Thirty years of Alzheimer's disease genetics: the implications of systematic meta-analyses

By Lars Bertram, Rudolph E. Tanzi. Nature Reviews Neuroscience, 2008

788 citations recorded by the source corpus.

Subfields: Molecular Biology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/0ecfdfcbe7678b46830a21ff7ce49aeb2904b1c3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Pharmacology

In Physiology

Citations in the corpus

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”
Mechanisms Underlying Inflammation in Neurodegeneration (2010, neutral): “Rare mutations in APP and the presenilin components of g-secretase are causes of familial AD, providing one line of evidence for the hypothesis that Ab contributes to the pathogenesis of AD (Bertram and Tanzi, 2008).”
The genetics of Alzheimer disease. (2012, background): “(Modified from Bertram and Tanzi 2008; reprinted with permission from the author.)”
The genetics of Alzheimer disease: back to the future. (2010, background): “The outcomes have been inconsistent; of the nearly 700 candidate AD genes investigated over the past 30 years, only few show significant risk effects when data from all available studies are combined (Bertram and Tanzi, 2008) (for an up-to-date overview see the AlzGene Database).”
Clinical epidemiology of Alzheimer’s disease: assessing sex and gender differences (2014, neutral): “Compared to non-carriers, heterozygous carriers of one ε4 allele are 3–4 times more likely to develop AD, whereas the risk for homozygous carriers is even higher.(87,88) The APOE ε4 allele is specifically associated with an earlier age of onset of AD.”
Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy (2009, background): “Individuals with one e4 allele are three to four times as likely to develop AD than those without e4 allele”
Oxidative stress in neurodegenerative diseases (2012, background): “The main histological features are extracellular protein deposits called senile Aβ-amyloid plaques and intraneuronal neurofibrillary tangles [73] .”
Alzheimer's disease: strategies for disease modification (2010, background): “Of all the possible genetic causes of AD, e4 is the one involved in most case”
The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease (2011, background): “Mutations in three genes—amyloid precursor protein, presenilin 1, and presenilin 2—cause an early onset, autosomal dominantly inherited AD [17].”
Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s disease (2009, background): “Ab (38–43 amino acids) is a proteolytic by-product from the amyloid precursor protein (APP) generated by the sequential b-secretase and c-secretase cleavage.”
Principles of early drug discovery (2011, background): “For example, familial Alzheimer’s Disease (AD) patients commonly have mutations in the amyloid precursor protein or presenilin genes which lead to the production and deposition in the brain of increased amounts of the Abeta peptide, characteristic of AD (Bertram and Tanzi, 2008).”
The pathobiology of vascular dementia (2013, neutral): “Shortly after, mutations in the amyloid precursor protein (APP) gene were identified in familial forms of AD (Bertram and Tanzi, 2008).”