Brain atrophy in multiple sclerosis: mechanisms, clinical relevance and treatment options

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3185190 21 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Brain atrophy in multiple sclerosis: mechanisms, clinical relevance and
treatment options
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Multiple sclerosis (MS) is an immune-mediated disease of the central
nervous system characterized by focal or diffuse inflammation,
demyelination, axonal loss and neurodegeneration. Brain atrophy can be
seen in the earliest stages of MS, progresses faster compared to healthy
adults, and is a reliable predictor of future physical and cognitive
disability. In addition, it is widely accepted to be a valid, sensitive
and reproducible measure of neurodegeneration in MS. Reducing the rate
of brain atrophy has only recently been incorporated as a critical
endpoint into the clinical trials of new or emerging disease modifying
drugs (DMDs) in MS. With the advent of easily accessible neuroimaging
softwares along with the accumulating evidence, clinicians may be able
to use brain atrophy measures in their everyday clinical practice to
monitor disease course and response to DMDs. In this review, we will
describe the different mechanisms contributing to brain atrophy, their
clinical relevance on disease presentation and course and the effect of
current or emergent DMDs on brain atrophy and neuroprotection.
Έτος δημοσίευσης:
2019
Συγγραφείς:
Andravizou, Athina
Dardiotis, Efthimios
Artemiadis, Artemios and
Sokratous, Maria
Siokas, Vasileios
Tsouris, Zisis
Aloizou,
Athina-Maria
Nikolaidis, Ioannis
Bakirtzis, Christos and
Tsivgoulis, Georgios
Deretzi, Georgia
Grigoriadis, Nikolaos and
Bogdanos, Dimitrios P.
Hadjigeorgiou, Georgios M.
Περιοδικό:
Autoimmunity Highlights
Εκδότης:
Springer-Verlag
Τόμος:
10
Αριθμός / τεύχος:
1
Λέξεις-κλειδιά:
Multiple sclerosis; Bran; Atrophy; Neurodegeneration; Axon;
Inflammation; Neuroprotection; Drugs
Επίσημο URL (Εκδότης):
DOI:
10.1186/s13317-019-0117-5
Το ψηφιακό υλικό του τεκμηρίου δεν είναι διαθέσιμο.