The genetics of Alzheimer disease.

By Rudolph E. Tanzi. Cold Spring Harbor Perspectives in Medicine, 2012

1,230 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/9d57bd2d1170bc5233ad75419aa9bbc298c65121

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Citations in the corpus

Hallmarks of neurodegenerative diseases. (2023, neutral): “3,9 A close relationship between lipid metabolism and microglial activation is emerging as lipid related genes are upregulated in the transition from homeostatic to damage-associated microglia.”
2016 Alzheimer's disease facts and figures (2016, neutral): “Genetic mutations A small percentage of Alzheimer’s cases (an estimated 1 percent or less) [26] develop as a result of mutations to any of three specific genes.”
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “Links between Aβ and tau pathogenesis Unlike mutations in APP and PS1/2 that affect Aβ generation in early onset familial AD [285, 286], mutations in MAPT have not been associated with AD [287, 288], suggesting that tau pathogenesis may occur downstream of Aβ accumulation [289].”
Super-enhancers in the control of cell identity and disease. (2013, neutral): “Alzheimer’s disease is a common form of dementia characterized by progressive neurodegeneration and loss of cognitive functions of the brain, and much of the genetic variation implicated in Alzheimer’s disease is associated with amyloid precursor protein, transmembrane proteins, and apolipoprotein E”
The Amyloid-β Pathway in Alzheimer’s Disease (2021, background): “Over 200 mutations involving this complex have been observed [34].”
Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future (2023, background): “Lack of accurate animal models AD can be classified into a genetic and sporadic form of the disease.(441) More than 99% of AD cases occur at an age >60 years in a sporadic manner, potentiated by various risk factors related to lifestyle.”
Plasma Proteome Profiling to Assess Human Health and Disease. (2016, background): “The apolipoprotein allele APOE4 in the homozygous form is the largest known risk factor for late-onset Alzheimer’s diseasewith a 10-fold higher risk compared with the homozygous APOE3 form (Tanzi, 2012).”
TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques (2016, background): “The origin of nonfamilial AD is less well understood and may depend on a combination of genetic and nongenetic risk factors (Tanzi, 2012).”