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1. High levels of neurofilament light and YKL-40 in cerebrospinal fluid are related to poor outcome in ALS.

2. Myofiber Type Shift in Extraocular Muscles in Amyotrophic Lateral Sclerosis.

3. A novel homozygous p.Ser69Pro SOD1 mutation causes severe young-onset ALS with decreased enzyme activity.

4. Integrative genetic analysis illuminates ALS heritability and identifies risk genes.

5. Infantile SOD1 deficiency syndrome caused by a homozygous SOD1 variant with absence of enzyme activity.

6. De novo mutations in SOD1 are a cause of ALS.

7. Neurofilaments can differentiate ALS subgroups and ALS from common diagnostic mimics.

9. Inflammatory profiles relate to survival in subtypes of amyotrophic lateral sclerosis.

10. Misfolded SOD1 inclusions in patients with mutations in C9orf72 and other ALS/FTD-associated genes.

11. A novel phosphorylation site mutation in profilin 1 revealed in a large screen of US, Nordic, and German amyotrophic lateral sclerosis/frontotemporal dementia cohorts.

12. Disease-related changes in the cerebrospinal fluid metabolome in amyotrophic lateral sclerosis detected by GC/TOFMS.

13. Good practice in the management of amyotrophic lateral sclerosis: clinical guidelines. An evidence-based review with good practice points. EALSC Working Group.

15. Infantile SOD1 deficiency syndrome caused by a homozygous SOD1 variant with absence of enzyme activity.

16. De novo mutations in are a cause of ALS.

17. C9orf72 expansion is associated with accelerated decline of respiratory function and decreased survival in amyotrophic lateral sclerosis

18. Misfolded SOD1 inclusions in patients with mutations in and other ALS/FTD-associated genes.

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