Introduction to special issue: Neurovascular aging—A driving force for neurological dysfunction in stroke and neurodegenerative diseases

2017 ◽  
Vol 34 ◽  
pp. 1-2
Author(s):  
Steven H. Graham
2015 ◽  
Vol 36 (2) ◽  
pp. 72-77 ◽  
Author(s):  
Prajwal Ciryam ◽  
Rishika Kundra ◽  
Richard I. Morimoto ◽  
Christopher M. Dobson ◽  
Michele Vendruscolo

2021 ◽  
pp. 1-11
Author(s):  
Amir Mohammadi ◽  
Abasalt Hosseinzadeh Colagar ◽  
Ayeh Khorshidian ◽  
Seyed Mohammad Amini

Progressive abnormality and loss of axons and neurons in the central nervous system (CNS) cause neurodegenerative diseases (NDs). Protein misfolding and its collection are the most important pathological features of NDs. Astrocytes are the most plentiful cells in the mammalian CNS (about 20–40% of the human brain) and have several central functions in the maintenance of the health and correct function of the CNS. Astrocytes have an essential role in the preservation of brain homeostasis, and it is not surprising that these multifunctional cells have been implicated in the onset and progression of several NDs. Thus, they become an exciting target for the study of NDs. Over almost 15 years, it was revealed that curcumin has several therapeutic effects in a wide variety of diseases’ treatment. Curcumin is a valuable ingredient present in turmeric spice and has several essential roles, including those which are anticarcinogenic, hepatoprotective, thrombosuppressive, cardioprotective, anti-arthritic, anti-inflammatory, antioxidant, chemopreventive, chemotherapeutic, and anti-infectious. Furthermore, curcumin can suppress inflammation; promote angiogenesis; and treat diabetes, pulmonary problems, and neurological dysfunction. Here, we review the effects of curcumin on astrocytes in NDs, with a focus on Alzheimer’s disease, Parkinson’s disease, multiple scleroses, Huntington’s disease, and amyotrophic lateral sclerosis.


2020 ◽  
Vol 6 (1) ◽  
pp. 1-15
Author(s):  
Jordi Tejel ◽  
Ramazan Hakkı Öztan

This special issue approaches the study of refugees and forcibly displaced persons in the Middle East beyond the analytic bounds dictated by states, nations and regions. Each author is interested in showing connections, influences, and far-reaching consequences that cut across analytic boundaries. By challenging state-centred accounts and instead placing refugees, institutions, and states in a mutually interactive framework, each contributor frames refugees as the driving force behind various historical processes. By providing a range of case studies drawn from the Middle East, the volume also marks a step away from the Euro-centrism that so often defines the study of refugees and shows the centrality of the developments in Europe for the Middle East and the developments in the Middle East for Europe. We therefore propose the connected histories of refugeedom as the historiographical way forward in the study of refugees.


2021 ◽  
Vol 63 (1) ◽  
Author(s):  
Geoffrion Karine ◽  
Viviane Cretton

For a number of migrant actors, bureaucratic processes related to immigration constitute the greater part of the route toward their aspired destination and significantly shape their experience of migration and forced immobility. This special issue takes a look at the meaningful ways in which migrant actors interact with immigration bureaucracies and at how administrative procedures, with their highly emotional potential, shape in turn the subjectivity, decisions and actions of migrant actors. All the articles here analyse immigration bureaucracy as a dynamic process mediated by a network of people and by material objects (for example, documents, forms). Whether work, marriage or refuge is the reason for migration, the period of waiting in administrative limbo — which can last years — is crucial to our understanding of the bureaucratic encounter as a social force. This issue, dedicated to migrants’ lived experience of paperwork, clerks and other immigration intermediaries, explores two aspects of migrant actors’ encounters with immigration bureaucracies that go beyond the specificities of each individual’s personal background and trajectory: the production of affects and bureaucratic agency; the former often being the driving force behind the latter.


2019 ◽  
Author(s):  
Adi Minis ◽  
Jose Rodriguez ◽  
Avi Levin ◽  
Kai Liu ◽  
Eve-Ellen Govek ◽  
...  

AbstractProteasome-mediated degradation of intracellular proteins is essential for cell function and survival. The proteasome-binding protein PI31 (Proteasomal Inhibitor of 31kD) promotes 26S assembly and functions as an adapter for proteasome transport in axons. As localized protein synthesis and degradation is especially critical in neurons, we generated a conditional loss of PI31 in spinal motor neurons (MNs) and cerebellar Purkinje cells (PCs). A cKO of PI31 in these neurons caused axon degeneration, neuronal loss and progressive spinal and cerebellar neurological dysfunction. For both MNs and PCs, markers of proteotoxic stress preceded axonal degeneration and motor dysfunction, indicating a critical role for PI31 in neuronal homeostasis. The time course of the loss of MN and PC function in developing mouse CNS suggests a key role for PI31 in human developmental neurological disorders.Statement of SignificanceThe conserved proteasome-binding protein PI31 serves as an adapter to couple proteasomes with cellular motors to mediate their transport to distal tips of neurons where protein breakdown occurs. We generated global and conditional PI31 knockout mouse strains and show that this protein is required for protein homeostasis, and that its conditional inactivation in neurons disrupts synaptic structures and long-term survival. This work establishes a critical role for PI31 and local protein degradation in the maintenance of neuronal architecture, circuitry and function. Because mutations that impair PI31 function cause neurodegenerative diseases in humans, reduced PI31 activity may contribute to age-related neurodegenerative diseases.


2020 ◽  
Vol 295 (19) ◽  
pp. 6652-6664 ◽  
Author(s):  
Sophie A. Morgan ◽  
Isabelle Lavenir ◽  
Juan Fan ◽  
Masami Masuda-Suzukake ◽  
Daniela Passarella ◽  
...  

Assembled α-synuclein in nerve cells and glial cells is the defining pathological feature of neurodegenerative diseases called synucleinopathies. Seeds of α-synuclein can induce the assembly of monomeric protein. Here, we used sucrose gradient centrifugation and transiently transfected HEK 293T cells to identify the species of α-synuclein from the brains of homozygous, symptomatic mice transgenic for human mutant A53T α-synuclein (line M83) that seed aggregation. The most potent fractions contained Sarkosyl-insoluble assemblies enriched in filaments. We also analyzed six cases of idiopathic Parkinson's disease (PD), one case of familial PD, and six cases of multiple system atrophy (MSA) for their ability to induce α-synuclein aggregation. The MSA samples were more potent than those of idiopathic PD in seeding aggregation. We found that following sucrose gradient centrifugation, the most seed-competent fractions from PD and MSA brains are those that contain Sarkosyl-insoluble α-synuclein. The fractions differed between PD and MSA, consistent with the presence of distinct conformers of assembled α-synuclein in these different samples. We conclude that α-synuclein filaments are the main driving force for amplification and propagation of pathology in synucleinopathies.


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