Editorial for the Genetics of Alzheimer’s Disease Special Issue: October 2021

Alzheimer’s disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of β-amyloid (Aβ) and tau proteins in the brain, loss of gray matter, and neuronal death [...]

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Published inGenes Vol. 12; no. 11; p. 1794
Main Authors Ibanez, Laura, Miller, Justin B.
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 14.11.2021
MDPI
Subjects
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Animals
Biomarkers
brain
Brain research
Conflicts of interest
Copy number
Cytokines
Data mining
Datasets
death
Etiology
Gene expression
Genetic diversity
Genetics
Grants
Growth factors
Health risk assessment
Humans
Immunomodulation
lifestyle
Medical imaging
Neurodegenerative diseases
neurons
Proteins
Quantitative trait loci
Risk factors
Tyrosine
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Abstract Alzheimer’s disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of β-amyloid (Aβ) and tau proteins in the brain, loss of gray matter, and neuronal death [...]
AbstractList Alzheimer's disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of β-amyloid (Aβ) and tau proteins in the brain, loss of gray matter, and neuronal death [...].
Alzheimer's disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of β-amyloid (Aβ) and tau proteins in the brain, loss of gray matter, and neuronal death [...].Alzheimer's disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of β-amyloid (Aβ) and tau proteins in the brain, loss of gray matter, and neuronal death [...].
Shaw, Katsumata [2] found that limitations inherent with stringent multiple testing correction may mask the ability to detect Alzheimer’s disease risk from complex copy number variations and genes with coupled expression within immunomodulatory tyrosine-phosphorylated inhibitory motifs (ITIMs) or activation motifs (ITAMs). Patel, Zhang [7] demonstrate that rare genetic variants significantly impact gene expression and gene co-expression in Alzheimer’s disease, indicating that set-based gene analyses are necessary to fully capture gene dynamics related to disease progression. Patel, D.; Zhang, X.; Farrell, J.J.; Lunetta, K.L.; Farre, L.A. Set-Based Rare Variant Expression Quantitative Trait Loci in Blood and Brain from Alzheimer Disease Study Participants.
Author Miller, Justin B.
Ibanez, Laura
AuthorAffiliation 1 Department of Psychiatry, Washington University in Saint Louis, St. Louis, MO 63110, USA
2 Department of Neurology, Washington University in Saint Louis, St. Louis, MO 63110, USA
3 Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
AuthorAffiliation_xml – name: 2 Department of Neurology, Washington University in Saint Louis, St. Louis, MO 63110, USA
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Cites_doi 10.3390/genes12060865
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2021 by the authors. 2021
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Snippet Alzheimer’s disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of...
Alzheimer's disease is a complex and multifactorial condition regulated by both genetics and lifestyle, which ultimately results in the accumulation of...
Shaw, Katsumata [2] found that limitations inherent with stringent multiple testing correction may mask the ability to detect Alzheimer’s disease risk from...
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StartPage 1794
SubjectTerms Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Animals
Biomarkers
brain
Brain research
Conflicts of interest
Copy number
Cytokines
Data mining
Datasets
death
Etiology
Gene expression
Genetic diversity
Genetics
Grants
Growth factors
Health risk assessment
Humans
Immunomodulation
lifestyle
Medical imaging
Neurodegenerative diseases
neurons
Proteins
Quantitative trait loci
Risk factors
Tyrosine
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Title Editorial for the Genetics of Alzheimer’s Disease Special Issue: October 2021
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