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Putative novel CSF biomarkers of Alzheimer’s disease based on the novel concept of generic protein misfolding and proteotoxicity: the PRAMA cohort Transl. Neurodegener. (IF 12.6) Pub Date : 2024-03-08 Alessandra Bigi, Giulia Fani, Valentina Bessi, Liliana Napolitano, Silvia Bagnoli, Assunta Ingannato, Lorenzo Neri, Roberta Cascella, Paolo Matteini, Sandro Sorbi, Benedetta Nacmias, Cristina Cecchi, Fabrizio Chiti
Alzheimer’s disease (AD) accounts for 60%–70% of cases of dementia worldwide (https://www.alz.org). The NIA-AA (American National Institute of Aging and Alzheimer’s Association) has proposed a research framework based on a biomarker-grounded biological, rather than syndromal, definition of AD, where the disease has to be regarded as a continuum [1]. In this spectrum, seven biomarkers have attained
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LRRK2 kinase inhibition reverses G2019S mutation-dependent effects on tau pathology progression Transl. Neurodegener. (IF 12.6) Pub Date : 2024-03-04 Noah Lubben, Julia K. Brynildsen, Connor M. Webb, Howard L. Li, Cheryl E. G. Leyns, Lakshmi Changolkar, Bin Zhang, Emily S. Meymand, Mia O’Reilly, Zach Madaj, Daniella DeWeerd, Matthew J. Fell, Virginia M. Y. Lee, Dani S. Bassett, Michael X. Henderson
Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson’s disease (PD). These mutations elevate the LRRK2 kinase activity, making LRRK2 kinase inhibitors an attractive therapeutic. LRRK2 kinase activity has been consistently linked to specific cell signaling pathways, mostly related to organelle trafficking and homeostasis, but its relationship to PD pathogenesis
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Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside Transl. Neurodegener. (IF 12.6) Pub Date : 2024-02-27 Yuan-Yuan Ma, Xin Li, Jin-Tai Yu, Yan-Jiang Wang
The aetiologies and origins of neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), are complex and multifaceted. A growing body of evidence suggests that the gut microbiome plays crucial roles in the development and progression of neurodegenerative diseases. Clinicians have come to realize that therapeutics
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α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes Transl. Neurodegener. (IF 12.6) Pub Date : 2024-02-21 Emmanouela Leandrou, Ioanna Chalatsa, Dimitrios Anagnostou, Christina Machalia, Maria Semitekolou, Vicky Filippa, Manousos Makridakis, Antonia Vlahou, Ema Anastasiadou, Kostas Vekrellis, Evangelia Emmanouilidou
It is now realized that Parkinson’s disease (PD) pathology extends beyond the substantia nigra, affecting both central and peripheral nervous systems, and exhibits a variety of non-motor symptoms often preceding motor features. Neuroinflammation induced by activated microglia and astrocytes is thought to underlie these manifestations. α-Synuclein aggregation has been linked with sustained neuroinflammation
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Emerging role of senescent microglia in brain aging-related neurodegenerative diseases Transl. Neurodegener. (IF 12.6) Pub Date : 2024-02-20 Chan Rim, Min-Jung You, Minyeop Nahm, Min-Soo Kwon
Brain aging is a recognized risk factor for neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease), but the intricate interplay between brain aging and the pathogenesis of these conditions remains inadequately understood. Cellular senescence is considered to contribute to cellular dysfunction and inflammaging. According
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Microstructural integrity of the locus coeruleus and its tracts reflect noradrenergic degeneration in Alzheimer’s disease and Parkinson’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2024-02-09 Chen-Pei Lin, Irene Frigerio, John G. J. M. Bol, Maud M. A. Bouwman, Alex J. Wesseling, Martin J. Dahl, Annemieke J. M. Rozemuller, Ysbrand D. van der Werf, Petra J. W. Pouwels, Wilma D. J. van de Berg, Laura E. Jonkman
Degeneration of the locus coeruleus (LC) noradrenergic system contributes to clinical symptoms in Alzheimer’s disease (AD) and Parkinson’s disease (PD). Diffusion magnetic resonance imaging (MRI) has the potential to evaluate the integrity of the LC noradrenergic system. The aim of the current study was to determine whether the diffusion MRI-measured integrity of the LC and its tracts are sensitive
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Life and disease status of patients with Parkinson’s disease during and after zero-COVID in China: an online survey Transl. Neurodegener. (IF 12.6) Pub Date : 2024-02-06 Pei Huang, Yu-Yan Tan, Biao Chen, Hui-Fang Shang, Li-Juan Wang, Chun-Feng Liu, Ling Chen, Ying Chang, Han Wang, Xue-Lian Wang, Xiao-Guang Lei, Li-Fen Yao, Yang Yu, Zheng Ye, Hai-Bo Chen, Sheng-Di Chen
Little is known about the impact of the COVID-19 pandemic on patients with Parkinson’s disease (PD) at different stages of the pandemic. This study aims to assess the lives and disease status of PD patients during the zero-COVID policy period and after ending the zero-COVID policy. This multicenter cross-sectional study included two online surveys among PD patients in China, from May 30 to June 30
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The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-23 Yuqing Liu, Yejun Tan, Zheyu Zhang, Min Yi, Lemei Zhu, Weijun Peng
Ageing is a crucial risk factor for Alzheimer’s disease (AD) and is characterised by systemic changes in both intracellular and extracellular microenvironments that affect the entire body instead of a single organ. Understanding the specific mechanisms underlying the role of ageing in disease development can facilitate the treatment of ageing-related diseases, such as AD. Signs of brain ageing have
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The therapeutic potential of probucol and probucol analogues in neurodegenerative diseases Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-22 Arazu Sharif, John Mamo, Virginie Lam, Hani Al-Salami, Armin Mooranian, Gerald F. Watts, Roger Clarnette, Giuseppe Luna, Ryu Takechi
Neurodegenerative disorders present complex pathologies characterized by various interconnected factors, including the aggregation of misfolded proteins, oxidative stress, neuroinflammation and compromised blood–brain barrier (BBB) integrity. Addressing such multifaceted pathways necessitates the development of multi-target therapeutic strategies. Emerging research indicates that probucol, a historic
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Correction: A novel transgenic mouse line with hippocampus-dominant and inducible expression of truncated human tau Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-11 Yang Gao, Yuying Wang, Huiyang Lei, Zhendong Xu, Shihong Li, Haitao Yu, Jiazhao Xie, Zhentao Zhang, Gongping Liu, Yao Zhang, Jie Zheng, Jian‑Zhi Wang
Correction: Translational Neurodegeneration 12:51 (2023) https://doi.org/10.1186/s40035-023-00379-5 Following publication of the original article [1], the authors reported an error in the Fig. 2: Figure 2e presented a typing error "HT7" was wrongly written as "HT1". See the Fig. 2 corrected Fig. 2 Increase of phosphorylated tau in the hippocampus of dox-administered hTau368 mice. a Diagram of human
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Death-associated protein kinase 1 as a therapeutic target for Alzheimer's disease Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-09 Tao Zhang, Byeong Mo Kim, Tae Ho Lee
Alzheimer’s disease (AD) is the most prevalent form of dementia in the elderly and represents a major clinical challenge in the ageing society. Neuropathological hallmarks of AD include neurofibrillary tangles composed of hyperphosphorylated tau, senile plaques derived from the deposition of amyloid-β (Aβ) peptides, brain atrophy induced by neuronal loss, and synaptic dysfunctions. Death-associated
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Increased cysteinyl-tRNA synthetase drives neuroinflammation in Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-08 Xiu-Hong Qi, Peng Chen, Yue-Ju Wang, Zhe-Ping Zhou, Xue-Chun Liu, Hui Fang, Chen-Wei Wang, Ji Liu, Rong-Yu Liu, Han-Kui Liu, Zhen-Xin Zhang, Jiang-Ning Zhou
Microglia-mediated neuroinflammation in Alzheimer’s disease (AD) is not only a response to pathophysiological events, but also plays a causative role in neurodegeneration. Cytoplasmic cysteinyl-tRNA synthetase (CARS) is considered to be a stimulant for immune responses to diseases; however, it remains unknown whether CARS is involved in the pathogenesis of AD. Postmortem human temporal cortical tissues
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Nanotechnology for microglial targeting and inhibition of neuroinflammation underlying Alzheimer’s pathology Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-04 Hoda M. Gebril, Aravind Aryasomayajula, Mariana Reis Nogueira de Lima, Kathryn E. Uhrich, Prabhas V. Moghe
Alzheimer's disease (AD) is considered to have a multifactorial etiology. The hallmark of AD is progressive neurodegeneration, which is characterized by the deepening loss of memory and a high mortality rate in the elderly. The neurodegeneration in AD is believed to be exacerbated following the intercoupled cascades of extracellular amyloid beta (Aβ) plaques, uncontrolled microglial activation, and
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Blockage of VEGF function by bevacizumab alleviates early-stage cerebrovascular dysfunction and improves cognitive function in a mouse model of Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2024-01-03 Min Zhang, Zhan Zhang, Honghong Li, Yuting Xia, Mengdan Xing, Chuan Xiao, Wenbao Cai, Lulu Bu, Yi Li, Tae-Eun Park, Yamei Tang, Xiaojing Ye, Wei-Jye Lin
Alzheimer's disease (AD) is a neurodegenerative disorder and the predominant type of dementia worldwide. It is characterized by the progressive and irreversible decline of cognitive functions. In addition to the pathological beta-amyloid (Aβ) deposition, glial activation, and neuronal injury in the postmortem brains of AD patients, increasing evidence suggests that the often overlooked vascular dysfunction
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Parkinson’s disease and gut microbiota: from clinical to mechanistic and therapeutic studies Transl. Neurodegener. (IF 12.6) Pub Date : 2023-12-15 Xuxiang Zhang, Beisha Tang, Jifeng Guo
Parkinson’s disease (PD) is one of the most prevalent neurodegenerative diseases. The typical symptomatology of PD includes motor symptoms; however, a range of nonmotor symptoms, such as intestinal issues, usually occur before the motor symptoms. Various microorganisms inhabiting the gastrointestinal tract can profoundly influence the physiopathology of the central nervous system through neurological
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Supplementation with high-GABA-producing Lactobacillus plantarum L5 ameliorates essential tremor triggered by decreased gut bacteria-derived GABA Transl. Neurodegener. (IF 12.6) Pub Date : 2023-12-13 Hao-Jie Zhong, Si-Qi Wang, Ruo-Xin Zhang, Yu-Pei Zhuang, Longyan Li, Shuo-Zhao Yi, Ying Li, Lei Wu, Yu Ding, Jumei Zhang, Xinqiang Xie, Xing-Xiang He, Qingping Wu
The γ-aminobutyric acid (GABA) hypothesis posits a role of GABA deficiency in the central nervous system in the pathogenesis and progression of essential tremor (ET). However, the specific causative factor for GABA deficiency is not clear. The gut microbiota in mammals has recently been considered as a significant source of GABA. Furthermore, the GABA-based signals originating from the intestine can
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Novel data-driven subtypes and stages of brain atrophy in the ALS–FTD spectrum Transl. Neurodegener. (IF 12.6) Pub Date : 2023-12-07 Ting Shen, Jacob W. Vogel, Jeffrey Duda, Jeffrey S. Phillips, Philip A. Cook, James Gee, Lauren Elman, Colin Quinn, Defne A. Amado, Michael Baer, Lauren Massimo, Murray Grossman, David J. Irwin, Corey T. McMillan
TDP-43 proteinopathies represent a spectrum of neurological disorders, anchored clinically on either end by amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD). The ALS–FTD spectrum exhibits a diverse range of clinical presentations with overlapping phenotypes, highlighting its heterogeneity. This study was aimed to use disease progression modeling to identify novel data-driven
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Inhibiting tau-induced elevated nSMase2 activity and ceramides is therapeutic in an Alzheimer’s disease mouse model Transl. Neurodegener. (IF 12.6) Pub Date : 2023-12-04 Carolyn Tallon, Benjamin J. Bell, Medhinee M. Malvankar, Pragney Deme, Carlos Nogueras-Ortiz, Erden Eren, Ajit G. Thomas, Kristen R. Hollinger, Arindom Pal, Maja Mustapic, Meixiang Huang, Kaleem Coleman, Tawnjerae R. Joe, Rana Rais, Norman J. Haughey, Dimitrios Kapogiannis, Barbara S. Slusher
Cognitive decline in Alzheimer’s disease (AD) is associated with hyperphosphorylated tau (pTau) propagation between neurons along synaptically connected networks, in part via extracellular vesicles (EVs). EV biogenesis is triggered by ceramide enrichment at the plasma membrane from neutral sphingomyelinase2 (nSMase2)-mediated cleavage of sphingomyelin. We report, for the first time, that human tau
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Neuronal and synaptic adaptations underlying the benefits of deep brain stimulation for Parkinson's disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-30 Wenying Xu, Jie Wang, Xin-Ni Li, Jingxue Liang, Lu Song, Yi Wu, Zhenguo Liu, Bomin Sun, Wei-Guang Li
Deep brain stimulation (DBS) is a well-established and effective treatment for patients with advanced Parkinson's disease (PD), yet its underlying mechanisms remain enigmatic. Optogenetics, primarily conducted in animal models, provides a unique approach that allows cell type- and projection-specific modulation that mirrors the frequency-dependent stimulus effects of DBS. Opto-DBS research in animal
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N6-methyladenosine-modified circRIMS2 mediates synaptic and memory impairments by activating GluN2B ubiquitination in Alzheimer's disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-28 Xiong Wang, Jiazhao Xie, Lu Tan, Yanjun Lu, Na Shen, Jiaoyuan Li, Hui Hu, Huijun Li, Xiaoguang Li, Liming Cheng
Synaptic degeneration occurs in the early stage of Alzheimer's disease (AD) before devastating symptoms, strongly correlated with cognitive decline. Circular RNAs (circRNAs) are abundantly enriched in neural tissues, and aberrant expression of circRNAs precedes AD symptoms, significantly correlated with clinical dementia severity. However, the direct relationship between circRNA dysregulation and synaptic
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A phase 1 open-label pilot study of low-dose interleukine-2 immunotherapy in patients with Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-16 Alireza Faridar, Abdulmunaim M. Eid, Aaron D. Thome, Weihua Zhao, David R. Beers, Maria B. Pascual, Mohammad O. Nakawah, Gustavo C. Roman, Charles S. Davis, Michael Grundman, Joseph C. Masdeu, Stanley H. Appel
ClinicalTrials.gov Identifier: NCT05821153, Registered April 20 2023, Retrospectively registered, https://classic.clinicaltrials.gov/ct2/show/NCT05821153
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Oligodendrocyte progenitor cells in Alzheimer’s disease: from physiology to pathology Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-14 Peibin Zou, Chongyun Wu, Timon Cheng-Yi Liu, Rui Duan, Luodan Yang
Oligodendrocyte progenitor cells (OPCs) play pivotal roles in myelin formation and phagocytosis, communicating with neighboring cells and contributing to the integrity of the blood–brain barrier (BBB). However, under the pathological circumstances of Alzheimer’s disease (AD), the brain’s microenvironment undergoes detrimental changes that significantly impact OPCs and their functions. Starting with
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A novel transgenic mouse line with hippocampus-dominant and inducible expression of truncated human tau Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-10 Yang Gao, Yuying Wang, Huiyang Lei, Zhendong Xu, Shihong Li, Haitao Yu, Jiazhao Xie, Zhentao Zhang, Gongping Liu, Yao Zhang, Jie Zheng, Jian-Zhi Wang
Intraneuronal accumulation of hyperphosphorylated tau is a defining hallmark of Alzheimer’s disease (AD). However, mouse models imitating AD-exclusive neuronal tau pathologies are lacking. We generated a new tet-on transgenic mouse model expressing truncated human tau N1-368 (termed hTau368), a tau fragment increased in the brains of AD patients and aged mouse brains. Doxycycline (dox) was administered
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Intranasal administration of induced pluripotent stem cell-derived cortical neural stem cell-secretome as a treatment option for Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-09 Hyunkyung Mo, Juryun Kim, Jennifer Yejean Kim, Jang Woon Kim, Heeju Han, Si Hwa Choi, Yeri Alice Rim, Ji Hyeon Ju
Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly, resulting in gradual destruction of cognitive abilities. Research on the development of various AD treatments is underway; however, no definitive treatment has been developed yet. Herein, we present induced pluripotent stem cell (iPSC)-derived cortical neural stem cell secretome (CNSC-SE) as a new treatment candidate
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NLRP3 inflammasome in cognitive impairment and pharmacological properties of its inhibitors Transl. Neurodegener. (IF 12.6) Pub Date : 2023-11-02 Yi Xu, Yanling Yang, Xi Chen, Danling Jiang, Fei Zhang, Yao Guo, Bin Hu, Guohai Xu, Shengliang Peng, Lidong Wu, Jialing Hu
Cognitive impairment is a multifactorial and multi-step pathological process that places a heavy burden on patients and the society. Neuroinflammation is one of the main factors leading to cognitive impairment. The inflammasomes are multi-protein complexes that respond to various microorganisms and endogenous danger signals, helping to initiate innate protective responses in inflammatory diseases.
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Metabolic regulation of microglial phagocytosis: Implications for Alzheimer's disease therapeutics Transl. Neurodegener. (IF 12.6) Pub Date : 2023-10-31 Izabela Lepiarz-Raba, Ismail Gbadamosi, Roberta Florea, Rosa Chiara Paolicelli, Ali Jawaid
Microglia, the resident immune cells of the brain, are increasingly implicated in the regulation of brain health and disease. Microglia perform multiple functions in the central nervous system, including surveillance, phagocytosis and release of a variety of soluble factors. Importantly, a majority of their functions are closely related to changes in their metabolism. This natural inter-dependency
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Janus kinase inhibitors are potential therapeutics for amyotrophic lateral sclerosis Transl. Neurodegener. (IF 12.6) Pub Date : 2023-10-12 Peter J. Richardson, Daniel P. Smith, Alex de Giorgio, Xenia Snetkov, Joshua Almond-Thynne, Sara Cronin, Richard J. Mead, Christopher J. McDermott, Pamela J. Shaw
Amyotrophic lateral sclerosis (ALS) is a poorly treated multifactorial neurodegenerative disease associated with multiple cell types and subcellular organelles. As with other multifactorial diseases, it is likely that drugs will need to target multiple disease processes and cell types to be effective. We review here the role of Janus kinase (JAK)/Signal transducer and activator of transcription (STAT)
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Pathological insights from amyotrophic lateral sclerosis animal models: comparisons, limitations, and challenges Transl. Neurodegener. (IF 12.6) Pub Date : 2023-09-20 Longhong Zhu, Shihua Li, Xiao-Jiang Li, Peng Yin
In order to dissect amyotrophic lateral sclerosis (ALS), a multigenic, multifactorial, and progressive neurodegenerative disease with heterogeneous clinical presentations, researchers have generated numerous animal models to mimic the genetic defects. Concurrent and comparative analysis of these various models allows identification of the causes and mechanisms of ALS in order to finally obtain effective
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Patient-derived iPSC models of Friedreich ataxia: a new frontier for understanding disease mechanisms and therapeutic application Transl. Neurodegener. (IF 12.6) Pub Date : 2023-09-20 Saumya Maheshwari, Gabriela Vilema-Enríquez, Richard Wade-Martins
Friedreich ataxia (FRDA) is a rare genetic multisystem disorder caused by a pathological GAA trinucleotide repeat expansion in the FXN gene. The numerous drawbacks of historical cellular and rodent models of FRDA have caused difficulty in performing effective mechanistic and translational studies to investigate the disease. The recent discovery and subsequent development of induced pluripotent stem
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Role of dopamine in the pathophysiology of Parkinson’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-09-18 Zhi Dong Zhou, Ling Xiao Yi, Dennis Qing Wang, Tit Meng Lim, Eng King Tan
A pathological feature of Parkinson’s disease (PD) is the progressive loss of dopaminergic neurons and decreased dopamine (DA) content in the substantia nigra pars compacta in PD brains. DA is the neurotransmitter of dopaminergic neurons. Accumulating evidence suggests that DA interacts with environmental and genetic factors to contribute to PD pathophysiology. Disturbances of DA synthesis, storage
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Research progress on the role of extracellular vesicles in neurodegenerative diseases Transl. Neurodegener. (IF 12.6) Pub Date : 2023-09-11 Zhengzhe Li, Xiaoling Wang, Xiaoxing Wang, Xiaomei Yi, Yin Kwan Wong, Jiyang Wu, Fangfang Xie, Die Hu, Qi Wang, Jigang Wang, Tianyu Zhong
Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, affect millions of people worldwide. Tremendous efforts have been put into disease-related research, but few breakthroughs have been made in diagnostic and therapeutic approaches. Extracellular vesicles (EVs) are heterogeneous cell-derived membrane structures that arise
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Large-scale proximity extension assay reveals CSF midkine and DOPA decarboxylase as supportive diagnostic biomarkers for Parkinson’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-09-04 Wojciech Paslawski, Shervin Khosousi, Ellen Hertz, Ioanna Markaki, Adam Boxer, Per Svenningsson
There is a need for biomarkers to support an accurate diagnosis of Parkinson’s disease (PD). Cerebrospinal fluid (CSF) has been a successful biofluid for finding neurodegenerative biomarkers, and modern highly sensitive multiplexing methods offer the possibility to perform discovery studies. Using a large-scale multiplex proximity extension assay (PEA) approach, we aimed to discover novel diagnostic
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Early GCase activity is a predictor of long-term cognitive decline in Parkinson’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-08-28 Linn Oftedal, Johannes Lange, Kenn Freddy Pedersen, Aleksander Hagen Erga, Ingvild Dalen, Ole-Bjørn Tysnes, Guido Alves, Jodi Maple-Grødem
Dementia is a serious complication for many patients with advanced Parkinson’s disease (PD) and its incidence is increased in PD patients harbouring a mutation in GBA1 [1]. However, cognitive impairment is not limited to late disease stages and can also manifest in patients with early untreated disease, leading to diminished social function and increased disability and caregiver burden. We have previously
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α-Synuclein-carrying astrocytic extracellular vesicles in Parkinson pathogenesis and diagnosis Transl. Neurodegener. (IF 12.6) Pub Date : 2023-08-25 Pan Wang, Guoyu Lan, Bin Xu, Zhenwei Yu, Chen Tian, Xia Lei, Wassilios G. Meissner, Tao Feng, Ying Yang, Jing Zhang
The accumulation of α-synuclein (α-syn), an essential step in PD development and progression, is observed not only in neurons but also in glia, including astrocytes. The mechanisms regulating astrocytic α-syn level and aggregation remain unclear. More recently, it has been demonstrated that a part of α-syn spreading occurs through extracellular vesicles (EVs), although it is unknown whether this process
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The potential impact of clinical factors on blood-based biomarkers for Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-08-18 Fengfeng Pan, Yan Lu, Qi Huang, Fang Xie, Jingye Yang, Qihao Guo
With the development of testing technologies, blood-based biomarkers for Alzheimer’s disease (AD) such as amyloid-β (Aβ), phosphorylated tau (P-tau), and neurofilament light (NfL) have shown potential value in predicting AD pathology and disease progression [1]. To better interpret the detection results, it is essential to understand what factors would affect the concentrations of these biomarkers
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Multidimensional biomarkers for multiple system atrophy: an update and future directions Transl. Neurodegener. (IF 12.6) Pub Date : 2023-07-28 Linlin Wan, Sudan Zhu, Zhao Chen, Rong Qiu, Beisha Tang, Hong Jiang
Multiple system atrophy (MSA) is a fatal progressive neurodegenerative disease. Biomarkers are urgently required for MSA to improve the diagnostic and prognostic accuracy in clinic and facilitate the development and monitoring of disease-modifying therapies. In recent years, significant research efforts have been made in exploring multidimensional biomarkers for MSA. However, currently few biomarkers
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Clinical evidence of human pathogens implicated in Alzheimer’s disease pathology and the therapeutic efficacy of antimicrobials: an overview Transl. Neurodegener. (IF 12.6) Pub Date : 2023-07-26 Celso S. G. Catumbela, Vijayasree V. Giridharan, Tatiana Barichello, Rodrigo Morales
A wealth of pre-clinical reports and data derived from human subjects and brain autopsies suggest that microbial infections are relevant to Alzheimer’s disease (AD). This has inspired the hypothesis that microbial infections increase the risk or even trigger the onset of AD. Multiple models have been developed to explain the increase in pathogenic microbes in AD patients. Although this hypothesis is
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Animal models of Parkinson’s disease: bridging the gap between disease hallmarks and research questions Transl. Neurodegener. (IF 12.6) Pub Date : 2023-07-19 Axelle Dovonou, Cyril Bolduc, Victoria Soto Linan, Charles Gora, Modesto R. Peralta III, Martin Lévesque
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. More than 200 years after its first clinical description, PD remains a serious affliction that affects a growing proportion of the population. Prevailing treatments only alleviate symptoms; there is still neither a cure that targets the neurodegenerative processes nor therapies that modify
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Impact of seed amplification assay and surface-enhanced Raman spectroscopy combined approach on the clinical diagnosis of Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-07-12 Cristiano D’Andrea, Federico Angelo Cazzaniga, Edoardo Bistaffa, Andrea Barucci, Marella de Angelis, Martina Banchelli, Edoardo Farnesi, Panagis Polykretis, Chiara Marzi, Antonio Indaco, Pietro Tiraboschi, Giorgio Giaccone, Paolo Matteini, Fabio Moda
The current diagnosis of Alzheimer’s disease (AD) is based on a series of analyses which involve clinical, instrumental and laboratory findings. However, signs, symptoms and biomarker alterations observed in AD might overlap with other dementias, resulting in misdiagnosis. Here we describe a new diagnostic approach for AD which takes advantage of the boosted sensitivity in biomolecular detection, as
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Head-to-head comparison of plasma and PET imaging ATN markers in subjects with cognitive complaints Transl. Neurodegener. (IF 12.6) Pub Date : 2023-06-29 Jiaying Lu, Xiaoxi Ma, Huiwei Zhang, Zhenxu Xiao, Ming Li, Jie Wu, Zizhao Ju, Li Chen, Li Zheng, Jingjie Ge, Xiaoniu Liang, Weiqi Bao, Ping Wu, Ding Ding, Tzu-Chen Yen, Yihui Guan, Chuantao Zuo, Qianhua Zhao
Gaining more information about the reciprocal associations between different biomarkers within the ATN (Amyloid/Tau/Neurodegeneration) framework across the Alzheimer’s disease (AD) spectrum is clinically relevant. We aimed to conduct a comprehensive head-to-head comparison of plasma and positron emission tomography (PET) ATN biomarkers in subjects with cognitive complaints. A hospital-based cohort
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Brain metabolism in Alzheimer’s disease: biological mechanisms of exercise Transl. Neurodegener. (IF 12.6) Pub Date : 2023-06-26 Longfei Xu, Ran Liu, Yingkai Qin, Tianhui Wang
Alzheimer’s disease (AD) is a major subtype of neurodegenerative dementia caused by long-term interactions and accumulation of multiple adverse factors, accompanied by dysregulation of numerous intracellular signaling and molecular pathways in the brain. At the cellular and molecular levels, the neuronal cellular milieu of the AD brain exhibits metabolic abnormalities, compromised bioenergetics, impaired
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Update on the pathological roles of prostaglandin E2 in neurodegeneration in amyotrophic lateral sclerosis Transl. Neurodegener. (IF 12.6) Pub Date : 2023-06-19 Hiroshi Nango, Komugi Tsuruta, Hiroko Miyagishi, Yuri Aono, Tadashi Saigusa, Yasuhiro Kosuge
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. The pathogenesis of ALS remains largely unknown; however, inflammation of the spinal cord is a focus of ALS research and an important pathogenic process in ALS. Prostaglandin E2 (PGE2) is a major lipid mediator generated by the arachidonic-acid cascade
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Reciprocal effects of alpha-synuclein aggregation and lysosomal homeostasis in synucleinopathy models Transl. Neurodegener. (IF 12.6) Pub Date : 2023-06-13 Alice Drobny, Fanni Annamária Boros, Denise Balta, Susy Prieto Huarcaya, Deniz Caylioglu, Niyeti Qazi, Julia Vandrey, Yanni Schneider, Jan Philipp Dobert, Caleb Pitcairn, Joseph Robert Mazzulli, Friederike Zunke
Lysosomal dysfunction has been implicated in a number of neurodegenerative diseases such as Parkinson’s disease (PD). Various molecular, clinical and genetic studies have highlighted a central role of lysosomal pathways and proteins in the pathogenesis of PD. Within PD pathology the synaptic protein alpha-synuclein (αSyn) converts from a soluble monomer to oligomeric structures and insoluble amyloid
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Defective lysosomal acidification: a new prognostic marker and therapeutic target for neurodegenerative diseases Transl. Neurodegener. (IF 12.6) Pub Date : 2023-06-08 Chih Hung Lo, Jialiu Zeng
Lysosomal acidification dysfunction has been implicated as a key driving factor in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease. Multiple genetic factors have been linked to lysosomal de-acidification through impairing the vacuolar-type ATPase and ion channels on the organelle membrane. Similar lysosomal abnormalities are also present in sporadic
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Cognitive dysfunction of patients infected with SARS-CoV-2 omicron variant in Shanghai, China Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-24 Ping Yuan, Yong Bi, Yu Luo, Quan Tao, Sugang Gong, Yi Wang, Lize Xiong, Xiaohuan Xia, Jialin C. Zheng
Previous studies have reported that nearly one-fourth of coronavirus disease 2019 (COVID-19) survivors suffer from persistent cognitive impairment, including impaired memory, attention, concentration, executive function, and speed of information processing [1,2,3]. Omicron is the latest severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variant of concern (VOC) reported in November 2021 [4]
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Longitudinal evolution of cortical thickness signature reflecting Lewy body dementia in isolated REM sleep behavior disorder: a prospective cohort study Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-22 Jung Hwan Shin, Heejung Kim, Yu Kyeong Kim, Eun Jin Yoon, Hyunwoo Nam, Beomseok Jeon, Jee-Young Lee
The isolated rapid-eye-movement sleep behavior disorder (iRBD) is a prodromal condition of Lewy body disease including Parkinson's disease and dementia with Lewy bodies (DLB). We aim to investigate the longitudinal evolution of DLB-related cortical thickness signature in a prospective iRBD cohort and evaluate the possible predictive value of the cortical signature index in predicting dementia-first
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An open-label multiyear study of sargramostim-treated Parkinson’s disease patients examining drug safety, tolerability, and immune biomarkers from limited case numbers Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-22 Katherine E. Olson, Mai M. Abdelmoaty, Krista L. Namminga, Yaman Lu, Helen Obaro, Pamela Santamaria, R. Lee Mosley, Howard E. Gendelman
The clinical utility and safety of sargramostim has previously been reported in cancer, acute radiation syndrome, autoimmune disease, inflammatory conditions, and Alzheimer’s disease. The safety, tolerability, and mechanisms of action in Parkinson’s disease (PD) during extended use has not been evaluated. As a primary goal, safety and tolerability was assessed in five PD patients treated with sargramostim
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Perivascular spaces relate to the course and cognition of Huntington’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-15 Xiao-Yan Li, Juan-Juan Xie, Jin-Hong Wang, Yu-Feng Bao, Yi Dong, Bin Gao, Ting Shen, Pei-Yu Huang, Hao-Chao Ying, Han Xu, Anna Wang Roe, Hsin-Yi Lai, Zhi-Ying Wu
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease that is caused by a cytosine-adenine-guanine (CAG) expansion in the first exon of the huntingtin (HTT) gene, which codes for the huntingtin protein. It typically manifests with a triad of symptoms, including motor disorders, cognitive impairment and psychiatric disturbances [1]. HD primarily affects the basal ganglia (BG)
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Early life adversity as a risk factor for cognitive impairment and Alzheimer’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-12 Zhihai Huang, J. Dedrick Jordan, Quanguang Zhang
Neurological conditions, including cognitive impairment and Alzheimer’s disease (AD), impose a huge burden on society, affecting millions of people globally. In addition to genetic factors, recent studies indicate that environmental and experiential factors may contribute to the pathogenesis of these diseases. Early life adversity (ELA) has a profound impact on brain function and health later in life
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A phase 1b randomized clinical trial of CT1812 to measure Aβ oligomer displacement in Alzheimer’s disease using an indwelling CSF catheter Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-12 Kelsie M. LaBarbera, Yvette I. Sheline, Nicholas J. Izzo, Carla M. Yuede, Lora Waybright, Raymond Yurko, Hannah M. Edwards, Woodrow D. Gardiner, Kaj Blennow, Henrik Zetterberg, Anne Börjesson-Hanson, Roger Morgan, Charles S. Davis, Robert J. Guttendorf, Lon S. Schneider, Steven DeKosky, Harry LeVine, Michael Grundman, Anthony O. Caggiano, John R. Cirrito, Susan M. Catalano, Mary E. Hamby
Trial Registration: May 11th, 2018 ClinicalTrials.gov Identifier: NCT03522129 https://clinicaltrials.gov/ct2/show/NCT03522129. Investigational therapies for Alzheimer's disease (AD) target a wide range of mechanisms, yet promising disease-modifying therapies remain a huge unmet need. Much evidence indicates that the oligomeric form of amyloid-beta (Aβ) is a toxic species contributing to AD through
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Correction: Links between COVID-19 and Parkinson’s disease/Alzheimer’s disease: reciprocal impacts, medical care strategies and underlying mechanisms Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-12 Pei Huang, Lin-Yuan Zhang, Yu-Yan Tan, Sheng-Di Chen
Correction to: Translational Neurodegeneration (2023) 12:5 https://doi.org/10.1186/s40035-023-00337-1 Following publication of this article [1], three errors were identified about the reference. Correction 1: 136. Crocker TF, Brown L, Lam N, Wray F, Knapp P, Forster A. Information provision for stroke survivors and their carers. Cochrane Database Syst Rev. 2021;11:CD001919. Should be corrected as follows:
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Correction: Starburst amacrine cells, involved in visual motion perception, lose their synaptic input from dopaminergic amacrine cells and degenerate in Parkinson’s disease patients Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-10 Xavier Sánchez‑Sáez, Isabel Ortuño‑Lizarán, Carla Sánchez‑Castillo, Pedro Lax, Nicolás Cuenca
Correction: Translational Neurodegeneration (2023) 12:17 (2023) https://doi.org/10.1186/s40035-023-00348-y Following publication of the original article [1], the authors reported an error in the article title. “Lose” was mistakenly typed as “loose” in the original title. The correct title should read: Starburst amacrine cells, involved in visual motion perception, lose their synaptic input from dopaminergic
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Correction: Plasma glial fibrillary acidic protein and neurofilament light chain for the diagnostic and prognostic evaluation of frontotemporal dementia Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-09 Nuole Zhu, Miguel Santos-Santos, Ignacio Illán-Gala, Victor Montal, Teresa Estellés, Isabel Barroeta, Miren Altuna, Javier Arranz, Laia Muñoz, Olivia Belbin, Isabel Sala, Maria Belén Sánchez-Saudinós, Andrea Subirana, Laura Videla, Jordi Pegueroles, Rafael Blesa, Jordi Clarimón, Maria Carmona-Iragui, Juan Fortea, Alberto Lleó, Daniel Alcolea
Correction: Translational Neurodegeneration (2021) 10:50 https://doi.org/10.1186/s40035-021-00275-w Following publication of this article [1], the below funding information is missing. European Union's Horizon 2020, 'MES-CoBraD' (H2020-SC1-BHC-2018-2020/GA 965422 to JF). The original article [1] has been corrected. Zhu, et al. Translational Neurodegeneration. 2021;10:50. Article CAS PubMed PubMed Central
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Microtubule acetylation dyshomeostasis in Parkinson’s disease Transl. Neurodegener. (IF 12.6) Pub Date : 2023-05-08 Padmashri Naren, Khan Sabiya Samim, Kamatham Pushpa Tryphena, Lalitkumar K. Vora, Saurabh Srivastava, Shashi Bala Singh, Dharmendra Kumar Khatri
The inter-neuronal communication occurring in extensively branched neuronal cells is achieved primarily through the microtubule (MT)-mediated axonal transport system. This mechanistically regulated system delivers cargos (proteins, mRNAs and organelles such as mitochondria) back and forth from the soma to the synapse. Motor proteins like kinesins and dynein mechanistically regulate polarized anterograde
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An AARS1 variant identified to cause adult-onset leukoencephalopathy with neuroaxonal spheroids and pigmented glia Transl. Neurodegener. (IF 12.6) Pub Date : 2023-04-28 Jingying Wu, Taotao Liu, Benyan Zhang, Chang Liu, Xinghua Luan, Li Cao
Adult-onset leukoencephalopathy with spheroids and pigmented glia (ALSP) is a genetic disease characterized by progressive cognitive, movement and neuropsychiatric disorders, bilateral periventricular white matter hyperintensity in fluid attenuated inversion recovery (FLAIR) and diffuse weighted imaging (DWI) sequences, and axonal spheroids and pigmented microglia by brain biopsy. Heterozygous variants
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Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases Transl. Neurodegener. (IF 12.6) Pub Date : 2023-04-14 Sina Shadfar, Sonam Parakh, Md Shafi Jamali, Julie D. Atkin
Redox homeostasis refers to the balance between the production of reactive oxygen species (ROS) as well as reactive nitrogen species (RNS), and their elimination by antioxidants. It is linked to all important cellular activities and oxidative stress is a result of imbalance between pro-oxidants and antioxidant species. Oxidative stress perturbs many cellular activities, including processes that maintain
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Starburst amacrine cells, involved in visual motion perception, loose their synaptic input from dopaminergic amacrine cells and degenerate in Parkinson’s disease patients Transl. Neurodegener. (IF 12.6) Pub Date : 2023-04-03 Xavier Sánchez-Sáez, Isabel Ortuño-Lizarán, Carla Sánchez-Castillo, Pedro Lax, Nicolás Cuenca
The main clinical symptoms characteristic of Parkinson’s disease (PD) are bradykinesia, tremor, and other motor deficits. However, non-motor symptoms, such as visual disturbances, can be identified at early stages of the disease. One of these symptoms is the impairment of visual motion perception. Hence, we sought to determine if the starburst amacrine cells, which are the main cellular type involved
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Argyrophilic grain disease is common in older adults and may be a risk factor for suicide: a study of Japanese forensic autopsy cases Transl. Neurodegener. (IF 12.6) Pub Date : 2023-04-01 Koji Yoshida, Yukiko Hata, Shojiro Ichimata, Keitaro Okada, Naoki Nishida
Neuropathological diagnosis of argyrophilic grain disease (AGD) is currently based primarily on the combination of argyrophilic grain (AG) visualized using Gallyas–Braak silver staining, phosphorylated tau-positive pretangles, coiled bodies, and ballooned neuron detection. Although AGD is common in patients with dementia and/or prominent psychiatric symptoms, whether it is a distinct neurological disease
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Modulating arousal to overcome gait impairments in Parkinson’s disease: how the noradrenergic system may act as a double-edged sword Transl. Neurodegener. (IF 12.6) Pub Date : 2023-03-26 Anouk Tosserams, Bastiaan R. Bloem, Kaylena A. Ehgoetz Martens, Rick C. Helmich, Roy P. C. Kessels, James M. Shine, Natasha L. Taylor, Gabriel Wainstein, Simon J. G. Lewis, Jorik Nonnekes
In stressful or anxiety-provoking situations, most people with Parkinson’s disease (PD) experience a general worsening of motor symptoms, including their gait impairments. However, a proportion of patients actually report benefits from experiencing—or even purposely inducing—stressful or high-arousal situations. Using data from a large-scale international survey study among 4324 people with PD and
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Toward a biomarker panel measured in CNS-originating extracellular vesicles for improved differential diagnosis of Parkinson’s disease and multiple system atrophy Transl. Neurodegener. (IF 12.6) Pub Date : 2023-03-20 Hash Brown Taha, Simon Hornung, Suman Dutta, Leony Fenwick, Otmane Lahgui, Kathryn Howe, Nour Elabed, Irish del Rosario, Darice Y. Wong, Aline Duarte Folle, Daniela Markovic, Jose-Alberto Palma, Un Jung Kang, Roy N. Alcalay, Miriam Sklerov, Horacio Kaufmann, Brent L. Fogel, Jeff M. Bronstein, Beate Ritz, Gal Bitan
Synucleinopathies are neurodegenerative diseases characterized by accumulation of misfolded α-synuclein (α-syn) inclusions in neuronal and/or glial cells. Despite differences in the underlying pathophysiology, synucleinopathies often are misdiagnosed, especially in early stages, due to the overlapping clinical symptoms [1]. Recently, our group has shown that α-syn measured in both neuronal extracellular