Nolz1 expression is required in dopaminergic axon guidance and striatal innervation.

Midbrain dopaminergic (DA) axons make long longitudinal projections towards the striatum. Despite the importance of DA striatal innervation, processes involved in establishment of DA axonal connectivity remain largely unknown. Here we demonstrate a striatal-specific requirement of transcriptional regulator Nolz1 in establishing DA circuitry formation.

Glatiramer acetate as a clinically and cost-effective treatment of relapsing multiple sclerosis over 10 years of use within the National Health Service: Final results from the UK Risk Sharing Scheme.

Background: The UK Risk Sharing Scheme (RSS) provided information on the effect of first-line multiple sclerosis (MS) disease-modifying treatments on long-term disability.

Objective: The aim is to provide results specific to glatiramer acetate (GA; Copaxone®) from the final 10-year analysis of the RSS.

Methods: A Markov model was used to assess clinical effectiveness measured as Expanded Disability Status Scale (EDSS) progression and utility loss.

SOX2 Regulates P63 and Stem/Progenitor Cell State in the Corneal Epithelium.

Mutations in key transcription factors SOX2 and P63 were linked with developmental defects and postnatal abnormalities such as corneal opacification, neovascularization, and blindness. The latter phenotypes suggest that SOX2 and P63 may be involved in corneal epithelial regeneration. Although P63 has been shown to be a key regulator of limbal stem cells, the expression pattern and function of SOX2 in the adult cornea remained unclear.

miRNAs-19b, -29b-2* and -339-5p show an early and sustained up-regulation in ischemic models of stroke.

Stroke, the loss of neurons after ischemic insult to the brain, is one of the leading causes of death and disability worldwide. Despite its prevalence and severity, current therapy is extremely limited, highlighting the importance of further understanding the molecular events underlying ischemia-induced neuronal cell death. An ischemic area can be subdivided into two separate pathophysiological regions: the rapidly dying necrotic core, and the potentially salvageable apoptotic penumbra.

Mitochondrial fragmentation and neuronal cell death in response to the Bcl-2/Bcl-x(L)/Bcl-w antagonist ABT-737.

Inhibition of pro-survival Bcl-2 family proteins by BH3-only proteins is a key initial step leading to apoptotic cell death. In neurons, investigating cell death pathways is often hampered by the multi-factorial nature of the stress stimuli employed. Here we investigate the action of ABT-737, a small molecule inhibitor which specifically targets the BH3-protein binding domain of pro-survival Bcl-2, Bcl-X(L) and Bcl-w.