Amyotrophic lateral sclerosis: Current perspectives from basic research to the clinic

R Mancuso, X Navarro - Progress in Neurobiology, 2015 - Elsevier
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by
progressive degeneration of upper and lower motoneurons, leading to muscle weakness …

Characterization of the contribution of genetic background and gender to disease progression in the SOD1 G93A mouse model of amyotrophic lateral sclerosis: a …

SR Pfohl, MT Halicek… - Journal of neuromuscular …, 2015 - content.iospress.com
Background: The SOD1 G93A mouse model of amyotrophic lateral sclerosis (ALS) is the
most frequently used model to examine ALS pathophysiology. There is a lack of …

Targeting mi R‐155 restores abnormal microglia and attenuates disease in SOD 1 mice

O Butovsky, MP Jedrychowski, R Cialic… - Annals of …, 2015 - Wiley Online Library
Objective To investigate miR‐155 in the SOD1 mouse model and human sporadic and
familial amyotrophic lateral sclerosis (ALS). Methods NanoString microRNA, microglia and …

Neuroprotective effects of the mitochondria-targeted antioxidant MitoQ in a model of inherited amyotrophic lateral sclerosis

E Miquel, A Cassina, L Martínez-Palma… - Free Radical Biology …, 2014 - Elsevier
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by
motor neuron degeneration that ultimately results in progressive paralysis and death …

Adult spinal motoneurones are not hyperexcitable in a mouse model of inherited amyotrophic lateral sclerosis

N Delestrée, M Manuel, C Iglesias… - The Journal of …, 2014 - Wiley Online Library
Key points Intrinsic hyperexcitability of spinal motoneurones is thought to contribute to
excitotoxicity during amyotrophic lateral sclerosis (ALS), but it has never been demonstrated …

The vulnerability of spinal motoneurons and soma size plasticity in a mouse model of amyotrophic lateral sclerosis

SS Dukkipati, TL Garrett… - The Journal of …, 2018 - Wiley Online Library
Key points Motoneuron soma size is a largely plastic property that is altered during
amyotrophic lateral sclerosis (ALS) progression. We report evidence of systematic spinal …

Activity-dependent neuroprotective protein deficiency models synaptic and developmental phenotypes of autism-like syndrome

G Hacohen-Kleiman, S Sragovich… - The Journal of …, 2018 - Am Soc Clin Investig
Previous findings showed that in mice, complete knockout of activity-dependent
neuroprotective protein (ADNP) abolishes brain formation, while haploinsufficiency (Adnp+ …

Modulation of astrocytic mitochondrial function by dichloroacetate improves survival and motor performance in inherited amyotrophic lateral sclerosis

E Miquel, A Cassina, L Martínez-Palma, C Bolatto… - PloS one, 2012 - journals.plos.org
Mitochondrial dysfunction is one of the pathogenic mechanisms that lead to
neurodegeneration in Amyotrophic Lateral Sclerosis (ALS). Astrocytes expressing the ALS …

C57BL/6J congenic Prp-TDP43A315T mice develop progressive neurodegeneration in the myenteric plexus of the colon without exhibiting key features of ALS

T Hatzipetros, LP Bogdanik, VR Tassinari, JD Kidd… - Brain research, 2014 - Elsevier
ALS therapy development has been hindered by the lack of rodent animal models. The
discovery of TDP-43, a transcription factor that accumulates in the cytoplasm of motor …

Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of charcot-marie-tooth neuropathy

M Barneo-Muñoz, P Juárez, A Civera-Tregón… - PLoS …, 2015 - journals.plos.org
Mutations in GDAP1, which encodes protein located in the mitochondrial outer membrane,
cause axonal recessive (AR-CMT2), axonal dominant (CMT2K) and demyelinating …