Alzheimer’s Disease

Alzheimer’s Disease is a chronic neurodegenerative disease that generally worsens over time. It is the most common cause of dementia and can lead to difficulty in memory, problems with language, disorientation, mood swings, personality changes, and lack of self care.

The cause of Alzheimer’s Disease is not well understood. The disease process is characterized by neurofibrillary tangles and plaque development within the brain.

Unfortunately, there is no cure for Alzheimer’s Disease and treatment is limited to temporarily relieving symptoms.

Many researchers are looking toward stem cell treatments to try and cure Alzheimer’s Disease, but at this time the most successful trials have only aided in slowing down or temporarily stopping the progression of the disease. The goal of stem cell treatment for Alzheimer’s Disease is to improve the patient’s quality of life and try and regain some of the memory and functionality that they have lost.

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The most current research regarding stem cells and Alzheimer’s Disease is given below:

Human Umbilical Cord Blood-Derived Monocytes Improve Cognitive Deficits and Reduce Amyloid-β Pathology in PSAPP Mice
Donna Darlington, Song Li, Huayan Hou, Ahsan Habib, Jun Tian,* Yang Gao,* Jared Ehrhart,§ Paul R Sanberg,‡ Darrell Sawmiller,* Brian Giunta,*† Takashi Mori, and Jun Tan

Abstract: Alzheimer’s disease (AD) is the fourth major cause of mortality in the elderly in the US and the leading cause of dementia worldwide. While pharmacological targets have been discovered, there are no true disease-modifying therapies. We have recently discovered that multiple low-dose infusions of human umbilical cord blood cells (HUCBCs) ameliorate cognitive impairments and reduce Aβ-associated neuropathology in PSAPP transgenic mice. However, the mechanism for these effects of HUCBCs remains unclear. In the present study, we examined whether monocytes, as important components of HUCBCs, would have beneficial outcomes on the reduction of AD-like pathology and associated cognitive impairments in PSAPP transgenic AD model mice. PSAPP mice and their wild-type littermates were treated monthly with an infusion of peripheral human umbilical cord blood cell (HUCBC)-derived monocytes over a period of 2 and 4 months, followed by behavioral evaluations, biochemical, and histological analyses.


The principal findings of the present study confirmed that monocytes derived from HUCBCs (CB-M) play a central role in HUCBC-mediated cognition-enhancing and Aβ pathology-ameliorating activities. Most importantly, we found that compared with CB-M, aged monocytes showed an ineffective phagocytosis of Aβ, while exogenous soluble amyloid precursor protein α (sAPPα) could reverse this deficiency. Pretreating monocytes with sAPPα upregulates Aβ internalization. Our further studies suggested that sAPPα could form a heterodimer with Aβs, with the APP672–688 (Aβ1–16) region being responsible for this effect. This in turn promoted binding of these heterodimers to monocyte scavenger receptors and thus promoted enhanced Aβ clearance. In summary, our findings suggest an interesting hypothesis that peripheral monocytes contribute to Aβ clearance through heterodimerization of sAPPα with Aβ. Further, declined or impaired sAPPα production, or reduced heterodimerization with Aβ, would cause a deficiency in Aβ clearance and thus accelerate the pathogenesis of AD.