APOE4 gene variant reliably causes Alzheimer's disease in those with two copies.
APOE4 homozygotes exhibit AD pathology and higher levels of AD biomarkers than those with one or no copies.
APOE4 homozygotes have earlier symptom onset at an average of 65.1 years old.
Approximately 2% of population has two copies of APOE4 and nearly all develop Alzheimer's disease.
In a groundbreaking discovery, researchers have identified a distinct genetic form of Alzheimer's disease, finding that having two copies of the gene variant APOE4 reliably causes the development of the condition. This new understanding challenges previous beliefs that APOE4 merely increased the risk of developing Alzheimer's, and instead confirms it as a cause. Approximately 2% of the general population has two copies of ApoE4, and nearly all develop Alzheimer's disease (AD). The findings reveal that almost all individuals with two copies of the APOE4 gene variant exhibit AD pathology and have significantly higher levels of AD biomarkers compared to those with one or no copies. By age 65, nearly all APOE4 homozygotes have abnormal amyloid levels in cerebrospinal fluid, and 75% have positive amyloid scans. The age of symptom onset was also found to be earlier in APOE4 homozygotes at an average of 65.1 years old, with a narrower range of prediction than those with APOE3 homozygotes. These results indicate that APOE4 homozygosity represents a unique and distinct genetic form of Alzheimer's disease, mirroring the predictability of symptom onset and sequence of biomarker changes in autosomal dominant Alzheimer's and Down syndrome. This new understanding has significant implications for future research, diagnosis, and treatment options for those with APOE4 homozygosity.
Alzheimer’s disease may be inherited more often than previously known, with 1 in 6 cases considered to be inherited or familial.
People with two copies of the APOE4 gene have an elevated risk of developing Alzheimer’s disease, and it should be viewed as an inherited form of the disease.
APOE4 reliably causes the creation of beta amyloid plaques in the brain but having one or two copies of this gene doesn’t always lead to cognitive decline.
APOE4 is semi-dominant, and it is one of the most prevalent inherited diseases, with about 2% of the general population carrying two copies.
Accuracy
No Contradictions at Time
Of
Publication
Deception
(0%)
The article states that having two copies of the APOE4 gene should be considered a genetic form of Alzheimer's disease, not merely a risk for it. This is a significant shift in understanding and classification of the disease. The author, Brenda Goodman, presents this as a new study's finding without disclosing that she is also affiliated with the research. This omission of her conflict of interest deceives readers by not allowing them to assess the credibility and impartiality of the report.
The authors of the study, published Monday in the journal Nature Medicine, say that this might even be considered a distinct, inherited form of the disease and that different approaches to testing and treatment may be needed.
Fallacies
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None Found At Time Of
Publication
Bias
(95%)
The author uses language that depicts people with two copies of the APOE4 gene as having 'assured' or 'virtually assured' development of Alzheimer's disease, and describes their condition as a 'distinct, inherited form of the disease'. This language implies a bias towards viewing this genetic factor as causing the disease rather than just increasing risk.
Among people diagnosed with Alzheimer’s, researchers recognize familial forms of the disease and sporadic cases. Most cases are thought to be sporadic, which develop later in life. Familial forms, caused by mutations in any of three genes, tend to strike earlier and are known to be rare, accounting for about 2% of all Alzheimer’s diagnoses. Under the new paradigm, 1 in 6 cases of Alzheimer’s would be considered to be inherited.
APOE4 shouldn't just be recognized as a risk factor, it should be viewed as an inherited form of the disease.
Having two copies of APOE4 is about as prevalent as Down syndrome and sickle cell anemia.
Not only were people with two copies of the APOE4 gene much more likely to develop the biological changes that lead to Alzheimer’s disease, similar to people with other genetic forms of the disease, they were almost assured the diagnosis:
The important takeaway from the study is that Alzheimer’s disease shouldn’t be treated as a monolith. Rather, it shows that there are different forms of the disease that need personalized treatment.
APOE4 homozygotes exhibit AD pathology and have significantly higher levels of AD biomarkers from age 55 compared to APOE3 homozygotes.
By age 65, nearly all APOE4 homozygotes had abnormal amyloid levels in cerebrospinal fluid, and 75% had positive amyloid scans.
The age of symptom onset was earlier in APOE4 homozygotes at 65.1, with a narrower 95% prediction interval than APOE3 homozygotes.
APOE4 homozygotes mirror the predictability of symptom onset and sequence of biomarker changes in autosomal dominant AD and Down syndrome.
Accuracy
No Contradictions at Time
Of
Publication
Deception
(100%)
None Found At Time Of
Publication
Fallacies
(95%)
No dichotomous depictions found. No appeals to authority found. Inflammatory rhetoric is absent. There are formal fallacies present, specifically: the author makes a sweeping generalization about APOE4 homozygotes exhibiting AD pathology and having significantly higher levels of AD biomarkers without providing specific references or data points for each individual case. Additionally, there's an overgeneralization when stating that 'nearly all' APOE4 homozygotes had abnormal amyloid levels in cerebrospinal fluid and positive amyloid scans by age 65. Lastly, the author uses the term 'near-full penetrance', which is a misleading way to describe the prevalence of AD biology in APOE4 homozygotes.
Almost all APOE4 homozygotes exhibited AD pathology
APOE4 homozygotes had significantly higher levels of AD biomarkers from age 55 compared to APOE3 homozygotes
Nearly all had abnormal amyloid levels in cerebrospinal fluid and 75% had positive amyloid scans by age 65
The study concludes that APOE4 homozygotes represent a genetic form of AD
Researchers have identified that having two copies of the gene variant ApoE4 is a distinct genetic form of Alzheimer’s disease.
Approximately 2% of the general population has two copies of ApoE4.
Accuracy
Almost everyone with two copies of ApoE4 goes on to develop Alzheimer’s disease.
By age 65, almost all individuals with two copies of ApoE4 have abnormal levels of amyloid beta in their cerebrospinal fluid and positive amyloid scans.
Researchers have identified a genetic form of late-in-life Alzheimer’s disease caused by inheriting two copies of the gene APOE4.
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Accuracy
Approximately 15% of Alzheimer’s patients carry two copies of APOE4.
People with two copies of the APOE4 gene have an elevated risk of developing Alzheimer’s disease.
APOE4 reliably causes the creation of beta amyloid plaques in the brain but having one or two copies of this gene doesn’t always lead to cognitive decline.
Almost everyone with two copies of ApoE4 goes on to develop Alzheimer’s disease.
Deception
(100%)
None Found At Time Of
Publication
Fallacies
(95%)
The article does not contain any formal fallacies or appeals to authority. There are no dichotomous depictions or inflammatory rhetoric. However, there is an example of a complex situation being simplified which can be considered an informal fallacy known as 'hasty generalization'. The author states that “An estimated 15% of Alzheimer’s patients carry two copies of APOE4, meaning those cases “can be tracked back to a cause and the cause is in the genes.” This oversimplifies the relationship between APOE4 and Alzheimer's as it implies that all cases with two copies of APOE4 are caused by this gene. In reality, while it is true that having two copies of APOE4 increases the risk for developing Alzheimer's, other factors also contribute to the development of the disease. This oversimplification can lead readers to a misunderstanding of the complexity of Alzheimer's and its relationship with genetics.
An estimated 15% of Alzheimer’s patients carry two copies of APOE4, meaning those cases “can be tracked back to a cause and the cause is in the genes.”
