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Stanley H. Appel

Researcher at Houston Methodist Hospital

Publications -  451
Citations -  33577

Stanley H. Appel is an academic researcher from Houston Methodist Hospital. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Acetylcholine receptor. The author has an hindex of 97, co-authored 443 publications receiving 31282 citations. Previous affiliations of Stanley H. Appel include University of Pennsylvania & Baylor University.

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Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways

Elizabeth T. Cirulli, +70 more
- 27 Mar 2015 - 
TL;DR: A moderate-scale sequencing study aimed at increasing the number of genes known to contribute to predisposition for ALS found several known ALS genes were found to be associated, and TBK1 (the gene encoding TANK-binding kinase 1) was identified as an ALS gene.
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Prevalence and patterns of cognitive impairment in sporadic ALS.

TL;DR: These data confirm the presence of cognitive impairment in 50% of patients with ALS and particularly implicate executive dysfunction and mild memory decline in the disease process and have features consistent with FTD.
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A unifying hypothesis for the cause of amyotrophic lateral sclerosis, Parkinsonism, and Alzheimer disease

TL;DR: It is presented that each of these disorders is due to lack of a disorder‐specific neurotrophic hormone, and central nervous system tissue culture provides a convenient system in which to assay these neurotrophic hormones and should permit a test of the hypothesis.
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Natural history of amyotrophic lateral sclerosis in a database population. Validation of a scoring system and a model for survival prediction.

TL;DR: In this paper, a Cox proportional hazards model was used to predict survival time in ALS patients, which proved highly accurate for the 80% of patients at intermediate risk, and a second model was developed which accurately predicted, after an initial period of observation, the time over which ALS patients will decline a set number of points in total ALS score.
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Wild-type microglia extend survival in PU.1 knockout mice with familial amyotrophic lateral sclerosis

TL;DR: It is demonstrated that the expression of mSOD1G93A results in activated and neurotoxic microglia, and suggested that the lack of m SOD1 G93A expression inmicroglia may contribute to motoneuron protection, and confirmed the importance of microglio as a double-edged sword.