Tag Archives: aging

Could Young Blood Cure Alzheimer’s Disease?

You may have heard the buzz lately about research surrounding the use of young people’s blood to treat Alzheimer’s disease. The latest findings were presented at the recent Clinical Trials on Alzheimer’s Disease conference, as reported by TIME Magazine. After previous studies showed that injecting an old mouse with the blood of a younger mouse (a process called parabiosis) caused improved memory and cognition, neuroscientists have been curious to see whether the same effect could be true in humans.

A group of researchers from Stanford conducted a small clinical trial to test this idea. They recruited 18 elderly volunteers and injected them weekly with young people’s blood plasma (taken from a local blood bank) or a placebo over the course of four weeks. They found that those receiving the young plasma treatments showed significantly enhanced measures of independence, including ability to shop for themselves or balance their own checkbook. No harmful side effects were noted.

The researchers did not study the subjects’ memory or cognitive ability as part of the trial, but these measures are being planned for future studies with a larger sample size. While still very preliminary, this small trial does suggest that there could be some factors in young people’s blood that could improve cognition in older people. While it’s far too early to start storming the blood banks demanding a transfusion, the link between our brains and our blood suggests that we need to be paying particular attention to our cardiovascular health as we age.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!
Advertisements

How Alzheimer’s and Depression are Linked to Hearing Loss (Reblog)

Our article this week is a reblog from the New Generation Hearing Blog. It’s a fairly short article, but I like that sheds light on the little-known connection between brain health and hearing loss. Click the link below to give it a read!

 

There are at least 38 million people who suffer from hearing loss throughout America. Many senior citizens expect to lose their hearing over time but few know that it could increase the chances for depression and even increase the risk of Alzheimer’s disease. In fact, hearing loss can influence every aspect of an individual’s life […]

via How Alzheimer’s and Depression are Linked to Hearing Loss — New Generation Hearing Blog

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

An Often-Ignored Type of Brain Cell May Be the Key to Aging

As we age, a multitude of changes occur in our bodies at the genetic level. A gene is essentially just an instruction manual for building a particular protein. When the gene is activated, it’s like the book is wide open, allowing the cellular machinery to access the instructions and build the encoded protein. This is called “gene expression.” Genes can also be inactivated, like sealing a book shut so that the instructions can’t be accessed. When this happens, the protein that’s encoded by the gene cannot be synthesized.

This system of modifiable gene expression is necessary for complex multicellular organisms like ourselves to function. It’s what makes a heart cell different from a lung cell: even though their DNA sequence is the same, different genes are turned on and off in each type of cell. While the sequence of our DNA (i.e., the words written in all the instruction manuals) generally stays the same throughout our lifetime, a variety of factors can alter the pattern gene expression in individual cells. One of these factors is aging.

central-dogma-enhanced

An overview of gene expression. DNA is transcribed into an intermediate molecule called RNA, which then is translated into the final protein. Source

In a study published this week in Cell Reports, researchers from the UK examined all the changes in gene expression that occur in our brains during aging. They used a total of 480 post-mortem human brains from individuals aged 16 to 106 and performed a comprehensive analysis of gene expression based on specific regions of the brain. To their surprise, they found that neurons (the primary brain cells that are responsible for our actual “thinking”) had relatively small changes in regional gene expression over time.

In contrast, large changes were observed in non-neuronal brain cells called glia. Glia were once seen as just passive connective tissue, but we now know that they play a variety of important roles in the brain including maintaining the proper environment for neurons, aiding in the speed of neuronal transmissions, and protecting the brain from infection or injury. The glia’s gene expression changes were highly dependent on their region of the brain, with the most prominent shifts being observed in the hippocampus and the substantia nigra, structures associated with Alzheimer’s and Parkinson’s diseases, respectively.

The researchers also found that genes specific to microglia, a type of glial cell that serves as the brain’s primary immune system, had higher gene expression overall in older brains compared to younger brains. In contrast, genes specific to neurons or oligodendrocytes (another type of glia) had lower overall expression in older brains. These changes were accompanied by greater numbers of microglial cells and fewer neurons and oligodendrocytes in specific areas of the brain.

Overall, the changes in glial gene expression were a better predictor of age than changes in neuronal gene expression. This suggests that glia may be the primary driving force behind the process of brain aging, highlighting the importance of future research on these once-ignored cells.

1209_glial_cells_of_the_cns-02

This illustration shows neurons in yellow and various type of glia in teal or red. Glia play many important roles in the brain and are closely linked to aging. Source

A notable limitation of this study is that their calculations were based on levels of RNA rather than protein. RNA is an intermediate molecule between DNA and proteins, but the amount of protein produced from a particular RNA molecular is highly variable. Thus, it’s hard to determine from this study how much the proteins encoded by these genes were actually altered during aging.

Regardless, these results provide strong evidence that glia play a much greater role in aging than previously thought. This reflects a change that has gradually started occurring in the neuroscience community in which some of the focus is shifted from neurons to glia. Perhaps these poorly-understood cells will turn out to be the key to brain aging.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

A New Approach to Predicting Risk of Alzheimer’s Disease

Background

An individual’s risk for Alzheimer’s disease is affected by a variety of genetic and environmental factors. While the causes of early-onset Alzheimer’s are well understood, the genetic factors underlying late-onset Alzheimer’s disease (LOAD), which makes up 95% of total cases, are less clear. The APOE4 allele is considered the major risk factor for this form of Alzheimer’s, as it can increase your risk by 2-3 times if you have one copy of the allele or up to 15 times if you have two copies. APOE4 does not guarantee that an individual will develop LOAD, and researchers have been searching for other genes that may be involved. (For more background see The Genetics of Alzheimer’s Disease).

Genome-wide association studies, which systematically analyze the 0.1% of DNA sequence that varies between individuals, have linked at least 21 other genes to an increased risk of LOAD. Individually, each of these genes has only a small influence in comparison to APOE4, often increasing one’s risk by only a few percentage points. However, when many of these small genetic risk factors are combined, they can greatly affect an individual’s chances of developing LOAD.

Overall, studies suggest that approximately 33% of an individual’s risk for developing LOAD is attributable to genetics, with the rest being due to lifestyle choices and environmental factors. Of this, APOE and the 21 already-identified genes account for less than 25% of the genetic risk, suggesting that the majority of genetic risk factors for Alzheimer’s disease remain unknown.

New Results

In a recent study published in the journal Neurology, a group of researchers from the Alzheimer’s Disease Neuroimaging Initiative searched for other genes, outside of the 21 already identified, that could also act as slight risk factors for Alzheimer’s. They used data collected from the International Genomics of Alzheimer’s Project to compute polygenetic risk scores, or PGRS, for both young and elderly adults who did not have dementia. Each person’s PGRS was calculated using his or her unique combination of small genetic risk factors (including many that were not statistically significant in genome-wide association studies) in order to estimate the genetic risk for LOAD. The researchers then analyzed whether PGRS were associated with biological markers of preclinical Alzheimer’s disease.

In elderly subjects who did not have dementia, high PGRS was associated with poorer memory, smaller volume of the hippocampus (the part of the brain that helps us form new memories), and increased levels of toxic beta-amyloid in the brain. High PGRS in these individuals also correlated with an increased rate of cognitive decline and a greater probability of later being diagnosed with Alzheimer’s disease. The researchers also computed PGRS for younger subjects under the age of 35. They found that a high PGRS was associated with reduced hippocampal volume, similarly to the older subjects.

Together, these results suggest that more genes besides the currently-identified 21 may need to be considered when evaluating an individual’s risk for LOAD. The researchers plan to repeat this study using a larger sample size to verify the results. Future studies also will track younger subjects to see if PGRS can predict their risk for Alzheimer’s as they age, and compare these results to less comprehensive systems of genetic prediction. The hope is that by refining PGRS, we may one day be able to develop better genetic tests for young people that yield more accurate predictions of future Alzheimer’s risk.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email or like us on Facebook!