Alterations in the Brain May Occur as Early as 34 Years Before the Symptoms of Alzheimer’s Disease Appear

Researchers at Johns Hopkins School of Medicine found patients had increased levels of Tau, a biomarker of Alzheimer’s disease, as early as 34 years prior to the onset of symptoms.1

Note: Despite all advances in stem cells research and the application of these therapies in many countries all over the world, stem cells therapies are not legally approved yet in San Diego, Los Angeles, Chicago, Dallas, New York, Jacksonville, Seattle, Houston, San Francisco, Salt Lake City, Miami, Beverly Hills and other US cities. However, stem cell treatments are legal in Costa Rica.

The study, published in April, 2019 in Frontiers in Aging Neuroscience, was designed to identify changes in chemical biomarkers in the preclinical phase, or pre-symptomatic phase of Alzheimer’s disease.

About Alzheimer’s Disease

More than 35 million people are currently living with Alzheimer’s disease and the number of people living with the disease is expected to double in the next 10 years. Being able to diagnose the disease earlier could impact treatments and outcomes for patients at risk of developing the leading cause of dementia.

Dementia is a fatal disease characterized by chronic inflammation and neuronal loss resulting in amnesia, progressive cognitive impairment, and disorientation.

Alzheimer’s disease is the most common form of dementia with more than 5 million people in the United States living with this devastating disease, and it is the 6th leading cause of death, killing more people than prostate cancer and breast cancer combined.2.

The exact cause of Alzheimer’s disease is unknown but there are four key features; 1. Amyloid-beta (Aß) plaques, 2. Neurofibrillary tangles, 3. Neuroinflammation, and 4. Mass neuronal and synaptic loss.

Amyloid-beta plaques are sticky clumps of protein fragments that accumulate and attack brain cells, leading to their death. Neurofibrillary tangles are twisted fibers of Tau protein that build up inside the neurons of Alzheimer’s patients damaging neural structures and inhibiting the transport of nutrients.

Neuroinflammation is caused by the activation of microglia which mediate immune responses. Microglia are activated and begin producing cytokines that increase neuroinflammation. All of these factors result in mass neuronal and synaptic loss causing the cortex region of the brain to atrophy, or decrease in size.3-7

Clinicians believe Alzheimer’s begins years before the appearance of symptoms but are unclear how early the changes begin and what specific changes occur in the brain. 

Study Design and Results

Investigators at Johns Hopkins reviewed the medical records of 306 study participants considered to have normal cognitive function, 40 years of age or older, with the majority of participants having at least one first-degree relative with Alzheimer’s disease, putting them at higher risk of developing the disease.

Every two years, the team of investigators evaluated 9 measurements from cerebrospinal fluid samples, MRI brain scans and five standard cognitive tests that evaluated memory, learning, reading.

By the end of the study, 81 participants had developed Alzheimer’s disease. Researchers used a changepoint model to determine which of the measurements had changed significantly over time prior to the onset of symptoms.

Results showed all 9 measurements had significant changes, however, the timepoint at which those changes took place varied. All cognitive tests showed changes at 10-15 years prior to the onset of symptoms while the measurement of tau protein showed the earliest changes, with increases detected as early as 34 years prior to the onset of symptoms.

The goal for investigators and treating physicians, is to find a combination or biomarkers that will accurately indicate who is at increased risk for Alzheimer’s disease to develop better diagnostic tools, allowing clinicians to accurately identify and treat patients earlier.

About Stem Cell Therapy

At the Stem Cells Transplant Institute, we are using umbilical cord mesenchymal stem cells (UC-MSCs) to treat the symptoms of Alzheimer’s disease.

Neural stem cells transplanted at sites of nerve injury are thought to promote functional recovery by producing trophic factors that induce survival and regeneration of host neurons.

Intravenously administered mesenchymal stem cells are also capable of crossing the blood-brain barrier and effectively migrating to regions of neural injury, without inducing tumor growth or an immune response.9

Research has shown mesenchymal stem cells have the potential to treat the symptoms of Alzheimer’s disease through multiple pathways, and can:

1. Decrease Amyloid-beta plaque formation,

2. Stimulate neurogenesis, synaptogenesis and neuronal differentiation,

3. Rescue spatial learning and memory deficits, and

4. Possibly decrease inflammation by upregulating neuroprotective cytokines and decreasing pro-inflammatory cytokines.

What are the challenges of stem cell therapy?

Alzheimer’s disease destroys many different types of neurons in the brain.

Successful treatment requires all the stem cells to travels to and differentiate into different types of neurons and other brain cells correctly.

At this time stem cell therapy does not stop the underlying cause of Alzheimer’s disease and patient may need more than one treatment due to a declining effect over time

Why choose the Stem Cells Transplant Institute?

In many parts of the world, experts in the field of regenerative medicine are using stem cell therapy to successfully treat patients with Alzheimer’s disease. At the Stem Cells Transplant Institute, we use umbilical cord derived mesenchymal stem cells for the treatment of Alzheimer’s disease.

We have developed a two-day treatment combining umbilical cord stem cell therapy with powerful antioxidants and ozone therapy to enhance and maximize results.

The advantages of therapy at the Stem Cells Transplant Institute Include:

  1. Umbilical cord stem cells
  2. Umbilical cord stem cells are young and more adaptable
  3. Umbilical cord stem cells are free from viruses and bacteria
  4. Umbilical cord stem cells divide much more rapidly
  5. We also treat patients using powerful antioxidants, ozone therapy and platelet-rich plasma therapy
  6. Increases potency of stem cells
  7. Improves stem cell differentiation
  8. Enhances the immune system
  9. Promotes T-cell formation
  10. Controls inflammation
  11. Decreases muscle damage
  12. Reduces recovery time
  13. Increases strength and performance
  14. Maintains cellular health
  15. Fights infection and helps prevent disease
  16. Helps detoxify the liver

Contact us today to learn more about the benefits of stem cell therapy at the Stem Cells Transplant Institute.

Scientific References:

  1. Laurent YounesMarilyn Albert, Abhay Moghekar, Anja Soldan, Corinne Pettigrew and Michael I. Miller Front. Aging Neurosci., 02 April 2019
  2. Alzheimer’s Association. 2017 Alzheimer’s Disease Facts and Figures. Alzheimer’s Dement 2017;13:325-373.
  3. Thomas Duncan and Michael Valenzuela. Alzheimer’s disease, dementia and stem cell therapy. Stem Cell Research & Therapy (2017) 8:111.
  4. Salloway S, Sperling R, Fox NC, Blennow K, Klunk W, Raskind M, Sabbagh M,Honig LS, Porsteinsson AP, Ferris S. Two phase 3 trials of bapineuzumab inmild-to-moderate Alzheimer’s disease. N Engl J Med. 2014;370:322–33.
  5. Doody RS, Raman R, Farlow M, Iwatsubo T, Vellas B, Joffe S, Kieburtz K, He F,Sun X, Thomas RG. A phase 3 trial of semagacestat for treatment of Alzheimer’s disease. N Engl J Med. 2013;369:341–50.
  6. Walker D, Lue LF. Investigations with cultured human microglia onpathogenic mechanisms of Alzheimer’s disease and other neurodegenerative diseases. J Neurosci Res. 2005;81:412–25.
  7. Delbeuck X, Van der Linden M, Collette F. Alzheimer’s disease as a disconnection syndrome? Neuropsychol Rev. 2003;13:79–92.
  8. Ra JC, Shin IS, Kim SH, Kang SK, Kang BC, Lee HY, Kim YJ, Jo JY, Yoon EJ, Choi HJ. Safety of intravenous infusion of human adipose tissue-derived mesenchymal stem cells in animals and humans. Stem Cells Dev. 2011;20:1297–308.