD). However, the functional role of CD2AP, especially its role in microglia during AD onset, remains elusive. CD2AP protein levels in cultured primary cells
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Correction: The Parkinson’s disease risk gene cathepsin B promotes fibrillar alpha-synuclein clearance, lysosomal function and glucocerebrosidase activity in dopaminergic neurons Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-18 Jace Jones-Tabah, Kathy He, Nathan Karpilovsky, Konstantin Senkevich, Ghislaine Deyab, Isabella Pietrantonio, Thomas Goiran, Yuting Cousineau, Daria Nikanorova, Taylor Goldsmith, Esther del Cid Pellitero, Carol X.-Q. Chen, Wen Luo, Zhipeng You, Narges Abdian, Jamil Ahmad, Jennifer A. Ruskey, Farnaz Asayesh, Dan Spiegelman, Stanley Fahn, Cheryl Waters, Oury Monchi, Yves Dauvilliers, Nicolas Dupré, Irina
Correction: Mol Neurodegeneration 19, 88 (2024) https://doi.org/10.1186/s13024-024-00779-9 The authors wish to note the Grant ID, MFFF – 007905 relating to the mentioned grants to ZGO and EAF from the Michael J. Fox Foundation which was mistakenly omitted from the original article [1]. The authors also wish to note that Lior Greenbaum is only affiliated to affiliation #14 (Sackler Faculty of Medicine
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Aging-associated sensory decline and Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-12-04 Suji Hong, Seung-Hyun Baek, Mitchell K. P. Lai, Thiruma V. Arumugam, Dong-Gyu Jo
Multisensory decline is common as people age, and aging is the primary risk of Alzheimer’s Disease (AD). Recent studies have begun to shed light on the possibility that age-related sensory decline could accelerate AD pathogenesis, or be a prodromal indicator of AD. Sensory impairments, specifically in taste and smell, often emerge before cognitive symptoms in AD, indicating their potential as early
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Seeding activity of skin misfolded tau as a biomarker for tauopathies Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-29 Zerui Wang, Ling Wu, Maria Gerasimenko, Tricia Gilliland, Zahid Syed Ali Shah, Evalynn Lomax, Yirong Yang, Steven A. Gunzler, Vincenzo Donadio, Rocco Liguori, Bin Xu, Wen-Quan Zou
Tauopathies are a group of age-related neurodegenerative diseases characterized by the accumulation of pathologically hyperphosphorylated tau protein in the brain, leading to prion-like aggregation and propagation. They include Alzheimer’s disease (AD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick’s disease (PiD). Currently, reliable diagnostic biomarkers that directly
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NOTCH2NLC GGC intermediate repeat with serine induces hypermyelination and early Parkinson’s disease-like phenotypes in mice Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-28 Haitao Tu, Xin Yi Yeo, Zhi-Wei Zhang, Wei Zhou, Jayne Yi Tan, Li Chi, Sook-Yoong Chia, Zhihong Li, Aik Yong Sim, Brijesh Kumar Singh, Dongrui Ma, Zhidong Zhou, Isabelle Bonne, Shuo-Chien Ling, Adeline S.L. Ng, Sangyong Jung, Eng-King Tan, Li Zeng
The expansion of GGC repeats (typically exceeding 60 repeats) in the 5’ untranslated region (UTR) of the NOTCH2NLC gene (N2C) is linked to N2C-related repeat expansion disorders (NREDs), such as neuronal intranuclear inclusion disease (NIID), frontotemporal dementia (FTD), essential tremor (ET), and Parkinson’s disease (PD). These disorders share common clinical manifestations, including parkinsonism
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Human VCP mutant ALS/FTD microglia display immune and lysosomal phenotypes independently of GPNMB Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-26 Benjamin E. Clarke, Oliver J. Ziff, Giulia Tyzack, Marija Petrić Howe, Yiran Wang, Pierre Klein, Claudia A. Smith, Cameron A. Hall, Adel Helmy, Michael Howell, Gavin Kelly, Rickie Patani
Microglia play crucial roles in maintaining neuronal homeostasis but have been implicated in contributing to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, the role of microglia in ALS/FTD remains incompletely understood. Here, we generated highly enriched cultures of VCP mutant microglia derived from human induced pluripotent stem cells (hiPSCs) to investigate their
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A novel AAV Vector for gene therapy of RPE-related retinal degenerative diseases via intravitreal delivery Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-25 Yajun Gong, Xianyu Huang, Tianxiang Tu, Cenfeng Chu, Chunrui Xian, Yushun Yuan, Xin Fu, Ruobi Li, Guisheng Zhong, Xiaolai Zhou
To the editor, Dysfunction of retinal pigment epithelium (RPE) cells leads to multiple blinding retinal degenerative diseases, including retinitis pigmentosa, age-related macular degeneration, and Stargardt disease [1]. Currently, no drug treatments are available to cure or slow the progression of these diseases, and gene therapy has been considered a promising approach. However, when delivered via
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The Parkinson’s disease risk gene cathepsin B promotes fibrillar alpha-synuclein clearance, lysosomal function and glucocerebrosidase activity in dopaminergic neurons Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-25 Jace Jones-Tabah, Kathy He, Nathan Karpilovsky, Konstantin Senkevich, Ghislaine Deyab, Isabella Pietrantonio, Thomas Goiran, Yuting Cousineau, Daria Nikanorova, Taylor Goldsmith, Esther del Cid Pellitero, Carol X.-Q. Chen, Wen Luo, Zhipeng You, Narges Abdian, Jamil Ahmad, Jennifer A. Ruskey, Farnaz Asayesh, Dan Spiegelman, Stanley Fahn, Cheryl Waters, Oury Monchi, Yves Dauvilliers, Nicolas Dupré, Irina
Variants in the CTSB gene encoding the lysosomal hydrolase cathepsin B (catB) are associated with increased risk of Parkinson’s disease (PD). However, neither the specific CTSB variants driving these associations nor the functional pathways that link catB to PD pathogenesis have been characterized. CatB activity contributes to lysosomal protein degradation and regulates signaling processes involved
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Nuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson’s and other related neurodegenerative diseases Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-23 Zainab Riaz, Gabriel S. Richardson, Huajun Jin, Gary Zenitsky, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G. Kanthasamy
Nuclear pore complexes (NPCs) are embedded in the nuclear envelope and facilitate the exchange of macromolecules between the nucleus and cytoplasm in eukaryotic cells. The dysfunction of the NPC and nuclear transport plays a significant role in aging and the pathogenesis of various neurodegenerative diseases. Common features among these neurodegenerative diseases, including Parkinson’s disease (PD)
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Regulation of disease-associated microglia in the optic nerve by lipoxin B4 and ocular hypertension Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-20 Shubham Maurya, Maggie Lin, Shruthi Karnam, Tanirika Singh, Matangi Kumar, Emily Ward, Jeremy Sivak, John G. Flanagan, Karsten Gronert
The resident astrocyte-retinal ganglion cell (RGC) lipoxin circuit is impaired during retinal stress, which includes ocular hypertension-induced neuropathy. Lipoxin B4 produced by homeostatic astrocytes directly acts on RGCs to increase survival and function in ocular hypertension-induced neuropathy. RGC death in the retina and axonal degeneration in the optic nerve are driven by the complex interactions
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Stearoyl-CoA desaturase-1: a potential therapeutic target for neurological disorders Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-19 Melanie Loix, Sam Vanherle, Marta Turri, Stephan Kemp, Karl J. L. Fernandes, Jerome J. A. Hendriks, Jeroen F. J. Bogie
Disturbances in the fatty acid lipidome are increasingly recognized as key drivers in the progression of various brain disorders. In this review article, we delve into the impact of Δ9 fatty acid desaturases, with a particular focus on stearoyl-CoA desaturase-1 (SCD1), within the setting of neuroinflammation, neurodegeneration, and brain repair. Over the past years, it was established that inhibition
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Are oligodendrocytes the missing link in Alzheimer’s disease and related dementia research? Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-17 Sharyn L. Rossi, Diane E. Bovenkamp
Oligodendrocytes (OLs) and their lineage progenitor (OPCs) and precursor cells are widely studied and recognized as promising therapeutic targets for multiple neurodegenerative diseases and disorders including multiple sclerosis, spinal cord injuries, traumatic brain injuries, stroke, Parkinson’s disease, ALS, and others. Yet, their role in Alzheimer’s disease and related dementias (ADRDs), despite
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Contribution of amyloid deposition from oligodendrocytes in a mouse model of Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-16 Akihiro Ishii, Joseph A. Pathoulas, Omar MoustafaFathy Omar, Yingying Ge, Annie Y. Yao, Tressa Pantalena, Neeraj Singh, John Zhou, Wanxia He, Patrick Murphy, Riqiang Yan, Xiangyou Hu
The accumulation of β-amyloid (Aβ) peptides into insoluble plaques is an early pathological feature of Alzheimer’s disease (AD). BACE1 is the sole β-secretase for Aβ generation, making it an attractive therapeutic target for AD therapy. While BACE1 inhibitors have been shown to reduce Aβ levels in people with AD, clinical trials targeting BACE1 have failed due to unwanted synaptic deficits. Understanding
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CSF proteins of inflammation, proteolysis and lipid transport define preclinical AD and progression to AD dementia in cognitively unimpaired individuals Mol. Neurodegener. (IF 14.9) Pub Date : 2024-11-11 Marta del Campo, Carlos Quesada, Lisa Vermunt, Carel F. W. Peeters, Yanaika S. Hok-A-Hin, Calvin Trieu, Anouk den Braber, Inge M. W. Verberk, Pieter J. Visser, Betty M. Tijms, Wiesje M. van der Flier, Charlotte E. Teunissen
This preclinical AD CSF proteome study identified a panel of 12-CSF markers detecting amyloid positivity and clinical progression to AD with high accuracy; some of these CSF proteins related to immune function, neurotrophic processes, energy metabolism and endolysosomal functioning (e.g., ITGB2, CLEC5A, IGFBP-1, CST3) changed before amyloid positivity is established.
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Proteomic analysis of APOEε4 carriers implicates lipid metabolism, complement and lymphocyte signaling in cognitive resilience Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-31 Keenan A. Walker, Yang An, Abhay Moghekar, Ruin Moaddel, Michael R. Duggan, Zhongsheng Peng, Qu Tian, Luke C. Pilling, Shannon M. Drouin, Mark A. Espeland, Stephen R Rapp, Kathleen M Hayden, Aladdin H. Shadyab, Ramon Casanova, Madhav Thambisetty, Peter R. Rapp, Dimitrios Kapogiannis, Luigi Ferrucci, Susan M. Resnick
Apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late onset Alzheimer’s disease (AD). This case-cohort study used targeted plasma biomarkers and large-scale proteomics to examine the biological mechanisms that allow some APOEε4 carriers to maintain normal cognitive functioning in older adulthood. APOEε4 carriers and APOEε3 homozygotes enrolled in the Women’s Health Initiative
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Repetitive transcranial magnetic stimulation alleviates motor impairment in Parkinson’s disease: association with peripheral inflammatory regulatory T-cells and SYT6 Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-25 Fen Xie, Bibiao Shen, Yuqi Luo, Hang Zhou, Zhenchao Xie, Shuzhen Zhu, Xiaobo Wei, Zihan Chang, Zhaohua Zhu, Changhai Ding, Kunlin Jin, Chengwu Yang, Lucia Batzu, K Ray Chaudhuri, Ling-Ling Chan, Eng-King Tan, Qing Wang
Repetitive transcranial magnetic stimulation (rTMS) has been used to treat various neurological disorders. However, the molecular mechanism underlying the therapeutic effect of rTMS on Parkinson’s disease (PD) has not been fully elucidated. Neuroinflammation like regulatory T-cells (Tregs) appears to be a key modulator of disease progression in PD. If rTMS affects the peripheral Tregs in PD remains
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HDGFL2 cryptic protein: a portal to detection and diagnosis in neurodegenerative disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-25 Ellen A. Albagli, Anna Calliari, Tania F. Gendron, Yong-Jie Zhang
In 2006, TAR DNA-binding protein of 43 kDa (TDP-43) was discovered as the major ubiquitinated and aggregated protein in approximately 95% of amyotrophic lateral sclerosis (ALS) cases and 45% of frontotemporal lobar degeneration (FTLD) cases [1]. Since then, TDP-43 pathology has been identified in Alzheimer’s disease (AD), limbic-predominant age-related TDP-43 encephalopathy (LATE), and other neurodegenerative
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Gut-first Parkinson’s disease is encoded by gut dysbiome Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-24 Mário F. Munoz-Pinto, Emanuel Candeias, Inês Melo-Marques, A. Raquel Esteves, Ana Maranha, João D. Magalhães, Diogo Reis Carneiro, Mariana Sant’Anna, A. Raquel Pereira-Santos, António E Abreu, Daniela Nunes-Costa, Susana Alarico, Igor Tiago, Ana Morgadinho, João Lemos, Pedro N. Figueiredo, Cristina Januário, Nuno Empadinhas, Sandra Morais Cardoso
In Parkinson's patients, intestinal dysbiosis can occur years before clinical diagnosis, implicating the gut and its microbiota in the disease. Recent evidence suggests the gut microbiota may trigger body-first Parkinson Disease (PD), yet the underlying mechanisms remain unclear. This study aims to elucidate how a dysbiotic microbiome through intestinal immune alterations triggers PD-related neurodegeneration
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Amyloid-β (Aβ) immunotherapy induced microhemorrhages are linked to vascular inflammation and cerebrovascular damage in a mouse model of Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-21 Xavier Taylor, Harun N. Noristani, Griffin J. Fitzgerald, Herold Oluoch, Nick Babb, Tyler McGathey, Lindsay Carter, Justin T. Hole, Pascale N. Lacor, Ronald B. DeMattos, Yaming Wang
Anti-amyloid-β (Aβ) immunotherapy trials have revealed amyloid-related imaging abnormalities (ARIA) as the most prevalent and serious adverse events linked to pathological changes in cerebral vasculature. Recent studies underscore the critical involvement of perivascular macrophages and the infiltration of peripheral immune cells in regulating cerebrovascular damage. Specifically, Aβ antibodies engaged
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Comparing anti-tau antibodies under clinical trials and their epitopes on tau pathologies Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-19 Ha-Lim Song, Min-Seok Kim, Woo-Young Cho, Ye-Seul Yoo, Jae-You Kim, Tae-Wook Kim, Hyori Kim, Dong-Hou Kim, Seung-Yong Yoon
To the Editor, Tauopathies, including Alzheimer’s disease (AD), are characterized by the accumulation of abnormal tau protein deposits in the brain. Tau exists in multiple heterogenous forms of various polypeptide fragments by enzymatic cleavage and post-translational modifications (PTMs) [1]. Insights from clinical trials of anti-β-amyloid (Aβ) antibodies highlight the importance of epitope selection
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Increased expression of mesencephalic astrocyte-derived neurotrophic factor (MANF) contributes to synapse loss in Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-18 Yiran Zhang, Xiusheng Chen, Laiqiang Chen, Mingting Shao, Wenzhen Zhu, Tingting Xing, Tingting Guo, Qingqing Jia, Huiming Yang, Peng Yin, Xiao-Xin Yan, Jiandong Yu, Shihua Li, Xiao-Jiang Li, Su Yang
The activation of endoplasmic reticulum (ER) stress is an early pathological hallmark of Alzheimer’s disease (AD) brain, but how ER stress contributes to the onset and development of AD remains poorly characterized. Mesencephalic astrocyte-derived neurotrophic factor (MANF) is a non-canonical neurotrophic factor and an ER stress inducible protein. Previous studies reported that MANF is increased in
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Retraction Note: Aging exacerbates the brain inflammatory micro-environment contributing to α-synuclein pathology and functional deficits in a mouse model of DLB/PD Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-16 Michiyo Iba, Ross A. McDevitt, Changyoun Kim, Roshni Roy, Dimitra Sarantopoulou, Ella Tommer, Byron Siegars, Michelle Sallin, Somin Kwon, Jyoti Misra Sen, Ranjan Sen, Eliezer Masliah
This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s13024-022-00564-6.
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Correction: Whole-genome sequencing analysis reveals new susceptibility loci and structural variants associated with progressive supranuclear palsy Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-14 Hui Wang, Timothy S. Chang, Beth A. Dombroski, Po-Liang Cheng, Vishakha Patil, Leopoldo Valiente-Banuet, Kurt Farrell, Catriona Mclean, Laura Molina-Porcel, Alex Rajput, Peter Paul De Deyn, Nathalie Le Bastard, Marla Gearing, Laura Donker Kaat, John C. Van Swieten, Elise Dopper, Bernardino F. Ghetti, Kathy L. Newell, Claire Troakes, Justo G. de Yébenes, Alberto Rábano-Gutierrez, Tina Meller, Wolfgang
Correction: Mol Neurodegeneration 19, 61 (2024) https://doi.org/10.1186/s13024-024-00747-3 The original article [1] erroneously gives a wrong affiliation for Ulrich Müller. His correct affiliation is Institute of Human Genetics, Justus-Liebig University Giessen, 35392 Giessen, Germany. Wang H, Chang TS, Dombroski BA, et al. Whole-genome sequencing analysis reveals new susceptibility loci and structural
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A perspective on Alzheimer’s disease: exploring the potential of terminal/paradoxical lucidity and psychedelics Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-12 Cong Lin, Xiubo Du, Xiaohui Wang
Alzheimer’s disease (AD) remains a formidable challenge in the field of neurodegenerative disorders, characterized by an insidious onset of memory impairment and a gradual cognitive decline. The molecular pathologies underlying AD are complex and multifactorial, involving a combination of genetic, biochemical, and immunological factors that contribute to its progression [1, 2]. The challenges in treating
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Correction: Network proteomics of the Lewy body dementia brain reveals presynaptic signatures distinct from Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-11 Anantharaman Shantaraman, Eric B. Dammer, Obiadada Ugochukwu, Duc M. Duong, Luming Yin, E. Kathleen Carter, Marla Gearing, Alice Chen-Plotkin, Edward B. Lee, John Q. Trojanowski, David A. Bennett, James J. Lah, Allan I. Levey, Nicholas T. Seyfried, Lenora Higginbotham
Molecular Neurodegeneration (2024) 19:60 https://doi.org/10.1186/s13024-024-00749-1 The authors mistakenly omitted two funding sources - The BrightFocus Foundation and The American Brain Foundation (both for Lenora Higginbotham - in the original article which they wish to acknowledge via this Correction article. Authors and Affiliations Center for Neurodegenerative Disease, Emory University School
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Correction: Sodium oligomannate alters gut microbiota, reduces cerebral amyloidosis and reactive microglia in a sex-specific manner Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-10 Megan E. Bosch, Hemraj B. Dodiya, Julia Michalkiewicz, Choonghee Lee, Shabana M. Shaik, Ian Q. Weigle, Can Zhang, Jack Osborn, Aishwarya Nambiar, Priyam Patel, Samira Parhizkar, Xiaoqiong Zhang, Marie L. Laury, Prasenjit Mondal, Ashley Gomm, Matthew John Schipma, Dania Mallah, Oleg Butovsky, Eugene B. Chang, Rudolph E. Tanzi, Jack A. Gilbert, David M. Holtzman, Sangram S. Sisodia
Molecular Neurodegeneration (2024) 19:18 https://doi.org/10.1186/s13024-023-00700-w The original article erroneously presents incorrect graph labels in the caption of Fig. 4. The corrected Fig. 4 caption alongside its respective figure can be viewed ahead in this Correction article. Fig. 4 GV-971 modifies cytokine and chemokine levels in peripheral blood and cortical tissues. (a) Quantification of
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Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-10 Xuemei Zeng, Tara K. Lafferty, Anuradha Sehrawat, Yijun Chen, Pamela C. L. Ferreira, Bruna Bellaver, Guilherme Povala, M. Ilyas Kamboh, William E. Klunk, Ann D. Cohen, Oscar L. Lopez, Milos D. Ikonomovic, Tharick A. Pascoal, Mary Ganguli, Victor L. Villemagne, Beth E. Snitz, Thomas K. Karikari
Blood-based biomarkers are gaining grounds for the detection of Alzheimer’s disease (AD) and related disorders (ADRDs). However, two key obstacles remain: the lack of methods for multi-analyte assessments and the need for biomarkers for related pathophysiological processes like neuroinflammation, vascular, and synaptic dysfunction. A novel proteomic method for pre-selected analytes, based on proximity
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α-Synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons at-risk in Parkinson’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-08 Fanni F. Geibl, Martin T. Henrich, Zhong Xie, Enrico Zampese, Jun Ueda, Tatiana Tkatch, David L. Wokosin, Elena Nasiri, Constantin A. Grotmann, Valina L. Dawson, Ted M. Dawson, Navdeep S. Chandel, Wolfgang H. Oertel, D. James Surmeier
Pathological accumulation of aggregated α-synuclein (aSYN) is a common feature of Parkinson’s disease (PD). However, the mechanisms by which intracellular aSYN pathology contributes to dysfunction and degeneration of neurons in the brain are still unclear. A potentially relevant target of aSYN is the mitochondrion. To test this hypothesis, genetic and physiological methods were used to monitor mitochondrial
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Heparin-enriched plasma proteome is significantly altered in Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-08 Qi Guo, Lingyan Ping, Eric B. Dammer, Duc M. Duong, Luming Yin, Kaiming Xu, Anantharaman Shantaraman, Edward J. Fox, Todd E Golde, Erik C.B. Johnson, Blaine R. Roberts, James J. Lah, Allan I. Levey, Nicholas T. Seyfried
Heparin binding proteins (HBPs) with roles in extracellular matrix assembly are strongly correlated to β-amyloid (Aβ) and tau pathology in Alzheimer’s disease (AD) brain and cerebrospinal fluid (CSF). However, it remains challenging to detect these proteins in plasma using standard mass spectrometry-based proteomic approaches. We employed heparin-affinity chromatography, followed by off-line fractionation
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Clarifying the association of CSF Aβ, tau, BACE1, and neurogranin with AT(N) stages in Alzheimer disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-10-08 Sylvain Lehmann, Susanna Schraen-Maschke, Luc Buée, Jean-Sébastien Vidal, Constance Delaby, Christophe Hirtz, Frédéric Blanc, Claire Paquet, Bernadette Allinquant, Stéphanie Bombois, Audrey Gabelle, Olivier Hanon
Current AT(N) stratification for Alzheimer’s disease (AD) accounts for complex combinations of amyloid (A), tau proteinopathy (T) and neurodegeneration (N) signatures. Understanding the transition between these different stages is a major challenge, especially in view of the recent development of disease modifying therapy. This is an observational study, CSF levels of Tau, pTau181, pTau217, Aβ38/40/42
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One immune cell to bind them all: platelet contribution to neurodegenerative disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-09-27 Gabriela Rodriguez Moore, Isabel Melo-Escobar, David Stegner, Oliver Bracko
Alzheimer’s disease (AD) and related dementias (ADRD) collectively affect a significant portion of the aging population worldwide. The pathological progression of AD involves not only the classical hallmarks of amyloid beta (Aβ) plaque buildup and neurofibrillary tangle development but also the effects of vasculature and chronic inflammatory processes. Recently, platelets have emerged as central players
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Regional desynchronization of microglial activity is associated with cognitive decline in Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-09-05 Artem Zatcepin, Johannes Gnörich, Boris-Stephan Rauchmann, Laura M. Bartos, Stephan Wagner, Nicolai Franzmeier, Maura Malpetti, Xianyuan Xiang, Yuan Shi, Samira Parhizkar, Maximilian Grosch, Karin Wind-Mark, Sebastian T. Kunte, Leonie Beyer, Carolin Meyer, Desirée Brösamle, Ann-Christin Wendeln, Collins Osei-Sarpong, Steffanie Heindl, Arthur Liesz, Sophia Stoecklein, Gloria Biechele, Anika Finze, Florian
Microglial activation is one hallmark of Alzheimer disease (AD) neuropathology but the impact of the regional interplay of microglia cells in the brain is poorly understood. We hypothesized that microglial activation is regionally synchronized in the healthy brain but experiences regional desynchronization with ongoing neurodegenerative disease. We addressed the existence of a microglia connectome
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Identification of a specific APOE transcript and functional elements associated with Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-08-29 Qiang Chen, Luis Aguirre, Guoming Liang, Huanhuan Zhao, Tao Dong, Felix Borrego, Itziar de Rojas, Qichan Hu, Christopher Reyes, Ling-Yan Su, Bao Zhang, James D. Lechleiter, Harald H. H. Göring, Philip L. De Jager, Joel E. Kleinman, Thomas M. Hyde, Pan P. Li, Agustín Ruiz, Daniel R. Weinberger, Sudha Seshadri, Liang Ma
The APOE gene is the strongest genetic risk factor for late-onset Alzheimer’s Disease (LOAD). However, the gene regulatory mechanisms at this locus remain incompletely characterized. To identify novel AD-linked functional elements within the APOE locus, we integrated SNP variants with multi-omics data from human postmortem brains including 2,179 RNA-seq samples from 3 brain regions and two ancestries
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Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency Mol. Neurodegener. (IF 14.9) Pub Date : 2024-08-26 Panpan Wang, Yaping Shao, Murad Al-Nusaif, Jun Zhang, Huijia Yang, Yuting Yang, Kunhyok Kim, Song Li, Cong Liu, Huaibin Cai, Weidong Le
Although WD repeat domain 45 (WDR45) mutations have been linked to $$\upbeta$$ -propeller protein-associated neurodegeneration (BPAN), the precise molecular and cellular mechanisms behind this disease remain elusive. This study aims to shed light on the impacts of WDR45-deficiency on neurodegeneration, specifically axonal degeneration, within the midbrain dopaminergic (DAergic) system. We hope to better
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Whole-genome sequencing analysis reveals new susceptibility loci and structural variants associated with progressive supranuclear palsy Mol. Neurodegener. (IF 14.9) Pub Date : 2024-08-16 Hui Wang, Timothy S. Chang, Beth A. Dombroski, Po-Liang Cheng, Vishakha Patil, Leopoldo Valiente-Banuet, Kurt Farrell, Catriona Mclean, Laura Molina-Porcel, Alex Rajput, Peter Paul De Deyn, Nathalie Le Bastard, Marla Gearing, Laura Donker Kaat, John C. Van Swieten, Elise Dopper, Bernardino F. Ghetti, Kathy L. Newell, Claire Troakes, Justo G. de Yébenes, Alberto Rábano-Gutierrez, Tina Meller, Wolfgang
Progressive supranuclear palsy (PSP) is a rare neurodegenerative disease characterized by the accumulation of aggregated tau proteins in astrocytes, neurons, and oligodendrocytes. Previous genome-wide association studies for PSP were based on genotype array, therefore, were inadequate for the analysis of rare variants as well as larger mutations, such as small insertions/deletions (indels) and structural
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Network proteomics of the Lewy body dementia brain reveals presynaptic signatures distinct from Alzheimer’s disease Mol. Neurodegener. (IF 14.9) Pub Date : 2024-08-06 Anantharaman Shantaraman, Eric B. Dammer, Obiadada Ugochukwu, Duc M. Duong, Luming Yin, E. Kathleen Carter, Marla Gearing, Alice Chen-Plotkin, Edward B. Lee, John Q. Trojanowski, David A. Bennett, James J. Lah, Allan I. Levey, Nicholas T. Seyfried, Lenora Higginbotham
Lewy body dementia (LBD), a class of disorders comprising Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB), features substantial clinical and pathological overlap with Alzheimer’s disease (AD). The identification of biomarkers unique to LBD pathophysiology could meaningfully advance its diagnosis, monitoring, and treatment. Using quantitative mass spectrometry (MS), we measured
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Single-cell peripheral immunoprofiling of lewy body and Parkinson’s disease in a multi-site cohort Mol. Neurodegener. (IF 14.9) Pub Date : 2024-08-01 Thanaphong Phongpreecha, Kavita Mathi, Brenna Cholerton, Eddie J. Fox, Natalia Sigal, Camilo Espinosa, Momsen Reincke, Philip Chung, Ling-Jen Hwang, Chandresh R. Gajera, Eloise Berson, Amalia Perna, Feng Xie, Chi-Hung Shu, Debapriya Hazra, Divya Channappa, Jeffrey E. Dunn, Lucas B. Kipp, Kathleen L. Poston, Kathleen S. Montine, Holden T. Maecker, Nima Aghaeepour, Thomas J. Montine
Multiple lines of evidence support peripheral organs in the initiation or progression of Lewy body disease (LBD), a spectrum of neurodegenerative diagnoses that include Parkinson’s Disease (PD) without or with dementia (PDD) and dementia with Lewy bodies (DLB). However, the potential contribution of the peripheral immune response to LBD remains unclear. This study aims to characterize peripheral immune