APOE Test: How Genotyping Supports New Treatments for Alzheimer’s Disease

Alzheimer’s disease is the most common cause of dementia worldwide and affects millions of people. In recent years, major advances in understanding the biological mechanisms underlying the disease have enabled the development of new therapies that directly target the accumulation of beta-amyloid protein in the brain, one of the processes involved in disease progression.

With these new treatment options, medicine is moving toward an increasingly personalized approach, in which each patient’s genetic characteristics can also contribute to clinical decision-making.

In this context, APOE gene genotyping has become more relevant. In addition to providing information about genetic predisposition to Alzheimer’s disease, the results can help assess patients who may be candidates for certain anti-amyloid therapies, particularly because of the association between APOE variants and the risk of treatment-related adverse events.

What is Alzheimer’s disease?

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive decline and memory loss. Its main pathological features include brain atrophy, neuroinflammation, beta-amyloid (Aβ) accumulation, and the formation of neurofibrillary tangles resulting from the accumulation of hyperphosphorylated tau protein (1, 2).

Alzheimer’s disease can be classified into two forms according to age at onset. Early-onset Alzheimer’s disease develops before the age of 65, accounts for approximately 2–10% of cases, and may be associated with autosomal dominant pathogenic variants in the APP, PSEN1, and PSEN2 genes (2, 3).

Late-onset Alzheimer’s disease, on the other hand, occurs at age 65 or older and has a strong association with genetic factors, particularly the APOE gene, whose variants influence the risk of developing the disease (4).

In addition to genetic predisposition, modifiable factors, such as diet and sleep quality, may also influence the risk and progression of the disease.

What is the APOE test, and what is it used for?

The APOE test identifies which genetic variants and alleles of the apolipoprotein E (APOE) gene a person carries. This gene is involved in important processes related to lipid transport and metabolism and also plays a role in neuronal maintenance and repair (5, 6).

Genetic analysis can determine the combination of alleles inherited from an individual’s parents, providing information about risk factors associated with late-onset Alzheimer’s disease. However, this is a genetic predisposition test, not a diagnostic test for the disease.

What is the function of the APOE gene in the body?

The APOE gene encodes apolipoprotein E, a protein responsible for transporting cholesterol and other lipids between cells and tissues. In the central nervous system, this protein contributes to maintaining neuronal integrity, repairing brain injury, and modulating inflammatory processes (5).

There are three main isoforms of apolipoprotein E—ApoE2, ApoE3, and ApoE4—which differ functionally and may influence the risk of developing Alzheimer’s disease (7). In addition, evidence suggests that different APOE gene variants influence the clearance of beta-amyloid protein from the brain, a process directly related to the pathophysiology of Alzheimer’s disease (5, 6).

ApoE4 is the main genetic risk factor for Alzheimer’s disease, increasing the risk of developing the disease approximately three- to fourfold in individuals carrying one copy of the allele and nine- to fifteenfold in those carrying two copies. It is implicated in 60–80% of AD cases and is associated with an earlier age at disease onset (8, 9).

Although APOE ε4 is associated with an increased risk of developing the disease, its presence alone does not mean that a person will develop Alzheimer’s disease.

What is the relationship between the APOE gene and Alzheimer’s disease?

Alzheimer’s disease is a multifactorial condition resulting from interactions among genetic, biological, environmental, and lifestyle-related factors. ApoE is the main apolipoprotein present in the central nervous system and contributes to the regulation of the brain vasculature, both in the presence and absence of pathological changes associated with neurodegeneration (9, 10).

In most cases, particularly in what is known as late-onset Alzheimer’s disease, the condition is not a classic hereditary disease caused by a single genetic alteration passed down through generations.

Among the known genetic factors, the APOE gene is considered the main susceptibility factor for sporadic late-onset Alzheimer’s disease. This gene influences several biological processes involved in brain health, including lipid transport, inflammatory responses, and the clearance of beta-amyloid protein, one of the proteins associated with the disease (7, 8).

Different APOE gene variants are associated with different levels of risk. The APOE ε4 allele is associated with a higher likelihood of developing the disease, whereas the APOE ε2 allele may have a protective effect in some individuals. However, these variants alone do not determine whether a person will develop Alzheimer’s disease (8, 11).

How does APOE gene genotyping work?

Genotyping is a molecular test performed on biological samples, usually peripheral blood or saliva, to identify the variants present in the APOE gene (11, 12).

There are three main APOE alleles:

• APOE ε2: associated with a lower risk of Alzheimer’s disease compared with the general population;
• APOE ε3: the most common variant in the population and considered neutral in terms of risk;
• APOE ε4: associated with an increased risk of late-onset Alzheimer’s disease.

Each individual inherits two copies of the gene, resulting in combinations such as ε3/ε3, ε3/ε4, or ε4/ε4 (5, 8).

How should genotyping results be interpreted?

Interpretation should always take the patient’s clinical context into account and be performed by a qualified healthcare professional. In general:

• ε3/ε3: genetic risk is generally considered intermediate or similar to that of the general population;
• ε3/ε4: increased relative risk of Alzheimer’s disease;
• ε4/ε4: significantly higher risk compared with non-carriers;
• ε2/ε2 or ε2/ε3: may be associated with a lower relative risk.

It is important to emphasize that the result has no standalone diagnostic value (11). Interpretation should always consider the patient’s clinical context and be performed by a qualified healthcare professional, since APOE genotyping provides information about genetic susceptibility but does not establish a diagnosis of the disease.

What role does APOE genotyping play in new treatments for Alzheimer’s disease?

APOE gene genotyping has gained importance with the development of anti-amyloid immunotherapies, such as lecanemab and donanemab, which are used to treat Alzheimer’s disease (AD) in its early stages. The test identifies the presence of the ε4 allele, a genetic variant associated with an increased risk of developing the disease and a higher likelihood of treatment-related adverse events known as amyloid-related imaging abnormalities (ARIA). These are changes detected on magnetic resonance imaging (MRI) that may include brain edema (ARIA-E) and microhemorrhages or other changes related to the presence of blood in the brain (ARIA-H). Although many cases are asymptomatic, some can cause serious clinical manifestations (13–15).

The APOE ε4 allele is the main genetic risk factor for sporadic Alzheimer’s disease. Compared with individuals with the ε3/ε3 genotype, those carrying one ε4 allele have an approximately three- to fourfold higher risk, while those carrying two copies may have a ten- to fifteenfold higher risk (13).

With the introduction of anti-amyloid therapies, knowing a patient’s APOE genotype has also become important for assessing the potential benefits and risks of treatment:

• Genotype-dependent efficacy: In phase 3 studies, lecanemab and donanemab showed significant slowing of cognitive decline in certain patient groups, including ε4 non-carriers and heterozygotes. Aducanumab, which has since been commercially discontinued, showed a response favoring ε4 carriers (13, 16);

• ARIA risk proportional to the number of ε4 alleles: The risk of these abnormalities is higher in ε4 carriers, particularly those with two copies of the allele. ARIA-E rates were 5.4% with lecanemab and 15.7% with donanemab in non-carriers; 10.9% and 22.8%, respectively, in heterozygotes; and 32.6% and 35.0%, respectively, in ε4/ε4 homozygotes. A recent meta-analysis also confirmed the association between the number of ε4 allele copies and ARIA risk. Compared with non-carriers, individuals with the ε4/ε4 genotype had approximately four times the odds of developing ARIA-E and more than three times the odds of developing ARIA-H (13, 17). These figures reflect the studies and treatment conditions analyzed and should not be interpreted as universal rates applicable to all patients;

• Individualized treatment assessment: APOE genotyping can contribute to the individualized assessment of patients who may be candidates for anti-amyloid therapies. However, recommendations vary according to the regulatory agency. While the FDA allows treatment in individuals homozygous for APOE ε4 (ε4/ε4), highlighting the increased risk of ARIA and the need for a medical discussion of risks and benefits, the EMA has adopted a more cautious position, considering that the benefit–risk balance may be less favorable in this group. For this reason, the European indication prioritizes patients who are non-carriers or heterozygous for the ε4 allele. These differences reflect the current complexity of interpreting safety and efficacy data for anti-amyloid therapies in individuals who are homozygous for ε4 (ε4/ε4) (14, 15);

• Strategies to improve treatment safety: Research is also exploring strategies to make anti-amyloid therapies safer. A modified donanemab titration regimen reduced the incidence of ARIA-E at 24 weeks from 23.7% to 13.7% and ARIA-H from 25.1% to 20.3%, compared with the standard titration regimen. These findings reinforce the importance of investigating strategies that may improve treatment safety (18);

• Genotyping recommendations: APOE genotyping is not recommended for asymptomatic individuals, since a positive result in this context does not lead to a specific therapeutic intervention. Testing should be restricted to candidates for anti-amyloid therapy (15).

What are the latest advances in anti-amyloid therapies?

Medications such as lecanemab and donanemab were developed to remove beta-amyloid deposits from the brain. Clinical studies have demonstrated a reduction in amyloid burden and a modest slowing of clinical progression in patients with early-stage Alzheimer’s disease (12).

These therapies represent the first treatments capable of directly modifying one of the underlying biological processes involved in the disease (12).

How is the APOE ε4 genotype related to ARIA risk?

One of the main adverse events associated with these therapies is the occurrence of ARIA (amyloid-related imaging abnormalities), detected through magnetic resonance imaging (MRI). These abnormalities may include brain edema and small hemorrhages.

Evidence shows that carriers of the APOE ε4 allele, particularly individuals with the ε4/ε4 genotype, have a higher risk of developing ARIA during treatment (12, 19).

For this reason, international recommendations suggest that APOE status should be discussed and taken into account during the pretreatment assessment (12).

Why can genotyping contribute to pretreatment assessment?

APOE genotyping is particularly relevant when assessing patients being considered for treatment with anti-amyloid antibodies. Knowing a patient’s APOE genotype can:

• Support discussions about the risks and benefits of therapy;
• Help clarify the risk of ARIA;
• Assist in planning MRI monitoring;
• Contribute to personalized decision-making involving the physician, patient, and family members.

Therefore, genotyping does not determine who can or cannot receive treatment. Instead, it provides additional information to support a more individualized decision-making process (12).

When may APOE genotyping be indicated?

The test may be considered in specific clinical settings, such as the further investigation of individuals with a relevant family history or within specialized clinical protocols for risk assessment. Testing should be requested within an appropriate medical counseling context.

Currently, one of its main clinical applications is the assessment of patients with biologically confirmed Alzheimer’s disease who are candidates for anti-amyloid therapies. In these cases, identifying the APOE ε4 allele helps assess the risk of adverse events, particularly amyloid-related imaging abnormalities (ARIA), supporting discussions about the risks and benefits of treatment (12).

Conversely, APOE genotyping is not recommended indiscriminately for asymptomatic individuals as a population screening tool. It should be requested in specific clinical settings and with appropriate medical guidance (15).

Thus, APOE genotyping is a relevant tool in personalized medicine, particularly because it contributes to the safety assessment of new therapies and supports individualized clinical decisions.

What is the difference between genetic predisposition and diagnosis?

Genetic predisposition refers to a higher or lower probability of developing a particular condition over the course of a person’s lifetime.

Diagnosis, on the other hand, relies on clinical assessment and, when indicated, the use of biomarkers and complementary tests capable of demonstrating changes consistent with active disease (11).

Which tests can complement the investigation of Alzheimer’s disease?

Recent advances have enabled the use of biomarkers capable of identifying biological changes characteristic of the disease, often years before more evident symptoms appear.

The guidelines of the Brazilian Academy of Neurology recommend that these tests be used as a complement to clinical assessment, particularly in complex diagnostic situations or when disease-modifying therapies are being considered.

Tests currently used include:

• Cerebrospinal fluid (CSF) biomarkers (Aβ42, Aβ42/Aβ40 ratio, and tau proteins): When assessed together, these biomarkers can provide strong evidence of Alzheimer’s pathology, even in the early stages of the disease;

• Amyloid PET: Amyloid positron emission tomography (PET) is a molecular imaging test that can identify beta-amyloid protein deposits in the brain;

• Tau PET: Tau PET allows direct visualization of tau protein accumulation in the brain;

• Plasma biomarkers: phosphorylated tau 217 (p-tau217) and phosphorylated tau 181 (p-tau181): Phosphorylated tau 181 (p-tau181) and phosphorylated tau 217 (p-tau217) reflect changes associated with the accumulation of abnormal tau protein, one of the main mechanisms involved in Alzheimer’s disease. P-tau181 was one of the first widely studied blood-based biomarkers and has demonstrated good ability to distinguish patients with Alzheimer’s disease from individuals without the disease or with other causes of cognitive impairment.
  More recently, studies have shown that p-tau217 may offer even greater diagnostic performance, with a strong correlation with amyloid PET and tau PET findings. In many cases, elevated p-tau217 levels can be detected years before the development of clinical dementia, making this marker a promising tool for patient screening and stratification.
  Although blood-based biomarkers represent a significant advance because they are less invasive and more accessible, their interpretation must take place within the appropriate clinical context;

• Brain magnetic resonance imaging (MRI): MRI remains one of the most widely used tests in the investigation of cognitive impairment. In addition to helping rule out other causes of dementia, such as tumors, hydrocephalus, or vascular lesions, it can reveal patterns of brain atrophy consistent with Alzheimer’s disease, particularly in structures associated with memory, such as the hippocampus.
  MRI also plays a key role in monitoring patients receiving the new anti-amyloid therapies, allowing the identification of ARIA (amyloid-related imaging abnormalities), a potential treatment-related adverse event.

According to the Brazilian Academy of Neurology guidelines, clinical assessment remains the first step in determining whether these biomarkers are appropriate (11).

To learn more about scientific advances and how each of these tests contributes to the investigation of the disease, read our related article on Alzheimer’s disease diagnosis.

Which tests does SYNLAB offer for the investigation of Alzheimer’s disease?

SYNLAB offers innovative tests to support diagnosis at different stages of clinical assessment:

• APOE genotyping

APOE genotyping is a molecular test that identifies the variants of the APOE gene carried by an individual. The analysis can determine the presence of the ε2, ε3, and ε4 alleles, which are associated with different risk profiles for Alzheimer’s disease;

• Plasma phosphorylated tau 217 (p-tau217) measurement

Measuring phosphorylated tau protein at threonine 217 (p-tau217) in plasma has proven to be a highly effective biomarker in the differential diagnosis of dementias, particularly Alzheimer’s disease. Its diagnostic performance is comparable to that of biomarkers measured in cerebrospinal fluid, potentially avoiding an invasive procedure such as a lumbar puncture;

• Plasma phosphorylated tau 181 (p-tau181) measurement

Plasma measurement of phosphorylated tau 181 is an important biomarker in the assessment of neurodegenerative processes, particularly Alzheimer’s disease. Elevated p-tau181 levels reflect the tau-related pathology associated with Alzheimer’s disease, offering a less invasive alternative to tests performed on cerebrospinal fluid and contributing to a more accurate differential diagnosis;

• Beta-Amyloid and Tau Panel

Beta-amyloid and tau biomarkers can be assessed in both cerebrospinal fluid and plasma, allowing the investigation of the main biochemical changes associated with Alzheimer’s disease. CSF analysis remains the gold standard for simultaneously detecting amyloid deposition and neuronal degeneration, while plasma measurements offer a less invasive alternative, supporting the diagnosis, monitoring, and clinical stratification of dementias;

• ADGEN: genetic test for assessing predisposition to Alzheimer’s disease

ADGEN is a genetic test that analyzes four genes associated with the development of Alzheimer’s disease—APP, PSEN1, PSEN2, and APOE—using next-generation sequencing (NGS). The variants analyzed are documented in established scientific databases and can help estimate genetic risk, supporting early detection and clinical planning. Since Alzheimer’s disease is influenced by multiple factors, including hereditary components, genetic analysis provides important complementary information for specialized follow-up.

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Frequently Asked Questions (FAQ)

Does the APOE test detect Alzheimer’s disease?

No. APOE gene genotyping does not diagnose Alzheimer’s disease. It identifies genetic variants associated with different risk profiles for developing the disease and may contribute to the assessment of patients who are candidates for certain anti-amyloid therapies. The diagnosis of Alzheimer’s disease depends on clinical assessment and, when indicated, complementary tests.

What is APOE genotyping used for?

The APOE test identifies which variants of the APOE gene are present in an individual. Its applications may include assessing genetic predisposition to Alzheimer’s disease and, in specific clinical settings, evaluating the risk of adverse events associated with certain anti-amyloid therapies. The decision to order the test should take into account its clinical purpose and the healthcare professional’s assessment.

How can I find out whether I carry the APOE4 allele?

The presence of the ε4 allele can be identified through APOE gene genotyping, performed on a biological sample, usually blood or saliva, depending on the method and the laboratory’s specifications. The result indicates whether an individual carries zero, one, or two copies of the ε4 allele. The decision to perform the test and the interpretation of the results should be discussed with a healthcare professional.

What is the relationship between APOE4 and Alzheimer’s disease?

The APOE gene has three main variants, known as ε2, ε3, and ε4. Among them, the ε4 allele is associated with an increased risk of developing Alzheimer’s disease, particularly the late-onset form. However, its presence does not mean that a person will necessarily develop the disease, just as its absence does not eliminate the risk. Other genetic, environmental, and lifestyle-related factors also influence this risk.

In addition, the ε4 allele is relevant to the safety assessment of certain anti-amyloid therapies because it is associated with a higher likelihood of amyloid-related imaging abnormalities (ARIA), which may include brain edema and microhemorrhages.

How is genotyping of the ε2, ε3, and ε4 alleles performed?

APOE genotyping identifies the genetic variants that distinguish the ε2, ε3, and ε4 alleles. This distinction is based primarily on two positions in the DNA sequence. The analysis can be performed using different molecular methods, such as real-time PCR with allelic discrimination or other laboratory-validated techniques. The combination of the identified alleles determines an individual’s genotype, such as ε2/ε3, ε3/ε3, ε3/ε4, or ε4/ε4, among other possibilities.

Is there a genetic test to detect Alzheimer’s disease?

Genetic tests can provide relevant information about the risk or cause of certain forms of Alzheimer’s disease, but they should not be confused with standalone diagnostic tests. APOE genotyping assesses variants associated with risk and may help evaluate the safety of certain therapies. The investigation of rare familial forms may involve genes such as APP, PSEN1, and PSEN2, particularly when there is a family history suggestive of early-onset disease.

Clinical diagnosis may include cognitive assessment, imaging tests, and, when indicated, disease biomarkers such as those related to beta-amyloid and tau protein. The choice of tests depends on clinical history and specialist assessment.

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