4 research outputs found
New insights into the genetic etiology of Alzheimer's disease and related dementias
- Author
- Aaltonen L.
- Aaltonen V.
- Aarsland Dag
- Aavikko M.
- Abalos M.S.
- Abdelnour Carla
- Abner E.
- Abraham R.
- Adams H.
- Adams P.M.
- Adarmes-GĂłmez A.
- Adarmes-GĂłmez A.D.
- Aguilera N.
- Aguilera N.
- Aguirre A.
- Ahmad S.
- Akinyemi R.O.
- Al-Chalabi A.
- AlarcĂłn-MartĂn Emilio
- Albert M.S.
- Albin R.L.
- Alcolea Daniel
- Alegret Montserrat
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- Allende I.R.
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- Publication venue
- Publication date
- 01/01/2022
- Field of study
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele
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A genetic study of cerebral atherosclerosis reveals novel associations with ntng1 and cnot3
- Author
- Publication venue
- 'MDPI AG'
- Publication date
- 01/01/2021
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Cerebral atherosclerosis is a leading cause of stroke and an important contributor to dementia. Yet little is known about its genetic basis. To examine the association of common single nucleotide polymorphisms with cerebral atherosclerosis severity, we conducted a genomewide association study (GWAS) using data collected as part of two community-based cohort studies in the United States, the Religious Orders Study (ROS) and Rush Memory and Aging Project (MAP). Both studies enroll older individuals and exclude participants with signs of dementia at baseline. From our analysis of 1325 participants of European ancestry who had genotype and neuropathologically assessed cerebral atherosclerosis measures available, we found a novel locus for cerebral atherosclerosis in NTNG1. The locus comprises eight SNPs, including two independent significant SNPs: rs6664221 (ÎČ = â0.27, 95% CI = (â0.35, â0.19), p = 1.29 Ă 10â10 ) and rs10881463 (ÎČ = â0.20, 95% CI = (â0.27, â0.13), p = 3.40 Ă 10â8 ). We further found that the SNPs may influence cerebral atherosclerosis by regulating brain protein expression of CNOT3. CNOT3 is a subunit of CCR4âNOT, which has been shown to be a master regulator of mRNA stability and translation and an important complex for cholesterol homeostasis. In summary, we identify a novel genetic locus for cerebral atherosclerosis and a potential mechanism linking this variation to cerebral atherosclerosis progression. These findings offer insights into the genetic effects on cerebral atherosclerosis. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]
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- A. Lin
- A. Shukla-Dave
- A.D. Laing
- A.J. Adamson
- A.P. Dagher
- A.Z. Latif
- AE Walker
- B. Wilken
- C.A. Meyers
- D. Miltenburg
- D. Zagzag
- D.W. Giang
- F. Benard
- G. Sze
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- G.L. Colice
- H. Itto
- H. Snyder
- I.F. Pollack
- J.J. Kepes
- J.S. Taylor
- J.S. Tsuruda
- K. Okamoto
- K.G. Go
- L.B. Morgenstern
- L.D. Prockop
- L.E. Becker
- L.M. DeAngelis
- L.S. Medina
- M. Barcikowska
- M. Castillo
- M. Salcman
- M.J. Kuhn
- N. Kurihara
- N. Stefano De
- N.J. Abbott
- P. Kleihues
- P. Kleihues
- P.A. Stewart
- P.A. Stewart
- P.A. Wingo
- P.C. Burger
- P.C. Burger
- P.C. Davis
- P.E. Ricci
- P.M. Parizel
- P.W. Schaefer
- R. Babu
- R. Golfieri
- R.A. Patchell
- R.J. Porter
- S. Cha
- S. Cha
- S. Sato
- S.C. Chang
- S.D. Rand
- S.H. Landis
- S.I. Blaser
- T. Ebisu
- T. Kimura
- T.S. Surawicz
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
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New insights into the genetic etiology of Alzheimerâs disease and related dementias
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Characterization of the genetic landscape of Alzheimerâs disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/âproxyâ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE Δ4 allele. © 2022, The Author(s)