Longevity Alzheimer’s Disease Blood Test
$299.00
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the gradual decline in cognitive function and memory loss. It is the most common cause of dementia, accounting for approximately 60-70% of cases. AD typically manifests in older adults, although early-onset forms can occur.
The hallmarks of Alzheimer’s disease include the accumulation of abnormal protein aggregates in the brain, namely beta-amyloid plaques and tau tangles. These pathological changes lead to neuronal damage and loss, disrupting communication between brain cells and impairing cognitive processes.
In Alzheimer’s disease (AD), abnormal accumulation of tau proteins within neurons is one of the key pathological hallmarks, alongside the deposition of beta-amyloid plaques. Tau proteins are essential for maintaining the structural integrity and function of neurons. However, in AD, tau proteins undergo abnormal changes, leading to the formation of insoluble aggregates known as neurofibrillary tangles (NFTs) inside neurons.
In Alzheimer’s disease, there is a decrease in the levels of acetylcholine due to the loss of cholinergic neurons in the brain. By inhibiting the enzyme cholinesterase, which breaks down acetylcholine, it is possible to maintain higher levels of acetylcholine in the brain, thereby improving communication between neurons and temporarily enhancing cognitive function.
Malondialdehyde (MDA) is a marker of oxidative stress and lipid peroxidation, which are processes implicated in the pathogenesis of Alzheimer’s disease (AD). Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to neutralize them with antioxidants. In Alzheimer’s disease, increased oxidative stress leads to damage to cellular components, including lipids, proteins, and DNA, contributing to neuronal dysfunction and neurodegeneration.
Longevity Alzheimer’s Disease Blood Test: 8 Analytes tested: Amyloid Beta (Aβ) Peptides 42/40, Acetylcholinesterase (AChE), Choline, Malondialdehyde (MDA), Neurofilament Light Chain (NfL), Phosphorylated Tau 181 (p-T181), Phosphorylated Tau 217 (p-T217), Total Tau Proteins (t-tau)
Description
About the Test
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the gradual decline in cognitive function and memory loss. It is the most common cause of dementia, accounting for approximately 60-70% of cases. AD typically manifests in older adults, although early-onset forms can occur.
The hallmarks of Alzheimer’s disease include the accumulation of abnormal protein aggregates in the brain, namely beta-amyloid plaques and tau tangles. These pathological changes lead to neuronal damage and loss, disrupting communication between brain cells and impairing cognitive processes.
In Alzheimer’s disease (AD), abnormal accumulation of tau proteins within neurons is one of the key pathological hallmarks, alongside the deposition of beta-amyloid plaques. Tau proteins are essential for maintaining the structural integrity and function of neurons. However, in AD, tau proteins undergo abnormal changes, leading to the formation of insoluble aggregates known as neurofibrillary tangles (NFTs) inside neurons.
In Alzheimer’s disease, there is a decrease in the levels of acetylcholine due to the loss of cholinergic neurons in the brain. By inhibiting the enzyme cholinesterase, which breaks down acetylcholine, it is possible to maintain higher levels of acetylcholine in the brain, thereby improving communication between neurons and temporarily enhancing cognitive function.
Malondialdehyde (MDA) is a marker of oxidative stress and lipid peroxidation, which are processes implicated in the pathogenesis of Alzheimer’s disease (AD). Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to neutralize them with antioxidants. In Alzheimer’s disease, increased oxidative stress leads to damage to cellular components, including lipids, proteins, and DNA, contributing to neuronal dysfunction and neurodegeneration.
Longevity Alzheimer’s Disease Blood Test: 8 Analytes tested: Amyloid Beta (Aβ) Peptides 42/40, Acetylcholinesterase (AChE), Choline, Malondialdehyde (MDA), Neurofilament Light Chain (NfL), Phosphorylated Tau 181 (p-T181), Phosphorylated Tau 217 (p-T217), Total Tau Proteins (t-tau)
Overview
The most common type of Alzheimer’s disease usually begins after age 65 (late-onset Alzheimer’s disease). The most common gene associated with late-onset Alzheimer’s disease is a risk gene called apolipoprotein E (APOE).
APOE has three common forms:
APOE e2 — the least common — appears to reduce the risk of Alzheimer’s
APOE e4 — a little more common — increases the risk of Alzheimer’s
APOE e3 — the most common — doesn’t seem to affect the risk of Alzheimer’s
Genes
1 Gene
APOE
Disorders
- Risk for Late Onset Alzheimer’s Disease
Gene Function
Because you inherit one APOE gene from your mother and another from your father, you have two copies of the APOE gene. Having at least one APOE e4 gene increases your risk of developing Alzheimer’s disease. If you have two APOE e4 genes, your risk is even higher.
But not everyone who has one or even two APOE e4 genes develops Alzheimer’s disease. And the disease occurs in many people who don’t even have an APOE e4 gene, suggesting that the APOE e4 gene affects risk but is not a cause. Other genetic and environmental factors likely are involved in the development of Alzheimer’s disease.
Clinical Utility
When To Order
Patients with a personal and/or family history of Parkinson’s disease, Alzheimer’s disease, and Dementia. Warning signs of these diseases include, but are not limited to, abnormal imaging of the brain, difficulty moving or controlling one’s movement, memory loss that interferes with daily life, changes in mood and personality, difficulty having a conversation or completing familiar tasks, and confusion with the time or place.
Benefit To Patient
Patients identified with a disease-causing change (a pathogenic or likely pathogenic variant) in a gene on this panel have an increased risk of developing the associated neurodegenerative disease. Genetic testing may be beneficial in the planning and decision-making process for treatment, psychosocial counseling, research study enrollment, and support programs for caregivers and patients. Your patient’s family members can also be tested to help define their risk. If a pathogenic variant is identified in your patient, close relatives (children, siblings, and parents) are up to 50% more likely to also be at increased risk.
Patient Advocacy
Alzheimer’s Disease, Parkinson Disease, and Dementia are conditions that affect the brain and spinal cord. They can cause serious complications, such as difficulty moving or experiencing involuntary movements (i.e. tremors), memory loss, and disruption of mental abilities (solving problems, controlling emotions, or chewing and swallowing).
Symptoms of these conditions typically begin after the age of 60, however, in some families symptoms can occur as early as the third decade of life. Research has shown that these diseases can sometimes be caused by abnormal changes in our genes, and these genetic changes can be inherited and passed down in families. Having a family history of Parkinson’s disease, Alzheimer’s disease, dementia, or a similar condition may increase your risk of having that condition.
There is no cure for Alzheimer’s disease, Parkinson’s disease, or Dementia; however, there are treatments available to provide temporary relief from symptoms. Surgery, such as deep brain stimulation, may also be considered. Genetic testing may identify individuals at increased risk and assist in the planning and decision-making process for treatment, psychosocial counseling, and support programs for caregivers and patients.
To learn more about these conditions, please visit:
- Parkinson’s Foundation
- NIH-National Institute of Neurological Disorders and Stroke
- American Parkinson Disease Association
- Alzheimer’s Association
Lab Method & Assay
- Next Generation Sequencing
- Deletion/Duplication Analyses
- Sanger Sequencing
Test Limitations
All sequencing technologies have limitations. This analysis is performed by Next Generation Sequencing (NGS) and is designed to examine coding regions and splicing junctions. Although next generation sequencing technologies and our bioinformatics analysis significantly reduce the contribution of pseudogene sequences or other highly-homologous sequences, these may still occasionally interfere with the technical ability of the assay to identify pathogenic variant alleles in both sequencing and deletion/duplication analyses. Sanger sequencing is used to confirm variants with low quality scores and to meet coverage standards. If ordered, deletion/duplication analysis can identify alterations of genomic regions which include one whole gene (buccal swab specimens and whole blood specimens) and are two or more contiguous exons in size (whole blood specimens only); single exon deletions or duplications may occasionally be identified, but are not routinely detected by this test. Identified putative deletions or duplications are confirmed by an orthogonal method (qPCR or MLPA). This assay will not detect certain types of genomic alterations which may cause disease such as, but not limited to, translocations or inversions, repeat expansions (eg. trinucleotides or hexanucleotides), alterations in most regulatory regions (promoter regions) or deep intronic regions (greater than 20bp from an exon). This assay is not designed or validated for the detection of somatic mosaicism or somatic mutations.
Test Code
Specimen Requirements
Buccal swab
Turn Around Time
3 – 5 weeks
CPT Codes
81479×1
NOTE: The CPT codes listed on the website are in accordance with Current Procedural Terminology, a publication of the American Medical Association. CPT codes are provided here for the convenience of our clients. Clients who bill for services should make the final decision on which codes to use.
