The genetics of Alzheimer disease: back to the future.

By Lars Bertram, Christina M. Lill, Rudolph E. Tanzi. Neuron, 2010

866 citations recorded by the source corpus.

Subfields: Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/15ff492b14e783cea9867bea4fd1f55625dba6ba

How researchers see this paper

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

In Genetics

1. Rudolph E. Tanzi
2. Eric E. Schadt
3. Radu Dobrin
4. Lars Bertram

In Physiology

1. Kaj Blennow
2. Reisa A. Sperling
3. Rudolph E. Tanzi
4. Clifford R. Jack Jr.
5. Harald Hampel
6. P. Aisen
7. Lars Bertram
8. Philip Scheltens

Citations in the corpus

• The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy (2016, background): “Additionally, there are genetic risk factors for AD including the APOE ɛ4 allele (Bertram et al., 2010).”
• The genetics of Alzheimer disease. (2012, background): “Recently, our family-based and others’ case–control GWASs (reviewed in Bertram et al. 2009, 2010) led to the elucidation of novel susceptibility variants, all of which confer only small effects on risk.”
• Alzheimer’s Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta (2013, neutral): “LOAD has a strong genetic component and is probably caused by a combination of multiple risk alleles, each with modest and partially penetrant effects, and environmental factors (Bertram et al., 2010).”
• The Gut Microbiota and Alzheimer’s Disease (2017, neutral): “4 is a high-risk allele (for review, see [36, 37]).”
• Integrated systems approach identifies genetic nodes and networks in late-onset Alzheimer's disease (2013, background): “Progress in LOAD research is fundamentally limited by our reliance on mouse models of severe familial/ early-onset Alzheimer’s disease; therefore, our primary knowledge of LOAD is in actuality based on the downstream effects of three rare mutations in APP, PSEN1, and PSEN2 (Bertram et al., 2010).”
• Preclinical Alzheimer’s disease: Definition, natural history, and diagnostic criteria (2016, background): “To date, APOE ε4 represents the strongest and bestestablished genetic risk factor for sporadic AD [37,128,129].”
• The diagnosis of mild cognitive impairment due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease (2011, neutral): “It has been hypothesized that many additional genes play an important, but smaller role than APOE; these additional genes will also confer changes in risk for progression to AD dementia [13].”