Excessive synaptic loss is thought to be one of the earliest events in Alzheimer’s disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunctio...
Authors: Anthony Bosson, Adrien Paumier, Sylvie Boisseau, Muriel Jacquier-Sarlin, Alain Buisson and Mireille Albrieux
Alpha-synuclein (α-syn) aggregation represents the pathological hallmark of α-synucleinopathies like Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Toll-like rece...
Authors: Serena Venezia, Violetta Refolo, Alexia Polissidis, Leonidas Stefanis, Gregor K. Wenning and Nadia Stefanova
Given multiple studies of brain microRNA (miRNA) in relation to Alzheimer’s disease (AD) with few consistent results and the heterogeneity of this disease, the objective of this study was to explore their mech...
Authors: Ellis Patrick, Sathyapriya Rajagopal, Hon-Kit Andus Wong, Cristin McCabe, Jishu Xu, Anna Tang, Selina H. Imboywa, Julie A. Schneider, Nathalie Pochet, Anna M. Krichevsky, Lori B. Chibnik, David A. Bennett and Philip L. De Jager
Tauopathies are a broad set of neurodegenerative dementias characterized by aggregation of the tau protein into filamentous inclusions that can be found in neurons and glial cells. Activated microglia, astrocy...
Alzheimer’s Disease (AD) is the most prevalent progressive neurodegenerative disease; to date, no AD therapy has proven effective in delaying or preventing the disease course. In the search for novel therapeut...
Authors: Hunter S. Futch, Cara L. Croft, Van Q. Truong, Eric G. Krause and Todd E. Golde
Presenilins play a major role in the pathogenesis of Alzheimer’s disease, in which the hippocampus is particularly vulnerable. Previous studies of Presenilin function in the synapse, however, focused exclusive...
Authors: Sang Hun Lee, David Lutz, Mohanad Mossalam, Vadim Y. Bolshakov, Michael Frotscher and Jie Shen
Microglia are known as resident immune cells in the brain. β-amyloid (Aβ) plaques in the brain of Alzheimer’s disease (AD) are surrounded by microglia, but whether and how microglia affect the formation and ma...
Authors: Ruohe Zhao, Wanling Hu, Julia Tsai, Wei Li and Wen-Biao Gan
Amyotrophic Lateral Sclerosis (ALS) is a fatal and progressive neurodegenerative disorder with identified genetic causes representing a significant minority of all cases. A GGGGCC hexanucleotide repeat expansi...
Authors: Rustam Esanov, Gabriela Toro Cabrera, Nadja S. Andrade, Tania F. Gendron, Robert H. Brown Jr., Michael Benatar, Claes Wahlestedt, Christian Mueller and Zane Zeier
Parkinson’s’ disease (PD) and Multiple System Atrophy (MSA) are progressive brain disorders characterized by intracellular accumulations of α-synuclein and nerve cell loss in specific brain areas. This loss ca...
Authors: Tomasz Brudek, Kristian Winge, Jonas Folke, Søren Christensen, Karina Fog, Bente Pakkenberg and Lars Østergaard Pedersen
Parkinson’s disease is a multifactorial neurodegenerative disorder, the aetiology of which remains elusive. The primary clinical feature of progressively impaired motor control is caused by a loss of midbrain ...
Authors: James A. Duce, Bruce X. Wong, Hannah Durham, Jean-Christophe Devedjian, David P. Smith and David Devos
Prionoid transmission of α-synuclein (αSyn) aggregates along neuroanatomically connected projections is posited to underlie disease progression in α-synucleinopathies. Here, we specifically wanted to study whe...
Authors: Zachary A. Sorrentino, Mieu M.T. Brooks, Vincent Hudson III, Nicola J. Rutherford, Todd E. Golde, Benoit I. Giasson and Paramita Chakrabarty
Alzheimer’s disease (AD) is a highly heritable complex disease with no current effective prevention or treatment. The majority of drugs developed for AD focus on the amyloid cascade hypothesis, which implicate...
Authors: Anastasia G. Efthymiou and Alison M. Goate
Persistent endoplasmic reticulum (ER) stress is thought to drive the pathology of many chronic disorders due to its potential to elicit aberrant inflammatory signaling and facilitate cell death. In neurodegene...
Authors: Neil T. Sprenkle, Savannah G. Sims, Cristina L. Sánchez and Gordon P. Meares
Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and re...
Authors: Takashi Miyamoto, Liana Stein, Reuben Thomas, Biljana Djukic, Praveen Taneja, Joseph Knox, Keith Vossel and Lennart Mucke
Hyperphosphorylation of microtubule-associated protein tau is a distinct feature of neurofibrillary tangles (NFTs) that are the hallmark of neurodegenerative tauopathies. O-GlcNAcylation is a lesser known post...
Authors: Nicholas B. Hastings, Xiaohai Wang, Lixin Song, Brent D. Butts, Diane Grotz, Richard Hargreaves, J. Fred Hess, Kwok-Lam Karen Hong, Cathy Ruey-Ruey Huang, Lynn Hyde, Maureen Laverty, Julie Lee, Diane Levitan, Sherry X. Lu, Maureen Maguire, Veeravan Mahadomrongkul…
Herpes simplex virus type 1 strain 129 (H129) has represented a promising anterograde neuronal circuit tracing tool, which complements the existing retrograde tracers. However, the current H129 derived tracers...
Mitochondrial dysfunction has been linked to the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Functional studies of mitochondrial bioenergetics have focused...
Authors: Hibiki Kawamata, Pablo Peixoto, Csaba Konrad, Gloria Palomo, Kirsten Bredvik, Meri Gerges, Federica Valsecchi, Leonard Petrucelli, John M. Ravits, Anatoly Starkov and Giovanni Manfredi
To assess stages of Alzheimer's disease (AD) pathogenesis and the efficacy of drugs during clinical trials, there has been immense interest in the field to establish baseline cerebrospinal fluid (CSF) concentr...
Authors: Brendan P. Lucey, Anne M. Fagan, David M. Holtzman, John C. Morris and Randall J. Bateman
The experience from clinical trials indicates that anti-Aβ immunotherapy could be effective in early/pre-clinical stages of AD, whereas at the late stages promoting the clearing of Aβ alone may be insufficient...
Authors: Michael G. Agadjanyan, Karen Zagorski, Irina Petrushina, Hayk Davtyan, Konstantin Kazarian, Maxim Antonenko, Joy Davis, Charles Bon, Mathew Blurton-Jones, David H. Cribbs and Anahit Ghochikyan
Amyotrophic lateral sclerosis (ALS) is a debilitating neurodegenerative condition that is characterized by progressive loss of motor neurons and the accumulation of aggregated TAR DNA Binding Protein-43 (TDP-4...
Authors: Peter E. A. Ash, Elizabeth A. Stanford, Ali Al Abdulatif, Alejandra Ramirez-Cardenas, Heather I. Ballance, Samantha Boudeau, Amanda Jeh, James M. Murithi, Yorghos Tripodis, George J. Murphy, David H. Sherr and Benjamin Wolozin
The impairment of histone acetylation is causally linked to the cognitive decline in Alzheimer’s disease (AD). In addition to histone acetyltransferases (HATs) and histone deacetylases (HDACs), inhibitor of ac...
Authors: Gao-Shang Chai, Qiong Feng, Zhi-Hao Wang, Yu Hu, Dong-Sheng Sun, Xiao-Guang Li, Dan Ke, Hong-Lian Li, Gong-Ping Liu and Jian-Zhi Wang
Mutations in PINK1 and PARKIN are the most common causes of recessive early-onset Parkinson’s disease (EOPD). Together, the mitochondrial ubiquitin (Ub) kinase PINK1 and the cytosolic E3 Ub ligase PARKIN direct a...
Authors: Maya Ando, Fabienne C. Fiesel, Roman Hudec, Thomas R. Caulfield, Kotaro Ogaki, Paulina Górka-Skoczylas, Dariusz Koziorowski, Andrzej Friedman, Li Chen, Valina L. Dawson, Ted M. Dawson, Guojun Bu, Owen A. Ross, Zbigniew K. Wszolek and Wolfdieter Springer
Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer’s disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomo...
Chemokine signalling is required for the homing of leukocytes during retinal inflammation, and is associated with pathogenesis of diseases such as age-related macular degeneration (AMD). Here, we explore the r...
Authors: Riccardo Natoli, Nilisha Fernando, Michele Madigan, Joshua A. Chu-Tan, Krisztina Valter, Jan Provis and Matt Rutar
Parkin (PARK2) is an E3 ubiquitin ligase that is commonly mutated in Familial Parkinson’s Disease (PD). In cell culture models, Parkin is recruited to acutely depolarised mitochondria by PINK1. PINK1 activates...
Authors: Aitor Martinez, Benoit Lectez, Juanma Ramirez, Oliver Popp, James D. Sutherland, Sylvie Urbé, Gunnar Dittmar, Michael J. Clague and Ugo Mayor
Light exposure triggers movement of certain signaling proteins within the cellular compartments of the highly polarized rod photoreceptor cell. This redistribution of proteins between the inner and outer segme...
Authors: Kasey Rose, Steven T. Walston and Jeannie Chen
Amyloid-β oligomers (oAβ) are thought to mediate neurotoxicity in Alzheimer’s disease (AD), and previous studies in AD transgenic mice suggest that calcium dysregulation may contribute to these pathological ef...
Authors: Michal Arbel-Ornath, Eloise Hudry, Josiah R. Boivin, Tadafumi Hashimoto, Shuko Takeda, Kishore V. Kuchibhotla, Steven Hou, Carli R. Lattarulo, Arianna M. Belcher, Naomi Shakerdge, Pariss B. Trujillo, Alona Muzikansky, Rebecca A. Betensky, Bradley T. Hyman and Brian J. Bacskai
FADD (Fas-associated death domain) adaptor is a crucial protein involved in the induction of cell death but also mediates non-apoptotic actions via a phosphorylated form (p-Ser194-FADD). This study investigate...
Authors: Alfredo Ramos-Miguel, Jesús A. García-Sevilla, Alasdair M. Barr, Thomas A. Bayer, Peter Falkai, Sue E. Leurgans, Julie A. Schneider, David A. Bennett, William G. Honer and M. Julia García-Fuster
The mechanisms behind Aβ-peptide accumulation in non-familial Alzheimer’s disease (AD) remain elusive. Proteins of the tetraspanin family modulate Aβ production by interacting to γ-secretase.
Previous studies regarding the lipid-cognition relation in older adults are limited and have generated mixed results. We thus examined whether higher blood cholesterol concentrations were associated with faste...
Authors: Chaoran Ma, Zhaoxue Yin, Pengfei Zhu, Jiesi Luo, Xiaoming Shi and Xiang Gao
Reduction or inhibition of histone deacetylase 6 (HDAC6) has been shown to rescue memory in mouse models of Alzheimer’s disease (AD) and is recently being considered a possible therapeutic strategy. However, t...
Authors: Heesun Choi, Haeng Jun Kim, Jisoo Kim, Soohyun Kim, Jinhee Yang, Wonik Lee, Yeonju Park, Seung Jae Hyeon, Dong-Sup Lee, Hoon Ryu, Junho Chung and Inhee Mook-Jung
The activation of the aspartate-specific cysteinyl protease, Caspase-6, is proposed as an early pathogenic event of Alzheimer disease (AD) and Huntington’s disease. Caspase-6 inhibitors could be useful against...
Authors: Prateep Pakavathkumar, Anastasia Noël, Clotilde Lecrux, Agne Tubeleviciute-Aydin, Edith Hamel, Jan-Eric Ahlfors and Andrea C. LeBlanc
The ubiquitin-proteasome-system (UPS) is the major intracellular pathway leading to the degradation of unwanted and/or misfolded soluble proteins. This includes proteins regulating cellular survival, synaptic ...
Authors: Tobias Engel, Jaime Martinez-Villarreal, Christine Henke, Eva M. Jimenez-Mateos, Amaya Sanz-Rodriguez, Mariana Alves, Yasmina Hernandez-Santana, Gary P. Brennan, Aidan Kenny, Aoife Campbell, Jose J. Lucas and David C. Henshall
The ability of oligodendrocyte progenitor cells (OPCs) to give raise to myelin forming cells during developmental myelination, normal adult physiology and post-lesion remyelination in white matter depends on f...
Authors: Camille Leonetti, Richard Macrez, Mathilde Pruvost, Yannick Hommet, Jérémie Bronsard, Antoine Fournier, Maxime Perrigault, Isabel Machin, Denis Vivien, Diego Clemente, Fernando De Castro, Eric Maubert and Fabian Docagne
Abnormal aggregation of tau in the brain is a major contributing factor in various neurodegenerative diseases. The role of tau phosphorylation in the pathophysiology of tauopathies remains unclear. Consequentl...
Authors: Laure Saint-Aubert, Laetitia Lemoine, Konstantinos Chiotis, Antoine Leuzy, Elena Rodriguez-Vieitez and Agneta Nordberg
Proteolytic degradation of amyloid β (Aβ) peptides has been intensely studied due to the central role of Aβ in Alzheimer’s disease (AD) pathogenesis. While several enzymes have been shown to degrade Aβ peptide...
Authors: Erik Portelius, Niklas Mattsson, Josef Pannee, Henrik Zetterberg, Magnus Gisslén, Hugo Vanderstichele, Eleni Gkanatsiou, Gabriela A. N. Crespi, Michael W. Parker, Luke A. Miles, Johan Gobom and Kaj Blennow
Reactive microglia have been associated with the histological changes that occur in Parkinson’s disease brains and mouse models of the disease. Multiple studies from autopsy brains have verified the presence o...
Authors: Gunjan Dhawan Manocha, Angela Marie Floden, Kendra Lynn Puig, Kumi Nagamoto-Combs, Clemens R. Scherzer and Colin Kelly Combs
Neuroinflammation is associated with a wide range of neurodegenerative disorders, however the specific contribution to individual disease pathogenesis and selective neuronal cell death is not well understood. ...
Authors: Michael Lattke, Stephanie N. Reichel, Alexander Magnutzki, Alireza Abaei, Volker Rasche, Paul Walther, Dinis P. Calado, Boris Ferger, Thomas Wirth and Bernd Baumann
Alzheimer’s disease (AD)-linked protein, presenilin 1 (PS1), is present at the synapse, and the knock-out of presenilin in mice leads to synaptic dysfunction. On the other hand, synaptic activity was shown to ...
Authors: Katarzyna Marta Zoltowska, Masato Maesako, Iryna Lushnikova, Shuko Takeda, Laura J. Keller, Galina Skibo, Bradley T. Hyman and Oksana Berezovska
Alzheimer’s disease (AD) is characterized by progressive cognitive decline and memory loss. Environmental factors and gene-environment interactions (GXE) may increase AD risk, accelerate cognitive decline, and...
Authors: Anna K. Engstrom, Jessica M. Snyder, Nobuyo Maeda and Zhengui Xia
TDP-43 proteinopathy is a prominent pathological feature that occurs in a number of human diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and inclusion body myositis (IBM...
Authors: Yun Ha Jeong, Jonathan P. Ling, Sophie Z. Lin, Aneesh N. Donde, Kerstin E. Braunstein, Elisa Majounie, Bryan J. Traynor, Katherine D. LaClair, Thomas E. Lloyd and Philip C. Wong
APOE genotype is the foremost genetic factor modulating β-amyloid (Aβ) deposition and risk of sporadic Alzheimer’s disease (AD). Here we investigated how APOE genotype influences respo...
Authors: Joanna E Pankiewicz, Jairo Baquero-Buitrago, Sandrine Sanchez, Jennifer Lopez-Contreras, Jungsu Kim, Patrick M. Sullivan, David M. Holtzman and Martin J. Sadowski
Converging evidence from genetic, pathological and experimental studies have increasingly suggested an important role for autophagy impairment in Parkinson’s Disease (PD). Genetic studies have identified mutat...
Authors: Tim E. Moors, Jeroen J. M. Hoozemans, Angela Ingrassia, Tommaso Beccari, Lucilla Parnetti, Marie-Christine Chartier-Harlin and Wilma D. J. van de Berg
Parkinson’s disease (PD) is a devastating and highly prevalent neurodegenerative disease for which only symptomatic treatment is available. In order to develop a truly effective disease-modifying therapy, impr...
Authors: Helena Xicoy, Bé Wieringa and Gerard J.M. Martens
LRRK2 mutations and risk variants increase susceptibility to inherited and idiopathic Parkinson’s disease, while recent studies have identified potential protective variants. This, and...
Authors: Daniel C. Berwick, Behzad Javaheri, Andrea Wetzel, Mark Hopkinson, Jonathon Nixon-Abell, Simone Grannò, Andrew A. Pitsillides and Kirsten Harvey
Glycerophosphodiester phosphodiesterase 2 (GDE2) is a six-transmembrane protein that cleaves glycosylphosphatidylinositol (GPI) anchors to regulate GPI-anchored protein activity at the cell surface. In the dev...
Authors: Clinton Cave, Sungjin Park, Marianeli Rodriguez, Mai Nakamura, Ahmet Hoke, Mikhail Pletnikov and Shanthini Sockanathan
Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple scle...
Authors: Merry W. Ma, Jing Wang, Quanguang Zhang, Ruimin Wang, Krishnan M. Dhandapani, Ratna K. Vadlamudi and Darrell W. Brann
The most frequent genetic cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) is the expansion of a GGGGCC hexanucleotide repeat in a non-coding region of the chromosome 9...
Authors: Yu Ohki, Andrea Wenninger-Weinzierl, Alexander Hruscha, Kazuhide Asakawa, Koichi Kawakami, Christian Haass, Dieter Edbauer and Bettina Schmid
Tau pathology in AD spreads in a hierarchical pattern, whereby it first appears in the entorhinal cortex, then spreads to the hippocampus and later to the surrounding areas. Based on this sequential appearance...
Authors: Yipeng Wang, Varun Balaji, Senthilvelrajan Kaniyappan, Lars Krüger, Stephan Irsen, Katharina Tepper, RamReddy Chandupatla, Walter Maetzler, Anja Schneider, Eckhard Mandelkow and Eva-Maria Mandelkow
Authors: Thiyagaragan M. Achariyar, Baoman Li, Weiguo Peng, Philip B. Verghese, Yang Shi, Evan McConnell, Abdellatif Benraiss, Tristan Kasper, Wei Song, Takahiro Takano, David M. Holtzman, Maiken Nedergaard and Rashid Deane
Citation:Molecular Neurodegeneration
2017
12:3
Published on: 12 January 2017
The
original article was published in Molecular Neurodegeneration
2016
11:74
