Results from a study published in Neurology in March 2019, showed a link between systemic inflammation during the mid-life years, and memory loss and cognitive decline later in life. Stem cell therapy at the Stem Cells Transplant Institute in Costa Rica may help improve the signs and symptoms of dementia by reducing inflammation by upregulating neuroprotective cytokines and decreasing pro-inflammatory cytokines.
For years scientists have been trying to treat Alzheimer’s disease by focusing their efforts on treating or preventing two of the four key features of Alzheimer’s disease, the amyloid-beta plaques and neurofibrillary tangles, but they have not yet been successful at finding an effective treatment.
Researchers decided to examine the long-term association between systemic inflammation and cognitive decline by evaluating data from the Atherosclerosis Risk in Communities (ARIC) study at Johns Hopkins University. https://n.neurology.org/content/92/11/e1256
Researchers measured blood biomarkers including fibrinogen, white blood cell count, von Willebrand factor, factor VIII and C-reactive protein (CRP) in a total of 12,336 participants with an average age of 57. Cognition was also assessed during 3 visits over 20 years using standard tests for memory and other brain functions.
The results showed adults with the highest levels of inflammatory markers in their mid-life years (40s, 50s and 60s) had a steeper rate of cognitive decline later in life. Participants with the highest levels of inflammation had a 7.8% steeper cognitive decline when compared to those who lad the lowest levels of inflammation. Researchers found C-reactive protein to be a critical marker with participants having the highest levels of CRP showing an 11.6% steeper cognitive decline.
Researchers concluded “midlife inflammatory markers were most consistently associated with declines in memory”.
Dementia including Alzheimer’s Disease
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.4-8
Stem Cell Therapy at the Stem Cells Transplant Institute
Stem cell therapy may help improve the signs and symptoms of dementia including Alzheimer’s disease. Human umbilical cord mesenchymal stem cells (hUC-MSCs) can promote the release of acetylcholine, promote neurogenesis and synaptic formation and can reduce oxidative stress and cell death. Research is showing hUC-MSCs to be a better alternative to allogeneic stem cells because of their hypo-immunogenicity, superior tropism, high differentiation potential and paracrine activity.10-13Evidence suggests HUC-MSCs can differentiate into a variety of neuro-regulatory molecules and can elevate several factors including brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), insulin-like growth factor 1 (IGF-1), Glucagon-like pepetide-1 (GLP-1), and vascular endothelial growth factor (VEGF).9Neural 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 affect Alzheimer’s through multiple pathways and can:
- Decrease Amyloid-beta plaque formation
- Stimulate neurogenesis, synaptogenesis and neuronal differentiation
- Rescue spatial learning and memory deficits
- Possibly decrease inflammation by upregulating neuroprotective cytokines and decreasing pro-inflammatory cytokines
The Stem Cells Transplant Institute Uses Human Umbilical Cord Stem Cells
What are the advantages of human umbilical cord mesenchymal stem cells?
- Abundant supply containing up to 10 times more stem cells than bone marrow or adipose derived stem cells
- hUC-MSC have immunosuppressors and immunomodulatory properties that allow their use in any individual without rejection- Human Leukocyte Antigen (HLA) matching is not necessary
- Greater proliferation ability than adult autologous stem cells
- They regenerate at a very rapid rate
- They are young and very adaptive
- They have not been impacted by the aging process
- They have not been affected by environmental toxins
- Umbilical cord stem cells can be administered multiple times over the course of days
- Eliminates the need to collect stem cells from the patient’s fat or hip bone reducing pain and recovery time
Why Treatment at The Stem Cells Transplant Institute is Different
- At the Stem Cells Transplant Institute, we believe every patient, not just the rich and famous, should be able to experience the powerful regenerative benefits of stem cell therapy.
- At our clinic, we tailor each stem cell treatment, based on the patient’s individual needs and goals.
- At the Stem Cells Transplant Institute, we use only adult mesenchymal stem cells, also called somatic stem cells.
- Our clinic offers mesenchymal stem cells derived and expanded from human umbilical cord tissue.
- The human umbilical cord stem cells are collected, expanded, and tested over a three-week period before use at the Stem Cells Transplant Institute
- The mission of the Stem Cells Transplant Institute in Costa Rica, is to provide the highest level of care, using the most advanced technologies, to every patient that wants to experience the life changing benefits of stem cell therapy.
Contact us at the Stem Cells Transplant Institute to learn more about the benefits of stem cell therapy for neurodegenerative diseases like Alzheimer’s disease.
- Systemic inflammation during midlife and cognitive change over 20 years Keenan A. Walker, Rebecca F. Gottesman, Aozhou Wu, David S.Knopman, Alden L. Gross, Thomas H. Mosley, Elizabeth Selvin, B. Gwen Windham
- Alzheimer’s Association. 2017 Alzheimer’s Disease Facts and Figures. Alzheimer’s Dement 2017;13:325-373.
- Tang Jun, How close is the stem cell cure to the Alzheimer’s disease: Future and Beyond? Neural Regen Res. 2012 Jan 5; 7(1): 66–71.
- Neurology Mar 2019, 92 (11) e1256-e1267; DOI:10.1212/WNL.000000000000709Thomas Duncan and Michael Valenzuela. Alzheimer’s disease, dementia and stem cell therapy. Stem Cell Research & Therapy (2017) 8:111.
- 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.
- 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.
- 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.
- Delbeuck X, Van der Linden M, Collette F. Alzheimer’s disease as a disconnection syndrome? Neuropsychol Rev. 2003;13:79–92.