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E Rogaeva

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Articles 46
Citations 4713
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Recent Articles
1.
Gillingham S, Yunusova Y, Ganda A, Rogaeva E, Black S, Stuss D, et al.
Amyotroph Lateral Scler Frontotemporal Degener . 2016 Dec; 18(3-4):182-192. PMID: 27931119
Objective: It is generally acknowledged that at least 50% of individuals with amyotrophic lateral sclerosis (ALS) will exhibit cognitive deficits outside of the characteristic motor neuron involvement. However, a specific...
2.
Gijselinck I, Van Mossevelde S, van der Zee J, Sieben A, Engelborghs S, De Bleecker J, et al.
Mol Psychiatry . 2015 Oct; 21(8):1112-24. PMID: 26481318
Pathological expansion of a G4C2 repeat, located in the 5' regulatory region of C9orf72, is the most common genetic cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS)....
3.
Lambert J, Ibrahim-Verbaas C, Harold D, Naj A, Sims R, Bellenguez C, et al.
Nat Genet . 2013 Oct; 45(12):1452-8. PMID: 24162737
Eleven susceptibility loci for late-onset Alzheimer's disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large,...
4.
Reitz C, Tosto G, Vardarajan B, Rogaeva E, Ghani M, Rogers R, et al.
Transl Psychiatry . 2013 May; 3:e256. PMID: 23673467
Genetic variants in the sortilin-related receptor (SORL1) and the sortilin-related vacuolar protein sorting 10 (VPS10) domain-containing receptor 1 (SORCS1) are associated with increased risk of Alzheimer's disease (AD), declining cognitive...
5.
Marras C, Schule B, Schuele B, Munhoz R, Rogaeva E, Langston J, et al.
Neurology . 2011 Jul; 77(4):325-33. PMID: 21753163
Objectives: Using a family study design, we describe the motor and nonmotor phenotype in probands with LRRK2 G2019S mutations and family members and compare these individuals to patients with idiopathic...
6.
Robertson J, Bilbao J, Zinman L, Hazrati L, Tokuhiro S, Sato C, et al.
Neurobiol Aging . 2010 Jun; 32(3):553.e27-30. PMID: 20561714
It has been shown that mutations in the Fused in Sarcoma gene (FUS) could explain up to 5% of cases with familial amyotrophic lateral sclerosis (ALS). Our mutation analysis of...
7.
Bruni A, Bernardi L, Colao R, Rubino E, Smirne N, Frangipane F, et al.
Neurology . 2010 Feb; 74(10):798-806. PMID: 20164095
Objective: Large kindreds segregating familial Alzheimer disease (FAD) offer the opportunity of studying clinical variability as observed for presenilin 1 (PSEN1) mutations. Two early-onset FAD (EOFAD) Calabrian families with PSEN1...
8.
Sidransky E, Nalls M, Aasly J, Aharon-Peretz J, Annesi G, Barbosa E, et al.
N Engl J Med . 2009 Oct; 361(17):1651-61. PMID: 19846850
Background: Recent studies indicate an increased frequency of mutations in the gene encoding glucocerebrosidase (GBA), a deficiency of which causes Gaucher's disease, among patients with Parkinson's disease. We aimed to...
9.
Zinman L, Liu H, Sato C, Wakutani Y, Marvelle A, Moreno D, et al.
Neurology . 2009 Apr; 72(13):1153-9. PMID: 19332692
Background: About 20% of familial amyotrophic lateral sclerosis (ALS) is caused by mutations in SOD1 and is typically transmitted as an autosomal dominant trait. However, due to reduced mutation penetrance,...
10.
Rajah M, Bastianetto S, Bromley-Brits K, Cools R, DEsposito M, Grady C, et al.
Ageing Res Rev . 2009 Mar; 8(2):140-6. PMID: 19274854
The Douglas Mental Health University Institute, in collaboration with the McGill Centre for Studies in Aging, organized a 2-day symposium entitled "Biological Changes Associated with Healthy Versus Pathological Aging" that...