From Plaque to Progress: The Evolving Science of Dementia
Many of you know I have mild cognitive impairment (MCI) which is similar to dementia. It’s a condition where I detected a noticeable decline in cognitive abilities.
MCI and dementia share a number of symptoms. A few of these are: difficulties finding the right word, trouble staying on task (I have trouble following plots…not a great spot for a writer to be in), remembering recent events and struggling with complex undertakings like managing finances.
Sometimes MCI is a precursor to dementia. In others, it could last a lifetime. The NIH (National Institute of Health) claims 22% of Americans have this condition.
There’s been a lot of activity in science labs concerning cognitive decline and I want to share with you some of what I’ve found.
Normal Memory Loss
The normal charges in memory loss generally appear in our 40s or 50s. They are mild and don’t impact an individual’s daily life to any significant degree. This might affect speed of recall, occasional word loss and forgetting where you placed an object, just to name a few characteristics.
As we age, subtle changes in the brain such as reduced blood flow or slower communications between nerve cells cause occasional forgetfulness like misplacing a wallet or missing a periodic word. These “senior moments” are not significant enough to interrupt daily life.
The synapses age and weaken. The prefrontal cortex is less effective with regards to concentrating and not becoming distracted.
From Virginia Tech, neuroscientist Tim Jarome and his team, assessed memory loss and determined that it’s linked to molecular changes in the brain’s hippocampus and amygdala. Using gene editing the team successfully removed “chemical tags” that silence memory-building genes. The memory in some test subjects improved dramatically. So there is some evidence that retention can be reistablished.
Statistics
According to Columbia University Irving Medical Center, one in ten Americans over the age of 65 has dementia. The average 55 year old has a 42% lifetime risk of developing dementia, 35% for men, 48% rate for women.
New York University says dementia cases are estimated to double by 2060. I’ve read this in many sources. The increase will be especially large for women, Black people and those of the age of 73 or more.
So our programs and laboratories should be busier than ever. But they’re not . Their budgets have been cut back; layoffs are more frequent. Private, capital and corporate contributions have dropped. On top of that, government funding has been reduced. For instance, the National Science Foundation’s funding has been cut in half and there’s a proposal to cut the NIH 40%.
We have a lot of work to do. So carry the story about dementia and its needs.
Medication
As many of you know, the laboratories made a giant leap with regards to the pharmaceutical world – medicine. Still in its infant stages the U.S. FDA-approved drugs have arrived.
Legembi (lecanemab) and Kinsunla (donanemab) have been prescribed for those with MCI and mild Alzheimer’s. They prevent amyloid plaque from clumping to its amount of protein deposits in the dementias, one of the causes of Alzheimer’s which slows down thinking and functioning.
Another drug Leukin (saracatinib),designed to be a possible treatment for cancer, is now being tested in humans with Alzheimer’s. In mice, this drug showed some reversal of memory loss and it was successful in improving synapses. It also reduces cell inflammation. It may stimulate the immune system thus helping to keep the brain safe from harmful proteins.
On the horizon
Lab after lab is working toward the understanding, treatment and elimination of dementia.
Assistant professor at the University of California San Francisco, Claire Clelland , and her colleagues used cells from patients with heredity-related backgrounds such as those with Alzheimer’s disease (ALS) and fronto-temporal dementia (FTD) to examine different CRISPR results.
Clelland became a physicianscientist in order to cure dementia.
The majority of cases of ALS and FTD share a common cause: a copy of the C9orf gene that has a “ repeat expansion” with a short DNA sequence. This sequence is repeated over and over much like a record skipping to its last refrain.
They tried a number of experiments to interrupt its string. Finally, they were able to cut out the expansion through using CRISPR.
CRISPR
Labiotech was one of the first U.S.companies to use CRISPR for the treatment of dementia. Early results using CRISPR with heart disease and tumors on the liver were very successful – so why not dementia?
CRISPR stands for Clustured Regulary Interespaced Short Palindrontic Repeats. Now you know why we call it CRISPR.
It’s a revolutionary gene editing tool that allows analysts to edit DNA sequences. Think of it like a molecular pair of scissors that could cut and paste a genetic code.
However, it’s much more complicated than that.
Using CRISPR, some studies have shown progress in cognitive functions by reducing amyloid plaque (which causes Alzheimer’s), in improving cognitive functioning in mice and modifying the APOE-04 gene, a strong Alzheimer’s risk factor in human and mouse subjects.
More studies
The Mayo Clinic is working with monoclonal antibodies which might keep amyloid from accumulating and may remove deposits and keeping new ones from forming.
The monoclonal (identical) antibodies mimic the antibodies the body naturally produces as part of the immune system’s natural response to foreign invaders like toxic proteins and some metals.
Also looking into the future, CRISPR might be utilized for:
· Gene therapy
· Cancer treatment
· Agriculture (for example, disease-resistant crops)
· Basic research
The science is booming – think breakthrough meds, game-changing technology, even the horizon of gene therapy. But with programs being cut, it’s up to us to keep the momentum going. It’s time to step up, share the urgency and ensure research and treatment continue. Collectively we can make a difference.
Please remember, you are not alone.
Till next Monday or in the chat….
Judi
“…every step forward in dementia research, no matter how small, is a victory. It fuels our determination to find answers.” Dr. Howard Federoff, professor and Executive Vice President for Health Services, Reno School of Medicine