This entire dietary thing needs more study on my part. I`ll read the links you and Dr.Scally posted and get back to you soon. Whats MCT oil? If there is any way that I might be able to help, just say it.
MESO-Rx
Anabolic Steroids
Alzheimer’s
- Thread starter Michael Scally MD
- Start date
This entire dietary thing needs more study on my part. I`ll read the links you and Dr.Scally posted and get back to you soon. Whats MCT oil? If there is any way that I might be able to help, just say it.
MCT = Medium Chain Triglycerides. The liver converts them to ketones. Coconut oil contains MCTs and I happened to have some to get my mother started on it. Pure MCT oil is available through nutrition/vitamin stores.
That's a deal, my friend. You've already helped; I didnt know about Aricept. I'll keep you posted.
I'll be happy to help you with any issues/concerns re the high fat diet. We're doing that with my mom too. No issues so far. Dad (age 80) has already been on it and had the same improvements in lipids I did...he stopped taking a statin.
Last edited:
Yes iI see what youre talking about re MCT and coconut oil.
Medium-chain triglycerides - Wikipedia, the free encyclopedia
[ame="http://en.wikipedia.org/wiki/Caprylic_acid"]Caprylic acid - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/File:Caprylic_acid.svg" class="image" title="Skeletal formula"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/d/d2/Caprylic_acid.svg/210px-Caprylic_acid.svg.png"@@AMEPARAM@@commons/thumb/d/d2/Caprylic_acid.svg/210px-Caprylic_acid.svg.png[/ame]
I think caprillic acid is the main component of an Rx AD treatment dietary supp[lement. Dont recall its name and cost an arm and leg (of course).
Effect of MCI in AD patients:
Effects of beta-hydroxybutyrate on cognition in me... [Neurobiol Aging. 2004] - PubMed result
Hypometabolism as a therapeutic target in Alzheime... [BMC Neurosci. 2008] - PubMed result
The Rx MCI dietary supplement:
Axona - A Heathier State of Mind
http://www.coconutresearchcenter.org/
"MCFA are very different from LCFA. They do not have a negative effect on cholesterol and help to protect against heart disease. MCFA help to lower the risk of both atherosclerosis and heart disease. It is primarily due to the MCFA in coconut oil that makes it so special and so beneficial."
http://www.coconutresearchcenter.org/ketone-bodies-as-a-theraputic.htm
MCI (ac1202) Clinical trials database
http://www.clinicaltrialssearch.org/13847-ketasyn-ac-1202-clinical-trials.html
Last edited:
And finally:
More research:
http://www.coconutresearchcenter.org/coconut-research.htm#Cardiovascular Health
http://www.coconutresearchcenter.org/coconut-research.htm#Epilepsy, Alzheimer’s, and other Neurological Disorders
Im convinced of its effectiveness in both AD and vascular sclerosis.
You mentioned that you were waiting on arrival of a more effective MCT than coconut oil?
Gotta link?????
In conclusion;
apparently you dont need to drive the body into wholesale ketone body metabolism ( strong carb restrictions) for MCI to have an effect on brain feeding, for lack of a better term. MCIs are converted into ketone bodies in the liver and become available for starving neuron within hours or less.
I have great hope for this and will implement action asap.
IN addition the brain is also able to metabolize lactose, found in high concentrations in milk. Milkfat is highly saturated and consists of LCTs (not good- for CAD but studies are inconclusive). skim milk 3xd for now.
Gimme your thoughts LW64 ( and anyone else who has something relevant)
More research:
http://www.coconutresearchcenter.org/coconut-research.htm#Cardiovascular Health
http://www.coconutresearchcenter.org/coconut-research.htm#Epilepsy, Alzheimer’s, and other Neurological Disorders
Im convinced of its effectiveness in both AD and vascular sclerosis.
You mentioned that you were waiting on arrival of a more effective MCT than coconut oil?
Gotta link?????
In conclusion;
apparently you dont need to drive the body into wholesale ketone body metabolism ( strong carb restrictions) for MCI to have an effect on brain feeding, for lack of a better term. MCIs are converted into ketone bodies in the liver and become available for starving neuron within hours or less.
I have great hope for this and will implement action asap.
IN addition the brain is also able to metabolize lactose, found in high concentrations in milk. Milkfat is highly saturated and consists of LCTs (not good- for CAD but studies are inconclusive). skim milk 3xd for now.
Gimme your thoughts LW64 ( and anyone else who has something relevant)
I ordered MCT Oil from Swanson:
http://www.swansonvitamins.com/NWF331/ItemDetail?n=0
AFAIK, you're right about there being no need to go into ketosis. Stick with the coconut oil for now. We're doing the same. This is a tough disease to deal with so we're going into this with no expectations.
Unless you're putting her on a low carb diet, I would stick with low-fat milk.
http://www.swansonvitamins.com/NWF331/ItemDetail?n=0
AFAIK, you're right about there being no need to go into ketosis. Stick with the coconut oil for now. We're doing the same. This is a tough disease to deal with so we're going into this with no expectations.
Unless you're putting her on a low carb diet, I would stick with low-fat milk.
I am quite optomistic about this, considering her Hx space cadet syndrome as mentioned somewhere.
Why low fat milk? there is a lot of research re the lack of detrimental effects of milkfat. thats right up your alley.
Thats a hellofa price on the C8,10 MCTs.
It is obvious that the AMA standard procedure is inadequate to deal with the problem in a timely manner in our case.
How much control of the situation are you intending to take?
ZKT, if you don't mind, how old is your wife that she is suffering from alzheimers? Is she taking any other drugs that may be causing memory loss issues?
I trust biochemistry a lot more than epi/cohort-studies. Fat plus protein plus small amounts of carbs is much better than fat plus protein plus a lot of carbs re the resulting insulin response. Chronically elevated insulin is clearly related to this condition. Insulin degrading enzyme (IDE) clears amyloid plaques but if insulin is always high the IDE will preferentially interact with insulin and leave the plaques alone...
I liked your MCT Oil choice better! I'm ordering that too! You've been a GREAT help, zkt!:tiphat
My father and I are being proactive with this. He knew about aricept and she didnt take it because of interactions with other meds.
Last edited:
She is 66. Not is hasnt gone that far yet. Progressive short term memory loss and MCI. Have ruled out meds as causative. Family Hx of AD.
Thanks. That makes sense.
What drugs and interactions specifically, if you dont mind my asking?
Ageing is considered to be the manifestation of stochastic damage to cells that accumulates over many years. The generation of reactive oxidative species (ROS), which are a product of respiration, is believed to contribute substantially to the ageing process. ROS are produced as unwanted by-products in electron transport during oxidative phosphorylation. Despite the presence of endogenous antioxidants, a significant portion of ROS go unsequestered in mitochondria, and eventually damage macromolecules such as membrane phospholipids, proteins, DNA, and RNA, rendering them impaired or entirely dysfunctional. Furthermore, accumulating ROS within the mitochondria can trigger apoptosis through the release of cytochrome c into the cytoplasm. Over time, biological tissue succumbs to ROS-mediated damage; ageing is therefore traditionally viewed as a disorganised and inevitable process.
Alzheimer’s disease is an age-related neurodegenerative condition that affects 35 million people worldwide, and is the leading cause of dementia among the elderly. Specifically, the incidence of Alzheimer’s disease is 15% among those 65 years and older, and is close to 50% for those aged over 85 years. The strong correlation between Alzheimer’s disease and age is suggested by some similarities in phenotypes of the two conditions. Most notably, normal ageing involves the gradual decline in memory and cognitive functions that are associated with neuronal networks of the mediotemporal lobe. The neurons of the parahippocampal region and hippocampal formation are particularly affected in the normally aged brain, and it is precisely these regions that are first affected in Alzheimer’s disease. Moreover, Alzheimer’s disease might be largely the result of years of accumulated oxidative damage and mitochondrial malfunction and, as stated above, ageing involves similar perturbations.
Calorie restriction (a dietary regimen that involves reducing caloric intake to about 30–40% of normal intake) has provided an interesting glimpse into the mechanisms that regulate ageing. Animals that undergo calorie restriction, including yeast, Caenorhabditis elegans, Drosophila melanogaster, and mice, have extended lifespans and reduced morbidity with ageing. These benefits have been shown to be partly mediated by a family of NAD+-dependent histone deacetylases, called the sirtuins. Furthermore, the correlation between ageing and neurodegeneration has led researchers to investigate the sirtuin pathway as it pertains to Alzheimer’s disease, and these data have yielded exciting insights. In particular, recent reports show that SIRT1 hyperactivity might be able to reduce Alzheimer’s disease pathology both in vitro and in vivo through the upregulation of the ADAM10 gene. In this Rapid Review, they discuss these results and their implications for the treatment of Alzheimer’s disease.
Bonda DJ, Lee HG, Camins A, et al. The sirtuin pathway in ageing and Alzheimer disease: mechanistic and therapeutic considerations. Lancet Neurol 2011;10(3):275-9. The sirtuin pathway in ageing and Alzheimer diseas... [Lancet Neurol. 2011] - PubMed result
BACKGROUND: Advances in gerontology have yielded crucial insights into the molecular and biochemical aspects of the ageing process. The sirtuin pathway, which is most notable for its association with the anti-ageing effects of calorie restriction, has received particular attention, and pharmacological or transgenic upregulation of the sirtuin pathway has shown promising results in laboratory models of ageing. Alzheimer's disease is a neurodegenerative disease that is imposing an increasing burden on society, and is the leading cause of senile dementia worldwide. The lack of therapies for Alzheimer's disease provides a strong incentive for the development of an effective treatment strategy and, interestingly, research has uncovered a mechanism of action of the sirtuin pathway that might have therapeutic potential for Alzheimer's disease.
RECENT DEVELOPMENTS: SIRT1, one of the seven mammalian proteins of the sirtuin family of NAD(+)-dependent deacetylases, has recently been shown to attenuate amyloidogenic processing of amyloid-beta protein precursor (APP) in cell culture studies in vitro and in transgenic mouse models of Alzheimer's disease. Mechanistically, SIRT1 increases alpha-secretase production and activity through activation of the alpha-secretase gene ADAM10. Because alpha-secretase is the enzyme responsible for the non-amyloidogenic cleavage of APP, upregulation of alpha-secretase shifts APP processing to reduce the pathological accumulation of the presumptive toxic Abeta species that results from beta-secretase and gamma-secretase activity. Interestingly, the spatial patterns of Abeta deposition in the brain might correlate with increased aerobic glycolysis in those regions. Because aerobic glycolysis depletes cellular levels of NAD(+) (through a decreased NAD(+)/NADH ratio), it is possible that a corresponding downregulation of the NAD(+)-dependent sirtuin pathway contributes to the amyloidogenic processing of APP.
WHERE NEXT?: The specific inhibition of Abeta generation by SIRT1 coupled with the potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtuin pathway has translational implications. On the one hand, the possible underlying role of the sirtuin pathway in Alzheimer's disease onset and development might increase our understanding of this devastating condition. On the other hand, therapeutic upregulation of SIRT1 might provide opportunities for the amelioration of Alzheimer's-disease-type neuropathology through inhibition of amyloidogenesis. Ultimately, further analysis into both aspects is necessary if any progress is to be made.
Alzheimer’s disease is an age-related neurodegenerative condition that affects 35 million people worldwide, and is the leading cause of dementia among the elderly. Specifically, the incidence of Alzheimer’s disease is 15% among those 65 years and older, and is close to 50% for those aged over 85 years. The strong correlation between Alzheimer’s disease and age is suggested by some similarities in phenotypes of the two conditions. Most notably, normal ageing involves the gradual decline in memory and cognitive functions that are associated with neuronal networks of the mediotemporal lobe. The neurons of the parahippocampal region and hippocampal formation are particularly affected in the normally aged brain, and it is precisely these regions that are first affected in Alzheimer’s disease. Moreover, Alzheimer’s disease might be largely the result of years of accumulated oxidative damage and mitochondrial malfunction and, as stated above, ageing involves similar perturbations.
Calorie restriction (a dietary regimen that involves reducing caloric intake to about 30–40% of normal intake) has provided an interesting glimpse into the mechanisms that regulate ageing. Animals that undergo calorie restriction, including yeast, Caenorhabditis elegans, Drosophila melanogaster, and mice, have extended lifespans and reduced morbidity with ageing. These benefits have been shown to be partly mediated by a family of NAD+-dependent histone deacetylases, called the sirtuins. Furthermore, the correlation between ageing and neurodegeneration has led researchers to investigate the sirtuin pathway as it pertains to Alzheimer’s disease, and these data have yielded exciting insights. In particular, recent reports show that SIRT1 hyperactivity might be able to reduce Alzheimer’s disease pathology both in vitro and in vivo through the upregulation of the ADAM10 gene. In this Rapid Review, they discuss these results and their implications for the treatment of Alzheimer’s disease.
Bonda DJ, Lee HG, Camins A, et al. The sirtuin pathway in ageing and Alzheimer disease: mechanistic and therapeutic considerations. Lancet Neurol 2011;10(3):275-9. The sirtuin pathway in ageing and Alzheimer diseas... [Lancet Neurol. 2011] - PubMed result
BACKGROUND: Advances in gerontology have yielded crucial insights into the molecular and biochemical aspects of the ageing process. The sirtuin pathway, which is most notable for its association with the anti-ageing effects of calorie restriction, has received particular attention, and pharmacological or transgenic upregulation of the sirtuin pathway has shown promising results in laboratory models of ageing. Alzheimer's disease is a neurodegenerative disease that is imposing an increasing burden on society, and is the leading cause of senile dementia worldwide. The lack of therapies for Alzheimer's disease provides a strong incentive for the development of an effective treatment strategy and, interestingly, research has uncovered a mechanism of action of the sirtuin pathway that might have therapeutic potential for Alzheimer's disease.
RECENT DEVELOPMENTS: SIRT1, one of the seven mammalian proteins of the sirtuin family of NAD(+)-dependent deacetylases, has recently been shown to attenuate amyloidogenic processing of amyloid-beta protein precursor (APP) in cell culture studies in vitro and in transgenic mouse models of Alzheimer's disease. Mechanistically, SIRT1 increases alpha-secretase production and activity through activation of the alpha-secretase gene ADAM10. Because alpha-secretase is the enzyme responsible for the non-amyloidogenic cleavage of APP, upregulation of alpha-secretase shifts APP processing to reduce the pathological accumulation of the presumptive toxic Abeta species that results from beta-secretase and gamma-secretase activity. Interestingly, the spatial patterns of Abeta deposition in the brain might correlate with increased aerobic glycolysis in those regions. Because aerobic glycolysis depletes cellular levels of NAD(+) (through a decreased NAD(+)/NADH ratio), it is possible that a corresponding downregulation of the NAD(+)-dependent sirtuin pathway contributes to the amyloidogenic processing of APP.
WHERE NEXT?: The specific inhibition of Abeta generation by SIRT1 coupled with the potential link between aerobic glycolysis, NAD(+) depletion, and amyloidogenesis through the sirtuin pathway has translational implications. On the one hand, the possible underlying role of the sirtuin pathway in Alzheimer's disease onset and development might increase our understanding of this devastating condition. On the other hand, therapeutic upregulation of SIRT1 might provide opportunities for the amelioration of Alzheimer's-disease-type neuropathology through inhibition of amyloidogenesis. Ultimately, further analysis into both aspects is necessary if any progress is to be made.
Alzheimer's Disease May Be Passed Down From Ailing Mothers, Study Suggests
Alzheimer's Disease May Be Passed Down From Ailing Mothers, Study Suggests - Bloomberg
By Nicole Ostrow - Feb 28, 2011
Mothers may be more likely to pass down Alzheimer’s disease to their children than fathers, a finding that may help identify patients earlier, researchers from the University of Kansas School of Medicine said.
Healthy older adults with no cognitive problems whose mothers had Alzheimer’s disease had more brain shrinkage than those who had a father or no parent with the disease, according to research published today in the journal Neurology.
About 5.3 million Americans have Alzheimer’s disease and the number may increase to as much as 16 million by 2050, according to the Alzheimer’s Association. Age and family history are the two biggest risk factors for developing the disease, the researchers said. Today’s study provides more details on the biology behind the disease, study author Jeffrey Burns said.
“Our data is another piece to this puzzle that suggests that maternal inheritance is more important than paternal,” said Burns, director of the Alzheimer and Memory Program at the University of Kansas Medical Center in Kansas City, in a Feb. 25 telephone interview. “It appears that maternal factors might be imparting some risk that we don’t see coming from paternal or lack of family history.”
Researchers analyzed 53 people ages 60 and older who had no signs of dementia. Of those, 11 had mothers with the disease and 10 had fathers with the condition. They then were given brain scans and cognitive tests over the two-year study.
Study Results
The brain’s gray matter, which is part of nerve cells responsible for processing signals, shrank twice as much over the two years in study participants who reported their mothers had Alzheimer’s compared with those who had a father with the disease or no family history of the illness, the researchers said. Those whose mothers had the condition also saw the size of their brains decrease more than those whose fathers had the disease, according to the researchers.
Brain atrophy, or shrinkage of the brain, occurs in Alzheimer’s disease, the researchers said.
Whether those in the study will develop Alzheimer’s disease remains to be seen, Burns said. The researchers are continuing to follow the participants. Also, larger studies are needed to replicate these findings, he said.
People whose mothers have Alzheimer’s shouldn’t panic after reading these results, said Marc L. Gordon, a neurologist and Alzheimer’s researcher at the Feinstein Institute for Medical Research in Manhasset, New York.
“It’s very important to recognize a risk factor is not the same thing as being absolutely certain someone will get the disease,” Gordon, who wasn’t an author on today’s paper, said in a Feb. 25 telephone interview. “It’s an increased risk but it doesn’t mean you will certainly get this.”
Honea RA, Swerdlow RH, Vidoni ED, Burns JM. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease. Neurology 2011;76(9):822-9. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease
Objective: Beyond age, having a family history is the most significant risk factor for Alzheimer disease (AD). This longitudinal brain imaging study examines whether there are differential patterns of regional gray matter atrophy in cognitively healthy elderly subjects with (FH+) and without (FH?) a family history of late-onset AD.
Methods: As part of the KU Brain Aging Project, cognitively intact individuals with a maternal history (FHm, n = 11), paternal history (FHp, n = 10), or no parental history of AD (FH?, n = 32) similar in age, gender, education, and Mini-Mental State Examination (MMSE) score received MRI at baseline and 2-year follow-up. A custom voxel-based morphometry processing stream was used to examine regional differences in atrophy between FH groups, controlling for age, gender, and APOE ?4 (APOE4) status. We also analyzed APOE4-related atrophy.
Results: Cognitively normal FH+ individuals had significantly increased whole-brain gray matter atrophy and CSF expansion compared to FH?. When FH+ groups were split, only FHm was associated with longitudinal measures of brain change. Moreover, our voxel-based analysis revealed that FHm subjects had significantly greater atrophy in the precuneus and parahippocampus/hippocampus regions compared to FH? and FHp subjects, independent of APOE4 status, gender, and age. Individuals with an ?4 allele had more regional atrophy in the frontal cortex compared to ?4 noncarriers.
Conclusions: We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus. These data complement and extend reports of regional cerebral metabolic differences and increases in amyloid-? burden in FHm subjects, which may be related to a higher risk for developing AD.
Alzheimer's Disease May Be Passed Down From Ailing Mothers, Study Suggests - Bloomberg
By Nicole Ostrow - Feb 28, 2011
Mothers may be more likely to pass down Alzheimer’s disease to their children than fathers, a finding that may help identify patients earlier, researchers from the University of Kansas School of Medicine said.
Healthy older adults with no cognitive problems whose mothers had Alzheimer’s disease had more brain shrinkage than those who had a father or no parent with the disease, according to research published today in the journal Neurology.
About 5.3 million Americans have Alzheimer’s disease and the number may increase to as much as 16 million by 2050, according to the Alzheimer’s Association. Age and family history are the two biggest risk factors for developing the disease, the researchers said. Today’s study provides more details on the biology behind the disease, study author Jeffrey Burns said.
“Our data is another piece to this puzzle that suggests that maternal inheritance is more important than paternal,” said Burns, director of the Alzheimer and Memory Program at the University of Kansas Medical Center in Kansas City, in a Feb. 25 telephone interview. “It appears that maternal factors might be imparting some risk that we don’t see coming from paternal or lack of family history.”
Researchers analyzed 53 people ages 60 and older who had no signs of dementia. Of those, 11 had mothers with the disease and 10 had fathers with the condition. They then were given brain scans and cognitive tests over the two-year study.
Study Results
The brain’s gray matter, which is part of nerve cells responsible for processing signals, shrank twice as much over the two years in study participants who reported their mothers had Alzheimer’s compared with those who had a father with the disease or no family history of the illness, the researchers said. Those whose mothers had the condition also saw the size of their brains decrease more than those whose fathers had the disease, according to the researchers.
Brain atrophy, or shrinkage of the brain, occurs in Alzheimer’s disease, the researchers said.
Whether those in the study will develop Alzheimer’s disease remains to be seen, Burns said. The researchers are continuing to follow the participants. Also, larger studies are needed to replicate these findings, he said.
People whose mothers have Alzheimer’s shouldn’t panic after reading these results, said Marc L. Gordon, a neurologist and Alzheimer’s researcher at the Feinstein Institute for Medical Research in Manhasset, New York.
“It’s very important to recognize a risk factor is not the same thing as being absolutely certain someone will get the disease,” Gordon, who wasn’t an author on today’s paper, said in a Feb. 25 telephone interview. “It’s an increased risk but it doesn’t mean you will certainly get this.”
Honea RA, Swerdlow RH, Vidoni ED, Burns JM. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease. Neurology 2011;76(9):822-9. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease
Objective: Beyond age, having a family history is the most significant risk factor for Alzheimer disease (AD). This longitudinal brain imaging study examines whether there are differential patterns of regional gray matter atrophy in cognitively healthy elderly subjects with (FH+) and without (FH?) a family history of late-onset AD.
Methods: As part of the KU Brain Aging Project, cognitively intact individuals with a maternal history (FHm, n = 11), paternal history (FHp, n = 10), or no parental history of AD (FH?, n = 32) similar in age, gender, education, and Mini-Mental State Examination (MMSE) score received MRI at baseline and 2-year follow-up. A custom voxel-based morphometry processing stream was used to examine regional differences in atrophy between FH groups, controlling for age, gender, and APOE ?4 (APOE4) status. We also analyzed APOE4-related atrophy.
Results: Cognitively normal FH+ individuals had significantly increased whole-brain gray matter atrophy and CSF expansion compared to FH?. When FH+ groups were split, only FHm was associated with longitudinal measures of brain change. Moreover, our voxel-based analysis revealed that FHm subjects had significantly greater atrophy in the precuneus and parahippocampus/hippocampus regions compared to FH? and FHp subjects, independent of APOE4 status, gender, and age. Individuals with an ?4 allele had more regional atrophy in the frontal cortex compared to ?4 noncarriers.
Conclusions: We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus. These data complement and extend reports of regional cerebral metabolic differences and increases in amyloid-? burden in FHm subjects, which may be related to a higher risk for developing AD.
When I read about activating SIRT1, the first thing I think of is resveratrol...
@zkt...still following up on meds...I dont see interactions with what I know shes taking...
@zkt...still following up on meds...I dont see interactions with what I know shes taking...
Last edited:
Maternal History Of Alzheimer Disease
Late-onset Alzheimer disease (AD) is a neurodegenerative disease caused by complex genetic and environmental mechanisms. Age is the most significant risk factor for developing AD, followed by a family history of AD, with maternal transmission significantly more frequent than paternal transmission. First-degree relatives of individuals with AD are at a 4- to 10-fold higher risk for AD compared to individuals with no family history. Since it is unknown how familial transmission of AD biologically increases susceptibility for AD, clarifying mechanisms of familial risk for AD are a step toward developing enhanced treatment and prevention strategies.
Various forms of neuroimaging have attempted to characterize genetic and familial risk factors for late-onset AD by studying heritable traits in healthy individuals with no cognitive impairment. There are several studies showing that individuals without dementia who are offspring of AD-affected mothers may have changes in memory performance, reductions in brain glucose metabolism in parietotemporal cortices and posterior cingulate, and increased A-beta load primarily in the frontal cortex, posterior cingulate, and precuneus. At cross-section, we found that cognitively normal individuals with a maternal history (FHm) of late-onset AD had reduced gray matter volume in AD-related brain regions compared to those with a paternal (FHp) or a negative family history (FH-) of AD. However, no studies have yet assessed if there is progressive atrophy over several years in individuals with a family history of AD.
Recently, 3-dimensional-mapping methods have been developed to characterize spatial patterns of atrophy as a biomarker for studying disease progression due to their ability to predict conversion from mild cognitive impairment (MCI) to AD. Researchers used an optimized voxel-based 3-dimensional longitudinal analysis method to identify brain atrophy in the absence of significant clinical progression over 2 years in individuals with risk for AD due to a first-degree family member with AD.
Honea RA, Swerdlow RH, Vidoni ED, Burns JM. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease. Neurology 2011;76(9):822-9. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease
Objective: Beyond age, having a family history is the most significant risk factor for Alzheimer disease (AD). This longitudinal brain imaging study examines whether there are differential patterns of regional gray matter atrophy in cognitively healthy elderly subjects with (FH+) and without (FH?) a family history of late-onset AD.
Methods: As part of the KU Brain Aging Project, cognitively intact individuals with a maternal history (FHm, n = 11), paternal history (FHp, n = 10), or no parental history of AD (FH?, n = 32) similar in age, gender, education, and Mini-Mental State Examination (MMSE) score received MRI at baseline and 2-year follow-up. A custom voxel-based morphometry processing stream was used to examine regional differences in atrophy between FH groups, controlling for age, gender, and APOE ?4 (APOE4) status. We also analyzed APOE4-related atrophy.
Results: Cognitively normal FH+ individuals had significantly increased whole-brain gray matter atrophy and CSF expansion compared to FH?. When FH+ groups were split, only FHm was associated with longitudinal measures of brain change. Moreover, our voxel-based analysis revealed that FHm subjects had significantly greater atrophy in the precuneus and parahippocampus/hippocampus regions compared to FH? and FHp subjects, independent of APOE4 status, gender, and age. Individuals with an ?4 allele had more regional atrophy in the frontal cortex compared to ?4 noncarriers.
Conclusions: We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus. These data complement and extend reports of regional cerebral metabolic differences and increases in amyloid-? burden in FHm subjects, which may be related to a higher risk for developing AD.
Late-onset Alzheimer disease (AD) is a neurodegenerative disease caused by complex genetic and environmental mechanisms. Age is the most significant risk factor for developing AD, followed by a family history of AD, with maternal transmission significantly more frequent than paternal transmission. First-degree relatives of individuals with AD are at a 4- to 10-fold higher risk for AD compared to individuals with no family history. Since it is unknown how familial transmission of AD biologically increases susceptibility for AD, clarifying mechanisms of familial risk for AD are a step toward developing enhanced treatment and prevention strategies.
Various forms of neuroimaging have attempted to characterize genetic and familial risk factors for late-onset AD by studying heritable traits in healthy individuals with no cognitive impairment. There are several studies showing that individuals without dementia who are offspring of AD-affected mothers may have changes in memory performance, reductions in brain glucose metabolism in parietotemporal cortices and posterior cingulate, and increased A-beta load primarily in the frontal cortex, posterior cingulate, and precuneus. At cross-section, we found that cognitively normal individuals with a maternal history (FHm) of late-onset AD had reduced gray matter volume in AD-related brain regions compared to those with a paternal (FHp) or a negative family history (FH-) of AD. However, no studies have yet assessed if there is progressive atrophy over several years in individuals with a family history of AD.
Recently, 3-dimensional-mapping methods have been developed to characterize spatial patterns of atrophy as a biomarker for studying disease progression due to their ability to predict conversion from mild cognitive impairment (MCI) to AD. Researchers used an optimized voxel-based 3-dimensional longitudinal analysis method to identify brain atrophy in the absence of significant clinical progression over 2 years in individuals with risk for AD due to a first-degree family member with AD.
Honea RA, Swerdlow RH, Vidoni ED, Burns JM. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease. Neurology 2011;76(9):822-9. Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease
Objective: Beyond age, having a family history is the most significant risk factor for Alzheimer disease (AD). This longitudinal brain imaging study examines whether there are differential patterns of regional gray matter atrophy in cognitively healthy elderly subjects with (FH+) and without (FH?) a family history of late-onset AD.
Methods: As part of the KU Brain Aging Project, cognitively intact individuals with a maternal history (FHm, n = 11), paternal history (FHp, n = 10), or no parental history of AD (FH?, n = 32) similar in age, gender, education, and Mini-Mental State Examination (MMSE) score received MRI at baseline and 2-year follow-up. A custom voxel-based morphometry processing stream was used to examine regional differences in atrophy between FH groups, controlling for age, gender, and APOE ?4 (APOE4) status. We also analyzed APOE4-related atrophy.
Results: Cognitively normal FH+ individuals had significantly increased whole-brain gray matter atrophy and CSF expansion compared to FH?. When FH+ groups were split, only FHm was associated with longitudinal measures of brain change. Moreover, our voxel-based analysis revealed that FHm subjects had significantly greater atrophy in the precuneus and parahippocampus/hippocampus regions compared to FH? and FHp subjects, independent of APOE4 status, gender, and age. Individuals with an ?4 allele had more regional atrophy in the frontal cortex compared to ?4 noncarriers.
Conclusions: We conclude that FHm individuals without dementia have progressive gray matter volume reductions in select AD-vulnerable brain regions, specifically the precuneus and parahippocampal gyrus. These data complement and extend reports of regional cerebral metabolic differences and increases in amyloid-? burden in FHm subjects, which may be related to a higher risk for developing AD.
I found this story of an AD patient who used Axona.
Axona, a 'medical food,' is tried by an Alzheimer's patient: Healthy Cleveland | cleveland.com
Axona, a 'medical food,' is tried by an Alzheimer's patient: Healthy Cleveland | cleveland.com
There you go !
Have you researched the doseage of the MCT (caprillic, capric acids only) oil as compared to Axona or the other Rx products? The shipment should arrive today.
There you go !
Have you researched the doseage of the MCT (caprillic, capric acids only) oil as compared to Axona or the other Rx products? The shipment should arrive today.
Yup.
Axona, MCT & Coconut Oil: Differences & Benefits | Dementia & Alzheimer's Weekly
The MCT oil should arrive today as well. She just went back to coconut oil (we ran out after she was on it for only three days and my father thought it perked her up a bit), so maybe this Saturday we'll start the MCT Oil.
Similar threads
