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1. Oligogenic inheritance of optineurin (OPTN) and C9ORF72 mutations in ALS highlights localisation of OPTN in the TDP‐43‐negative inclusions of C9ORF72‐ALS. Issue 2 (24th August 2015)

2. Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions. (27th May 2014)

3. Oligodendrocyte pathology exceeds axonal pathology in white matter in human amyotrophic lateral sclerosis. Issue 3 (8th June 2020)

4. SPG15 protein deficits are at the crossroads between lysosomal abnormalities, altered lipid metabolism and synaptic dysfunction. Issue 16 (21st March 2022)

5. C9ORF72 hexanucleotide repeat exerts toxicity in a stable, inducible motor neuronal cell model, which is rescued by partial depletion of Pten. (1st February 2017)

6. AMYOTROPHIC LATERAL SCLEROSIS ASSOCIATED WITH AN INTERMEDIATE LENGTH GGGGCC REPEAT EXPANSION HAS DISTINCT NEUROPATHOLOGY COMPARED TO PATIENTS WITH LARGER EXPANSIONS. Issue 10 (9th September 2014)

7. Loss of nuclear TDP‐43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones. Issue 6 (October 2014)

8. A neuronal DNA damage response is detected at the earliest stages of Alzheimer's neuropathology and correlates with cognitive impairment in the Medical Research Council's Cognitive Function and Ageing Study ageing brain cohort. (23rd April 2015)

9. Intermediate length C9orf72 expansion in an ALS patient without classical C9orf72 neuropathology. Issue 3 (June 2015)

10. The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy. (22nd June 2016)