In a previous blog post Tau vs. Amyloid - An Alzheimer's Dilemma
I wrote about Tau as a mitigating factor in AD. Lately there is more and more attention being paid about Tau.
In a recent published report* Tau has been referenced in a creative interpretation of zombie like cells, more scientifically referred to as senescent cells. In the life cycle of a cell there is a senescence period when the cell becomes stressed and has ceased it's normal function. At this stage it can actually cause more harm than good.
According to senior author Miranda E. Orr, Ph.D., VA research health scientist at the South Texas Veterans Health Care System, "When cells enter this stage, they change their genetic programming and become pro-inflammatory and toxic" These cells then secrete a substance that kills adjacent healthy cells.
Although the study was done in mice, it was found that tau proteins surrounding cells caused cell senescence. Furthermore, senescence was not found with amyloid. In other studies to confirm this, reducing tau genetically also reduced
senescence. The reverse also held true. Increasing tau genetically
increased senescence.
When the researchers used a combination of the drugs dasatinib and quercetin cellular senescence decreased and brain structure and function improved. In fact the drugs were able to clear the tau pathology and stop, or even reverse, the progression of AD.
While much work has to be done, the authors believe that the effects of the drug combination may work in human being to reduce senescence. More clinical studies are necessary.
*University of Texas Health Science Center at San Antonio. (2018, August 22). Stressed, toxic, zombie cells seen for 1st time in Alzheimer's: Finding may apply to 20 brain diseases; drug tandem stops decline in old mice. ScienceDaily. Retrieved November 20, 2018 from www.sciencedaily.com/releases/2018/08/180822092706.htm
Thursday, November 22, 2018
Thursday, November 1, 2018
Can the Eyes Have It? Can Eye Scans Predict Alzheimer's?
Here is some news hot off the press! This news was just released a few days ago.
Being a retired ophthalmologist, I find these findings are unusually interesting and dear to my heart. More importantly, they are phenomenally earth shattering if the results are independently confirmed in the future.
Two papers were presented at the 2018 meeting of the American Academy of Ophthalmology that may make the prediction of future Alzheimer's (AD) onset and progression earlier and less costly with relatively non-invasive eye tests.
1 - Retinal Thickness Study
The first study, as reported by Ygal Rotenstreich, MD, e.t al. of the Goldschleger Eye Institute at Sheba Medical Center, Tel Aviv, Israel. involved measuring the thickness of the retina (inner lining of the eye).
The study showed that people with a family history of Alzheimer's had thinner inner layers of their retinas and corresponding thinning of the hippocampus, which was separately measured by a brain scan. Of particular note is that none of the patients studied had any symptoms of AD or MCI.
The hippocampus is the part of the brain greatly responsible for memory and is invariably thinned as AD progresses.
Rotenstreich stated that “Inner retinal layer thickness is associated with cognitive function and hippocampal volume and may present a novel bio-marker for very early detection of Alzheimer's disease.”
The implication of this study means that AD can possibly be diagnosed much earlier than any study currently available.
2 - Retinal Blood Vessels Study
This study, led by Sharon Fekrat, MD, and Dilraj Singh Grewal, MD, both of Duke University in Durham, NC, consisted of multiple eye studies of patients over 50 years old from the Duke Memory Disorders Clinic with AD or MCI as well as community-based healthy volunteers without known memory problems. In short, it was found that blood vessels in the eye may be a predictor of the progression of AD.
Findings concluded that patients with AD had significantly reduced retinal small vessel density and perfusion density (flow characteristics) compared to patients with mild cognitive impairment (MCI) and the normal volunteers. Perfusion density was also lower in MCI patients compared to the normals.
The retinal microvasculature (very small blood vessels) was measured by optical coherence tomography angiography, which is a relatively non-invasive procedure compared to current diagnostic tools such as spinal taps or not readily available and expensive PET scans.
It was concluded that changes in the retinal micro-vasculature may mirror small-vessel cerebrovascular (brain) changes in Alzheimer disease. The findings suggest a continuum of decreasing retinal blood flow starting with normals, then progressing to MCI and eventually AD. These findings could make the progression of AD detectable earlier in the course of its illness.
Conclusion.
It is not really surprising that both studies were of the retina. Any eye doctor could tell you that the retina is considered an extension of the brain. Both studies offer hope that AD may be detected or measured at very early stages with relatively simple non-invasive tests. More conclusive testing is warranted for both studies.
Being a retired ophthalmologist, I find these findings are unusually interesting and dear to my heart. More importantly, they are phenomenally earth shattering if the results are independently confirmed in the future.
Two papers were presented at the 2018 meeting of the American Academy of Ophthalmology that may make the prediction of future Alzheimer's (AD) onset and progression earlier and less costly with relatively non-invasive eye tests.
1 - Retinal Thickness Study
The first study, as reported by Ygal Rotenstreich, MD, e.t al. of the Goldschleger Eye Institute at Sheba Medical Center, Tel Aviv, Israel. involved measuring the thickness of the retina (inner lining of the eye).
The study showed that people with a family history of Alzheimer's had thinner inner layers of their retinas and corresponding thinning of the hippocampus, which was separately measured by a brain scan. Of particular note is that none of the patients studied had any symptoms of AD or MCI.
The hippocampus is the part of the brain greatly responsible for memory and is invariably thinned as AD progresses.
Rotenstreich stated that “Inner retinal layer thickness is associated with cognitive function and hippocampal volume and may present a novel bio-marker for very early detection of Alzheimer's disease.”
The implication of this study means that AD can possibly be diagnosed much earlier than any study currently available.
2 - Retinal Blood Vessels Study
This study, led by Sharon Fekrat, MD, and Dilraj Singh Grewal, MD, both of Duke University in Durham, NC, consisted of multiple eye studies of patients over 50 years old from the Duke Memory Disorders Clinic with AD or MCI as well as community-based healthy volunteers without known memory problems. In short, it was found that blood vessels in the eye may be a predictor of the progression of AD.
Findings concluded that patients with AD had significantly reduced retinal small vessel density and perfusion density (flow characteristics) compared to patients with mild cognitive impairment (MCI) and the normal volunteers. Perfusion density was also lower in MCI patients compared to the normals.
The retinal microvasculature (very small blood vessels) was measured by optical coherence tomography angiography, which is a relatively non-invasive procedure compared to current diagnostic tools such as spinal taps or not readily available and expensive PET scans.
It was concluded that changes in the retinal micro-vasculature may mirror small-vessel cerebrovascular (brain) changes in Alzheimer disease. The findings suggest a continuum of decreasing retinal blood flow starting with normals, then progressing to MCI and eventually AD. These findings could make the progression of AD detectable earlier in the course of its illness.
Conclusion.
It is not really surprising that both studies were of the retina. Any eye doctor could tell you that the retina is considered an extension of the brain. Both studies offer hope that AD may be detected or measured at very early stages with relatively simple non-invasive tests. More conclusive testing is warranted for both studies.
Monday, July 9, 2018
Metal Iron and Alzheimers
As alluded to in previous posts, amyloid protein plaques in the brain are strongly associated with Alzheimer's disease (AD).
A recent study at the University of Warwick found that several varieties of iron, especially an iron oxide called magnetite, combined with amyloid plaques in the brains of people diagnosed with Alzheimer's. Plaques from the brains of two deceased patients were used in the study.
The study proposed that the interactions of iron and amyloid protein are responsible for the toxicity that leads to the death and/or the malfunction of brain cells. The understanding of the role of iron is exciting new information.
Dr. Joanna Collingwood, Associate Professor at the University of Warwick's School of Engineering commented: "Iron is an essential element in the brain, so it is critical to understand how its management is affected in Alzheimer's disease." She further noted that this new finding opens the door to possible new treatments of AD by the use of iron modifying drugs.
Dr. Collingwood was part of an international team that included researchers from University of Florida and The University of Texas at San Antonio.
A recent study at the University of Warwick found that several varieties of iron, especially an iron oxide called magnetite, combined with amyloid plaques in the brains of people diagnosed with Alzheimer's. Plaques from the brains of two deceased patients were used in the study.
The study proposed that the interactions of iron and amyloid protein are responsible for the toxicity that leads to the death and/or the malfunction of brain cells. The understanding of the role of iron is exciting new information.
Dr. Joanna Collingwood, Associate Professor at the University of Warwick's School of Engineering commented: "Iron is an essential element in the brain, so it is critical to understand how its management is affected in Alzheimer's disease." She further noted that this new finding opens the door to possible new treatments of AD by the use of iron modifying drugs.
Dr. Collingwood was part of an international team that included researchers from University of Florida and The University of Texas at San Antonio.
Monday, April 16, 2018
Cognitine Reserve
What is Cognitive Reserve?
The concept or theory of Cognitive Reserve (CR) began circulating in the 1980s.
CR, which sometimes may be referred to as brain reserve, is a concept that some damaged brains are resistant to conditions such as Alzheimer's or dementia. CR is an explanation of why people whose brains have Alzheimier's like structural damage do not get Alzheimer's.
People with a higher CR (often measured as a great number of years of formal education) have been found to be less susceptible to cognitive decline than people with similar brain pathology but with a lower CR. One can think of CR as a protective reserve that may limit or delay mental changes seen in Alzheimer's or dementia.
How Can Cognitive Reserve Be Developed?
Research models have demonstrated that intellectual enrichment is key factor in building CR. This can be achieved by continued and prolonged brain stimulation. There is objective evidence that years of higher education, or even being bi or multi-lingual, leads to higher levels of CR.
People with extensive brain pathology have better mental functioning if they have CR compared to people with similar brains but little to no CR.
Most interestingly, recent studies such as one conducted by Ozioma Okonkwo et.al. of the University of Wisconsin in Madison, suggest that CR itself may very well prevent brain pathology from forming. This is a new exciting paradigm that bears watching.
It should be noted that other factors associated with a college education, such as socioeconomic status, social interactions, and cognitive stimulation throughout life, all can play a role in beefing up the brain’s defenses, Okonkwo said. He also pointed out that other interconnecting factors include occupational attainment, exposure to toxins, physical activity and other health issues such as diabetes, obesity, and cardiovascular disease.
Not surprisingly, it should also be noted that these studies, like many other studies regarding Alzheimer's, are suggestive and not conclusive. Yet as in many studies, it does offer hope, which is always a positive thing.
The concept or theory of Cognitive Reserve (CR) began circulating in the 1980s.
CR, which sometimes may be referred to as brain reserve, is a concept that some damaged brains are resistant to conditions such as Alzheimer's or dementia. CR is an explanation of why people whose brains have Alzheimier's like structural damage do not get Alzheimer's.
People with a higher CR (often measured as a great number of years of formal education) have been found to be less susceptible to cognitive decline than people with similar brain pathology but with a lower CR. One can think of CR as a protective reserve that may limit or delay mental changes seen in Alzheimer's or dementia.
How Can Cognitive Reserve Be Developed?
Research models have demonstrated that intellectual enrichment is key factor in building CR. This can be achieved by continued and prolonged brain stimulation. There is objective evidence that years of higher education, or even being bi or multi-lingual, leads to higher levels of CR.
People with extensive brain pathology have better mental functioning if they have CR compared to people with similar brains but little to no CR.
Most interestingly, recent studies such as one conducted by Ozioma Okonkwo et.al. of the University of Wisconsin in Madison, suggest that CR itself may very well prevent brain pathology from forming. This is a new exciting paradigm that bears watching.
It should be noted that other factors associated with a college education, such as socioeconomic status, social interactions, and cognitive stimulation throughout life, all can play a role in beefing up the brain’s defenses, Okonkwo said. He also pointed out that other interconnecting factors include occupational attainment, exposure to toxins, physical activity and other health issues such as diabetes, obesity, and cardiovascular disease.
Not surprisingly, it should also be noted that these studies, like many other studies regarding Alzheimer's, are suggestive and not conclusive. Yet as in many studies, it does offer hope, which is always a positive thing.
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