Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis

SH Kang, Y Li, M Fukaya, I Lorenzini… - Nature …, 2013 - nature.com
Oligodendrocytes associate with axons to establish myelin and provide metabolic support to
neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes …

[HTML][HTML] TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

…, YI Zhang, ME Umoh, SW Vaughan, I Lorenzini… - Nature …, 2018 - nature.com
The cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43)
is a common histopathological hallmark of the amyotrophic lateral sclerosis and …

Molecular comparison of GLT1+ and ALDH1L1+ astrocytes in vivo in astroglial reporter mice

Y Yang, S Vidensky, L Jin, C Jie, I Lorenzini, M Frankl… - Glia, 2011 - Wiley Online Library
Astrocyte heterogeneity remains largely unknown in the CNS due to lack of specific astroglial
markers. In this study, molecular identity of in vivo astrocytes was characterized in BAC …

[PDF][PDF] Presynaptic regulation of astroglial excitatory neurotransmitter transporter GLT1

Y Yang, O Gozen, A Watkins, I Lorenzini, A Lepore… - Neuron, 2009 - cell.com
The neuron-astrocyte synaptic complex is a fundamental operational unit of the nervous
system. Astroglia regulate synaptic glutamate, via neurotransmitter transport by GLT1/EAAT2. …

[PDF][PDF] C9orf72 deficiency promotes microglial-mediated synaptic loss in aging and amyloid accumulation

D Lall, I Lorenzini, TA Mota, S Bell, TE Mahan… - Neuron, 2021 - cell.com
C9orf72 repeat expansions cause inherited amyotrophic lateral sclerosis (ALS)/frontotemporal
dementia (FTD) and result in both loss of C9orf72 protein expression and production of …

[HTML][HTML] Artificial intelligence in neurodegenerative disease research: use of IBM Watson to identify additional RNA-binding proteins altered in amyotrophic lateral …

N Bakkar, T Kovalik, I Lorenzini, S Spangler… - Acta …, 2018 - Springer
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease with no
effective treatments. Numerous RNA-binding proteins (RBPs) have been shown to be altered in …

Biosynthesis of the major brain gangliosides GD1a and GT1b

…, PHH Lopez, D Colacurcio, K Vajn, I Lorenzini… - …, 2012 - academic.oup.com
Gangliosides—sialylated glycosphingolipids—are the major glycoconjugates of nerve cells.
The same four structures—GM1, GD1a, GD1b and GT1b—comprise the great majority of …

[PDF][PDF] Post-transcriptional inhibition of Hsc70-4/HSPA8 expression leads to synaptic vesicle cycling defects in multiple models of ALS

AN Coyne, I Lorenzini, CC Chou, M Torvund… - Cell reports, 2017 - cell.com
Amyotrophic lateral sclerosis (ALS) is a synaptopathy accompanied by the presence of
cytoplasmic aggregates containing TDP-43, an RNA-binding protein linked to ∼97% of ALS …

Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS

E Manzo, I Lorenzini, D Barrameda, AG O'Conner… - Elife, 2019 - elifesciences.org
10.7554/eLife.45114.001 Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative
disorder, with TDP-43 inclusions as a major pathological hallmark. Using a Drosophila …

[HTML][HTML] Moderate intrinsic phenotypic alterations in C9orf72 ALS/FTD iPSC-microglia despite the presence of C9orf72 pathological features

I Lorenzini, E Alsop, J Levy, LM Gittings… - Frontiers in cellular …, 2023 - frontiersin.org
While motor and cortical neurons are affected in C9orf72 amyotrophic lateral sclerosis and
frontotemporal dementia (ALS/FTD), it remains largely unknown if and how non-neuronal …