Biomarkers of Alzheimer’s Disease

Posted on February 24th, 2017

Early detection of Alzheimer’s Disease is paramount to beginning early treatment. Early treatment – prior to high levels of amyloid beta tangles and permanent brain damage has a much higher chance of success.

This article is the most comprehensive online listing of the biomarkers of Alzheimer’s Disease compiled by anyone so far. Contact us if you would like to suggest a biomarker or know of a more comprehensive list.

Traditional markers of Alzheimer’s include tau proteins, amyloid precursor proteins and amyloid beta levels in cerebral spinal fluid (CSF). These markers are useful indicators of the progression of neurodegeneration in Alzheimer’s Disease. However, they are later stage markers that indicate the disease is in full force.

A decrease in hematopoetic stem cells that give rise to all the other blood cells through the process of haematopoiesis [W] and a decrease in neurotrophic factors have been shown to have negative consequences for repair of existing neurons. Neurotrophic factors are proteins and peptides that support the growth, survival, and differentiation of both developing and mature neurons – without which the brain is no longer able to repair itself or grow. Additionally, evidence of blockage of CSF circulation caused by whiplash and other traumatic neck injuries may result in reduced clearance of amyloid beta by immune cells. This CSF blockage may have early diagnostic potential in a new form of MRI test, called Upright MRI. [R]

Other major risk factors include midlife high blood pressure, diabetes, and APOE4 genetics. See below for a full list.

Early Indicators of Alzheimer’s Disease

Very Early Indicators of Alzheimer’s Disease Risk
(Less than 50 Years Old)

Genetic Risk Factors of Alzheimer’s Disease

Genetic Risk Factors for Alzheimer's Disease

Early Onset and Familial Alzheimer’s Disease

The early onset of Alzheimer’s is usually driven by extreme factors. Severe physical trauma to the brain like multiple concussions or a high level of toxicity is a good example. Another example, not to be forgotten, is severe emotional trauma. Post traumatic stress disorder symptoms appear identical to Alzheimer’s Disease in clinical presentation (what a patients acts, looks and feels like). Genetics often plays a part in accelerating early onset Alzheimer’s.

Purely genetics triggered Alzheimer’s Disease (without major trauma to the brain) is actually a different disease altogether called Familial Alzheimer’s Disease (FAD) and is quite rare. It is not something you need to worry about getting if your family does not have a history of early onset Alzheimer’s Disease. This is not an area of focus for Soldara research.  If you would like to learn more about it, a good place to start is the National Institute on Aging. FAD is driven by three known genes:

Late Onset Alzheimer’s Disease (LOAD)

Late onset Alzheimer’s Disease is not triggered by genetics. Genetics merely increase your risk. Knowing your genetics can can give you the information you need to build a healthy lifestyle personalized to your genetics.

References

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  3. Laske, Christoph, et al. “Decreased CXCL12 (SDF-1) plasma levels in early Alzheimer’s disease: a contribution to a deficient hematopoietic brain support?.” Journal of Alzheimer’s Disease 15.1 (2008): 83-95. [R]
  4. Laske, Christoph, et al. “Decreased plasma and cerebrospinal fluid levels of stem cell factor in patients with early Alzheimer’s disease.” Journal of Alzheimer’s Disease 15.3 (2008): 451-460. [R]
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