Tag Archives: Alzheimers

Human Umbilical Cord Blood: The Secret to Memory?

A recent study indicates that a specific protein in human umbilical cord blood plasma has the potential to improve learning and memory in aging, older mice.

In 1972, research demonstrated that when pairs of rats were surgically attached, older rats had increased lifespan when sharing a bloodstream with young rats. This particular study spearheaded a scientific effort surrounding the understanding and consensus of aging: certain materials from younger bodies or organisms can often improve or rejuvenate older ones, when transplanted.

Further findings produced exciting research; scientists have previously shown that young blood can restore cell activity in the muscles and livers of aging mice, and that linking older mice to young when helped reverse heart muscle thickening.

Although many of the findings have not been successfully replicated, there is a unanimous agreement that—like humans—as mice and rats age, their bodies and behavior change on profoundly fundamental levels. Joe Castellano, a neuroscientist at Stanford University School of Medicine, saw that older mice tended to stop building nests, and became increasingly forgetful.

Castellano and his colleagues collectively hypothesized that young human blood might produce beneficial effects for aging mice; in a report published in the journal Nature, they state that they have located a protein in human umbilical cord blood that can improve both learning and memory in aging mice—a significant and exciting finding in the field of regenerative medicine.

The team collected plasma, the ‘watery part of blood,’ from people of different ages, in addition to plasma from human umbilical cords. They then injected human plasma from those different age groups, and from umbilical cord blood, into mice continuously over several weeks. The mice were aged 12 and 14 months, which is calculated to be approximately the mouse equivalent of being in late 50s or 60s.

When the mouse brains were dissected and the hippocampi were inspected, it was found that certain genes linked to the creation of new memories had been turned on in some of the mice. “So, we had a hint early on that one of these donor groups, specifically the [umbilical] cord plasma, might be having an effect on the brain itself,” Castellano says.

Castellano and his team then injected more aging mice with human plasma, and tested the animals’ ability to remember things. They found that after cord plasma treatment, mice escaped from a maze more rapidly; the performance in most areas was increased and improved. Similarly, mice treated with human umbilical cord performed better on memory tests.

A series of further experiments led Castellano and his colleagues to conclude that one specific protein—TIMP2—in human umbilical cord blood was responsible for the improvements. “The really exciting thing about this study, and previous studies that have come before it, is that we’ve sort of tapped into previously unappreciated potential of our blood — our plasma — and what it can do for reversing the harmful effects of aging on the brain,” says Castellano.

The research potentially hints at possible treatments and therapies that might ultimately work to prevent age-related illnesses from developing, including Alzheimer’s disease.

Alzheimer’s & Glucose: Reducing Sugar Intake

While scientists have long known that excess glucose—or sugar—and its breakdown products have the potential to damage proteins and cells through a reaction called ‘glycation,’ the specific molecular link between sugar and Alzheimer’s disease was neither confirmed nor fully understood.

Yet scientists have recently confirmed a ‘tipping point’ molecular link between the blood sugar glucose and Alzheimer’s disease, as a study published in the journal Scientific Reports has demonstrated that excess glucose irreparably damages a critical enzyme is involved with inflammation response to the early stages ofAlzheimer’s.

Unusually high blood sugar levels, also called hyperglycemia, is a familiar characteristic of diabetes and obesity; indeed, patients with diabetes have been shown to have an increased risk of developing Alzheimer’s disease compared to healthy individuals. In the early stages of the disease, abnormal proteins aggregate to form ‘plaques and tangles’ in the brain, which progressively lead to severe cognitive decline.

By utilizing a sensitive technique to detect glycation through brain samples of people both with and without Alzheimer’s, a team of scientists discovered that—in the early stages of Alzheimer’s—glycation damages an enzyme called MIF (macropage migration inhibitory factor), which ultimately plays a role in immune response and insulin regulation. This enzyme is involved in the response of brain cells to the build-up of abnormal proteins in the brain during Alzheimer’s, and researchers believe that inhibition and reduction of MIF activity—caused by glycation—could be the proverbial ‘tipping point’ in disease progression. As Alzheimer’s disease progresses, so too does glycation of these enzymes increase.

Researchers articulate that this knowledge will be vital in developing a chronological trajectory of the progression of Alzheimer’s, and will assist in identifying those at risk, in addition to new preventive techniques and treatments. Moreover, this potential link with Alzheimer’s serves as another reason to curb and lower sugar intake.

Mark Rosenberg, MD, FMNM, a physician who has extensively studied the mechanisms of cancer treatment failure, and developed new preventive therapies, states: “Glucose or sugar, is a source of fuel for normal cells and malignant cells. The more resistant and aggressive cancer cells tend to rely on the metabolism of glucose through a process called glycolysis. These cells over-express GLUT-1 transporters, as well as insulin, to pull in as much sugar, as quickly as they can, so they can meet their energy requirements. There are multiple studies correlating elevated blood sugar, insulin resistance, and diabetes with the risk, as well as survival, for many cancers. Bottom line, from a cancer perspective: minimize sugar intake.”

Around 50 million people across the globe have been diagnosed with Alzheimer’s disease, a statistical figure predicted to rise to more than 125 million by2050. Researchers believe that the global cost of the disease will likely escalate into the hundreds of billions of dollars, as medical patients require further social and palliative care, due to the debilitating cognitive effects of the disease.

10 Proteins Top Alzheimer’s Biomarkers

Often, the biological processes of Alzheimer’s Disease begin many years prior to the display of symptoms, making the pursuit of predictive diagnostics a paramount effort.  Simon Lovestone, from King’s College London (United Kingdom), and colleagues analyzed blood samples from 1,148 people: 476 with Alzheimer’s, 220 with mild cognitive impairment and 452 elderly controls without dementia. The researchers honed in on 26 proteins previously found to be linked with Alzheimer’s Disease, and found that 16 of the  proteins were strongly associated with brain shrinkage in either mild cognitive impairment or Alzheimer’s.  The team then ran a second series of tests to see which of these could predict which patients would progress from mild cognitive impairment to Alzheimer’s; they identified a combination of 10 proteins capable of predicting with 87% accuracy whether people with mild cognitive impairment would develop Alzheimer’s disease within a year.  Writing that: “We have identified 10 plasma proteins strongly associated with [Alzheimer’s] disease severity and disease progression,” the study authors submit that:  “Such markers may be useful for patient selection for clinical trials and assessment of patients with predisease subjective memory complaints.”  For the news source visit: http://uk.reuters.com/article/2014/07/08/us-health-alzheimers-idUKKBN0FC2IC20140708

Hye A, Riddoch-Contreras J, Baird AL, Ashton NJ, Bazenet C, Lovestone S, et al.  “Plasma proteins predict conversion to dementia from prodromal disease.”  Alzheimers Dement. 2014 Jul 3.