Foods to Eat on the MIND Diet
Green leafy vegetables (kale, spinach, collard greens, lettuce): a minimum of 6 servings a week
Nuts (almonds, cashews, pistachios): a minimum of 5 servings a week
Berries (strawberries, blueberries, raspberries, blackberries): a minimum of 2 servings a week
Beans (black beans, pinto beans, kidney beans): a minimum of 3 servings a week
Whole grains (quinoa, oatmeal, brown rice, whole-grain pasta and bread): a minimum of 3 servings a day (5)
Fish (salmon, tuna, trout): at least 1 serving a week.
Poultry (chicken, turkey): at least twice a week
Olive oil as the primary oil used.
Wine: no more than 1 glass a day
Foods to Limit on the MIND Diet
Red meat (steak, ground beef, pork, lamb): no more than 4 servings a week
Butter and margarine: no more than 1 tablespoon daily
Cheese (brie, mozzarella, or cheddar): no more than 1 serving a week.
Sweets (cakes, brownies, ice cream): no more than 5 servings a week
Fried or fast food (french fries, chicken nuggets, onion rings, fried chicken, hamburgers): no more than 1 serving a week.
Sleeping pill reduces levels of Alzheimer’s proteins:
Sleep disturbances can be an early sign of Alzheimer’s disease. Many people eventually diagnosed with Alzheimer’s start having trouble falling and staying asleep years before cognitive problems such as memory loss and confusion emerge. It’s a vicious cycle: Alzheimer’s disease involves changes to the brain that disrupt sleep, and poor sleep accelerates harmful changes to the brain.
Researchers at Washington University School of Medicine in St. Louis have identified a possible way to help break that cycle. A small, two-night study has shown that people who took a sleeping pill before bed experienced a drop in the levels of key Alzheimer’s proteins — a good sign, since higher levels of such proteins tracks with worsening disease. The study, which involved a sleeping aid known as suvorexant that is already approved by the Food and Drug Administration (FDA) for insomnia, hints at the potential of sleep medications to slow or stop the progression of Alzheimer’s disease, although much more work is needed to confirm the viability of such an approach.
As a first step to assess the effect of orexin inhibitors on people, Lucey and colleagues recruited 38 participants ages 45 to 65 and with no cognitive impairments to undergo a two-night sleep study. The participants were given a lower dose (10 mg) of suvorexant (13 people), a higher dose (20 mg) of suvorexant (12 people) or a placebo (13 people) at 9 p.m. and then went to sleep in a clinical research unit at Washington University. Researchers withdrew a small amount of cerebrospinal fluid via spinal tap every two hours for 36 hours, starting one hour before the sleeping aid or placebo was administered, to measure how amyloid and tau levels changed over the next day and a half.
In the cerebrospinal fluid of people who had received the high dose of suvorexant, amyloid levels dropped 10% to 20% and levels of a key form of tau known as hyperphosphorylated tau dropped 10% to 15%, compared to people who had received placebo. Both differences are statistically significant. There was not a significant difference between the people who received a low dose of suvorexant and those who received the placebo.
The study is preliminary, since it only looked at the effect of two doses of the drug in a small group of participants. Lucey has studies underway to assess the longer-term effects of orexin inhibitors in people at higher risk of dementia.
“Future studies need to have people taking these drugs for months, at least, and measuring the effect on amyloid and tau over time,” Lucey said. “We’re also going to be studying participants who are older and may still be cognitively healthy, but who already have some amyloid plaques in their brains. This study involved healthy middle-aged participants; the results may be different in an older population.
LINK - https://medicine.wustl.edu/news/sleeping-pill-reduces-levels-of-alzheimers-proteins/
Green leafy vegetables (kale, spinach, collard greens, lettuce): a minimum of 6 servings a week
Nuts (almonds, cashews, pistachios): a minimum of 5 servings a week
Berries (strawberries, blueberries, raspberries, blackberries): a minimum of 2 servings a week
Beans (black beans, pinto beans, kidney beans): a minimum of 3 servings a week
Whole grains (quinoa, oatmeal, brown rice, whole-grain pasta and bread): a minimum of 3 servings a day (5)
Fish (salmon, tuna, trout): at least 1 serving a week.
Poultry (chicken, turkey): at least twice a week
Olive oil as the primary oil used.
Wine: no more than 1 glass a day
Foods to Limit on the MIND Diet
Red meat (steak, ground beef, pork, lamb): no more than 4 servings a week
Butter and margarine: no more than 1 tablespoon daily
Cheese (brie, mozzarella, or cheddar): no more than 1 serving a week.
Sweets (cakes, brownies, ice cream): no more than 5 servings a week
Fried or fast food (french fries, chicken nuggets, onion rings, fried chicken, hamburgers): no more than 1 serving a week.
Sleeping pill reduces levels of Alzheimer’s proteins:
Sleep disturbances can be an early sign of Alzheimer’s disease. Many people eventually diagnosed with Alzheimer’s start having trouble falling and staying asleep years before cognitive problems such as memory loss and confusion emerge. It’s a vicious cycle: Alzheimer’s disease involves changes to the brain that disrupt sleep, and poor sleep accelerates harmful changes to the brain.
Researchers at Washington University School of Medicine in St. Louis have identified a possible way to help break that cycle. A small, two-night study has shown that people who took a sleeping pill before bed experienced a drop in the levels of key Alzheimer’s proteins — a good sign, since higher levels of such proteins tracks with worsening disease. The study, which involved a sleeping aid known as suvorexant that is already approved by the Food and Drug Administration (FDA) for insomnia, hints at the potential of sleep medications to slow or stop the progression of Alzheimer’s disease, although much more work is needed to confirm the viability of such an approach.
As a first step to assess the effect of orexin inhibitors on people, Lucey and colleagues recruited 38 participants ages 45 to 65 and with no cognitive impairments to undergo a two-night sleep study. The participants were given a lower dose (10 mg) of suvorexant (13 people), a higher dose (20 mg) of suvorexant (12 people) or a placebo (13 people) at 9 p.m. and then went to sleep in a clinical research unit at Washington University. Researchers withdrew a small amount of cerebrospinal fluid via spinal tap every two hours for 36 hours, starting one hour before the sleeping aid or placebo was administered, to measure how amyloid and tau levels changed over the next day and a half.
In the cerebrospinal fluid of people who had received the high dose of suvorexant, amyloid levels dropped 10% to 20% and levels of a key form of tau known as hyperphosphorylated tau dropped 10% to 15%, compared to people who had received placebo. Both differences are statistically significant. There was not a significant difference between the people who received a low dose of suvorexant and those who received the placebo.
The study is preliminary, since it only looked at the effect of two doses of the drug in a small group of participants. Lucey has studies underway to assess the longer-term effects of orexin inhibitors in people at higher risk of dementia.
“Future studies need to have people taking these drugs for months, at least, and measuring the effect on amyloid and tau over time,” Lucey said. “We’re also going to be studying participants who are older and may still be cognitively healthy, but who already have some amyloid plaques in their brains. This study involved healthy middle-aged participants; the results may be different in an older population.
LINK - https://medicine.wustl.edu/news/sleeping-pill-reduces-levels-of-alzheimers-proteins/
Drinking coffee may reduce the risk of developing Alzheimer’s disease:
The study involved 227 adults aged 60 years or over, who did not have cognitive decline at the start of the study. The team used a questionnaire to gather information from the participants about the amount and frequency of coffee they consumed.
They then performed cognitive assessments using a selection of psychological measures at baseline and 18-month intervals. These assessments measured six cognitive areas: episodic recall memory, recognition memory, executive function, language, attention and processing speed, and the AIBL Preclinical Alzheimer Cognitive Composite (PACC).
Analysis of the data showed that habitual coffee drinking was positively associated with the cognitive areas of executive function, attention, and the PACC score. Drinking higher amounts of coffee was associated with slower cognitive decline in these areas over the course of the study.
Higher baseline coffee consumption was also linked to a slower accumulation of amyloid protein over the 126 months.
There did not seem to be a link between coffee intake and brain volume atrophy in this study.
The observed results suggest that increasing coffee intake from 1 to 2 cups per day could potentially reduce cognitive decline by up to 8% after 18 months. There could also be up to a 5% decrease in cerebral beta-amyloid accumulation over the same period.
Dr. Gardener told MNT, “[h]igher coffee intake was associated with slower accumulation of the sticky protein called beta-amyloid, which clumps together in the brains of those with Alzheimer’s disease.”
LINK - https://www.medicalnewstoday.com/articles/drinking-coffee-may-reduce-the-risk-of-developing-alzheimers-disease#Investigating-the-link
The study involved 227 adults aged 60 years or over, who did not have cognitive decline at the start of the study. The team used a questionnaire to gather information from the participants about the amount and frequency of coffee they consumed.
They then performed cognitive assessments using a selection of psychological measures at baseline and 18-month intervals. These assessments measured six cognitive areas: episodic recall memory, recognition memory, executive function, language, attention and processing speed, and the AIBL Preclinical Alzheimer Cognitive Composite (PACC).
Analysis of the data showed that habitual coffee drinking was positively associated with the cognitive areas of executive function, attention, and the PACC score. Drinking higher amounts of coffee was associated with slower cognitive decline in these areas over the course of the study.
Higher baseline coffee consumption was also linked to a slower accumulation of amyloid protein over the 126 months.
There did not seem to be a link between coffee intake and brain volume atrophy in this study.
The observed results suggest that increasing coffee intake from 1 to 2 cups per day could potentially reduce cognitive decline by up to 8% after 18 months. There could also be up to a 5% decrease in cerebral beta-amyloid accumulation over the same period.
Dr. Gardener told MNT, “[h]igher coffee intake was associated with slower accumulation of the sticky protein called beta-amyloid, which clumps together in the brains of those with Alzheimer’s disease.”
LINK - https://www.medicalnewstoday.com/articles/drinking-coffee-may-reduce-the-risk-of-developing-alzheimers-disease#Investigating-the-link
National Institute on Aging
What Do We Know About Diet and Prevention of Alzheimer’s Disease?
We don’t know for sure whether following a certain diet can help prevent Alzheimer’s dementia. Many studies are underway to see how food affects the aging brain.
Homotaurine – failed as Alzheimer’s drug, now used for memory protection:
Only 20% of the drugs that begin Phase I clinical trials ever get to market.1 The other 80%, despite the millions of dollars spent in research and development, are part of the cost of doing business for the pharmaceutical industry. One Canadian-based company is now taking the extraordinary step of trying to recoup this cost by marketing as a neutraceutical a drug that the Food and Drug Administration (FDA) refused to approve for marketing in the United States.2
OVOS Natural Health Inc., a subsidiary of Bellus Health Inc. (formerly known as Neurochem), has brought homotaurine, a modification of the amino acid taurine, to market under the trade name Vivimind. In clinical trials, this agent—studied for the treatment of Alzheimer’s disease (AD)—is also known as 3-amino-1-propane-sulfonic acid (3-APS), tramiprosate, and Alzhemed. Vivimind is currently being marketed in Canada and on the Internet to healthy baby boomers for memory protection. According to a representative from OVOS, Vivimind was to be accessible to U.S. residents in 2009 (OVOS Natural Health, personal communication, 2009 Jan 13). The following is a brief discussion on the history of this agent and a commentary on the decision to market it as a nutraceutical.
Link - https://academic.oup.com/ajhp/article-abstract/66/21/1950/5130452?redirectedFrom=fulltext
Apolipoprotein E (ApoE) genotype is the major genetic risk factor for late-onset AD. The APOE ε4 allele confers a 4- to 12-fold higher risk of AD and lowers the age of onset by ~10–15 years (15, 16). The ApoE ε4 allele may also play a role in early-onset AD, delaying the onset of symptoms (17), and in other neurodegenerative diseases, where APOE ε4 status is a risk factor for co-pathology and poor evolution (18). ApoE protein binds to soluble Aβ and affects aggregation, transport, and clearance of amyloid within the central nervous system (CNS), increasing Aβ oligomers in the brain, which would contribute to the loss of dendritic spines thus accelerating memory impairment and leading to earlier cognitive decline in AD (16, 19, 20).
Homotaurine (tramiprosate) :
Evidence Summary:
Although tramiprosate failed in a phase 3 clinical trial, a post-hoc analysis showed benefits in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Aging and related health concerns: N/A
Safety: Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
What is it?
Homotaurine (tramiprosate) was discovered in a screen for small molecules that inhibit amyloid beta aggregation. It is structurally similar to taurine except that it has an extra carbon. It was the first phase 3 study to test the ‘amyloid hypotheses. Although tramiprosate failed in phase 3 clinical trials, a subgroup analysis showed that it stabilized cognition in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients.
• One preclinical study.
Only 20% of the drugs that begin Phase I clinical trials ever get to market.1 The other 80%, despite the millions of dollars spent in research and development, are part of the cost of doing business for the pharmaceutical industry. One Canadian-based company is now taking the extraordinary step of trying to recoup this cost by marketing as a neutraceutical a drug that the Food and Drug Administration (FDA) refused to approve for marketing in the United States.2
OVOS Natural Health Inc., a subsidiary of Bellus Health Inc. (formerly known as Neurochem), has brought homotaurine, a modification of the amino acid taurine, to market under the trade name Vivimind. In clinical trials, this agent—studied for the treatment of Alzheimer’s disease (AD)—is also known as 3-amino-1-propane-sulfonic acid (3-APS), tramiprosate, and Alzhemed. Vivimind is currently being marketed in Canada and on the Internet to healthy baby boomers for memory protection. According to a representative from OVOS, Vivimind was to be accessible to U.S. residents in 2009 (OVOS Natural Health, personal communication, 2009 Jan 13). The following is a brief discussion on the history of this agent and a commentary on the decision to market it as a nutraceutical.
Link - https://academic.oup.com/ajhp/article-abstract/66/21/1950/5130452?redirectedFrom=fulltext
Apolipoprotein E (ApoE) genotype is the major genetic risk factor for late-onset AD. The APOE ε4 allele confers a 4- to 12-fold higher risk of AD and lowers the age of onset by ~10–15 years (15, 16). The ApoE ε4 allele may also play a role in early-onset AD, delaying the onset of symptoms (17), and in other neurodegenerative diseases, where APOE ε4 status is a risk factor for co-pathology and poor evolution (18). ApoE protein binds to soluble Aβ and affects aggregation, transport, and clearance of amyloid within the central nervous system (CNS), increasing Aβ oligomers in the brain, which would contribute to the loss of dendritic spines thus accelerating memory impairment and leading to earlier cognitive decline in AD (16, 19, 20).
Homotaurine (tramiprosate) :
Evidence Summary:
Although tramiprosate failed in a phase 3 clinical trial, a post-hoc analysis showed benefits in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Aging and related health concerns: N/A
Safety: Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
What is it?
Homotaurine (tramiprosate) was discovered in a screen for small molecules that inhibit amyloid beta aggregation. It is structurally similar to taurine except that it has an extra carbon. It was the first phase 3 study to test the ‘amyloid hypotheses. Although tramiprosate failed in phase 3 clinical trials, a subgroup analysis showed that it stabilized cognition in ApoE4 individuals.
Neuroprotective Benefit:
Phase 3 studies in Alzheimer’s patients failed to show a benefit with tramiprosate, but a sub-group analysis in ApoE4 individuals shows some promise.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients.
• One preclinical study.
OUP Academic
Homotaurine: A failed drug for Alzheimer’s disease and now a nutraceutical for memory protection
Only 20% of the drugs that begin Phase I clinical trials ever get to market.1 The other 80%, despite the millions of dollars spent in research and developm
A phase 2 study of 58 patients reported a dose dependent decrease in CSF Aβ42 over three months (up to 70% reduction from baseline in 150mg group) (Aisen et al, 2006). This is odd considering tramiprosate’s proposed mechanism of action is to prevent amyloid aggregation (a drug that reduced the aggregation of amyloid beta would expectedly increase CSF levels as amyloid is cleared) (Karran and Hardy, 2014). However, there were no differences in CSF Aβ40 or total tau. In an 18-month phase 3 study of 790 patients with mild-to-moderate Alzheimer’s disease, tramiprosate (100mg or 150mg bid) failed to provide cognitive benefits (Aisen et a, 2011). There was, however, a trend for less hippocampal volume loss. The study was powered to detect a 25% reduction in cognitive loss. For an unknown reason, there was a lot of variability between the study sites and the placebo group deteriorated less than is historically common. Therefore, the authors concluded that the study was insufficiently powered. Regardless, because of the failure in the trial, the company stopped another ongoing phase 3 study in Europe.
ApoE4:
Subgroup analyses of the two phase 3 trials reported a gene-dose effect with tramiprosate, showing no cognitive effect in ApoE4 non-carriers, intermediate benefits in ApoE4 heterozygotes, and the greatest cognitive benefit in ApoE4 homozygotes. In addition, patients on the higher dose of tramiprosate (150mg bid) and with mild (vs. moderate) Alzheimer have responded better to the drug. In fact, cognition in mild Alzheimer’s ApoE4 homozygotes stabilized with tramiprosate and was 40% better than placebo, which the authors claim is clinically meaningful. The authors speculate that since tramiprosate’s mechanism of action is to prevent amyloid aggregation, and since ApoE4 patients have a higher amyloid burden, it would be most beneficial in this group.
Safety:
Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients
The most common side effects of tramiprosate are gastrointestinal in nature (nausea and vomiting) and can occur in up to 23% of the patients on the drug (compared to 13% in placebo). However, they tend to be mild and moderate in nature. Syncope, pneumonia, and weight loss were also more common in the drug group (occurring in 3.8%, 2.3%, and 15% of patients, respectively) (Aisen et al, 2011). ApoE4 homozygotes also had an increased incidence of depression (13% vs. 9% for placebo) (Abusharkra et al, 2017). It is unclear what caused these drug effects in patients. Tramiprosate was not associated with Amyloid Related Imaging Abnormalities (ARIA) – abnormalities present on the MRI scans of some patients with other amyloid-related drugs.
Drug Interactions:
There is no information on potential drug interactions.
Availability/Dosing:
After the failure of phase 3 clinical trials, tramiprosate began to be sold as a supplement called VIVImind (later ActiveMind from Advances Orthomolecular Research). In clinical studies best results were seen at doses of 150mg twice per day.
Research underway:
Alzheon purchased the rights to tramiprosate after the failed clinical trials and created a new pro-drug ALZ-801 that is reported to have improved pharmacokinetics, tolerability, and metabolic stability. Although not listed on clinicaltrials.gov, Alzheon’s website reports that it is currently in phase 2 clinical trials for ApoE4 homozygotes and heterozygotes.
Link - https://www.alzdiscovery.org/uploads/cognitive_vitality_media/Homotaurine-tramiprosate-Cognitive-Vitality-For-Researchers.pdf
ApoE4:
Subgroup analyses of the two phase 3 trials reported a gene-dose effect with tramiprosate, showing no cognitive effect in ApoE4 non-carriers, intermediate benefits in ApoE4 heterozygotes, and the greatest cognitive benefit in ApoE4 homozygotes. In addition, patients on the higher dose of tramiprosate (150mg bid) and with mild (vs. moderate) Alzheimer have responded better to the drug. In fact, cognition in mild Alzheimer’s ApoE4 homozygotes stabilized with tramiprosate and was 40% better than placebo, which the authors claim is clinically meaningful. The authors speculate that since tramiprosate’s mechanism of action is to prevent amyloid aggregation, and since ApoE4 patients have a higher amyloid burden, it would be most beneficial in this group.
Safety:
Tramiprosate is associated with a number of mild side effects, mostly gastrointestinal in nature.
Types of evidence:
• One phase 2 and two phase 3 studies in Alzheimer’s patients
The most common side effects of tramiprosate are gastrointestinal in nature (nausea and vomiting) and can occur in up to 23% of the patients on the drug (compared to 13% in placebo). However, they tend to be mild and moderate in nature. Syncope, pneumonia, and weight loss were also more common in the drug group (occurring in 3.8%, 2.3%, and 15% of patients, respectively) (Aisen et al, 2011). ApoE4 homozygotes also had an increased incidence of depression (13% vs. 9% for placebo) (Abusharkra et al, 2017). It is unclear what caused these drug effects in patients. Tramiprosate was not associated with Amyloid Related Imaging Abnormalities (ARIA) – abnormalities present on the MRI scans of some patients with other amyloid-related drugs.
Drug Interactions:
There is no information on potential drug interactions.
Availability/Dosing:
After the failure of phase 3 clinical trials, tramiprosate began to be sold as a supplement called VIVImind (later ActiveMind from Advances Orthomolecular Research). In clinical studies best results were seen at doses of 150mg twice per day.
Research underway:
Alzheon purchased the rights to tramiprosate after the failed clinical trials and created a new pro-drug ALZ-801 that is reported to have improved pharmacokinetics, tolerability, and metabolic stability. Although not listed on clinicaltrials.gov, Alzheon’s website reports that it is currently in phase 2 clinical trials for ApoE4 homozygotes and heterozygotes.
Link - https://www.alzdiscovery.org/uploads/cognitive_vitality_media/Homotaurine-tramiprosate-Cognitive-Vitality-For-Researchers.pdf
Approximately 25% of the general population carries at least one ε4 allele of the Apolipoprotein E (APOE ε4), the strongest genetic risk factor for late onset Alzheimer’s disease. Beyond its association with late-onset dementia, the association between APOE ε4 and change in cognition over the adult life course remains uncertain. This study aims to examine whether the association between Apolipoprotein E (APOE) ε4 zygosity and cognition function is modified between midlife and old age.
Compared to non-carriers, heterozygote (prevalence 25%) and homozygote (prevalence 2%) APOE ε4 carriers had increased risk of dementia, sub-distribution hazard ratios 2.19 (95% CI 1.73, 2.77) and 5.97 (95% CI 3.85, 9.28) respectively. Using data spanning 45–85 years with non-ε4 carriers as the reference, ε4 homozygotes had poorer global cognitive score starting from 65 years; ε4 heterozygotes had better scores between 45 and 55 years, then no difference until poorer cognitive scores from 75 years onwards. In analysis of individual cognitive tests, better cognitive performance in the younger ε4 heterozygotes was primarily attributable to executive function.
The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late onset Alzheimer’s disease (AD) [1]. Around 25% of the Caucasian population carries at least one ε4 allele [2], with a 3-fold increased risk of AD for heterozygotes and a nearly 15-fold increased risk for homozygotes compared to the ε3 homozygotes, the most common genotype [3].
The mechanisms underlying the relationship between APOE ε4 and AD are thought to be complex [5], involving, e.g., β-amyloid (Aβ) peptide clearance [6], neuronal death [7], and phosphorylation of tau [8].
In addition to AD, APOE ε4 plays a role in other causes of dementia, including vascular dementia [9], and Lewy Body disease [10]. Although case-control and longitudinal studies have examined the association of APOE with dementia, its association with cognitive decline over the adult life course remains debated [11, 12]. Some studies show accelerated cognitive decline in APOE ε4 homozygotes but not heterozygotes [13,14,15].
Furthermore, the association between APOE ε4 and cognition is thought to be modified by age; some [16,17,18] but not all studies [19, 20] report better cognitive performance among ε4 carriers at younger ages. The antagonistic pleiotropy hypothesis [21, 22], whereby a gene is thought to have different effects on health during different life stages, is a possible explanation for the age-varying association of APOE ε4 with cognitive performance over the life course [18, 22, 23].
However, much of the research on APOE is based on adults older than 65 years, followed for less than 10 years, making it difficult to ascertain how APOE shapes cognitive performance over the life course.
Link - https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00740-0#Sec2
Compared to non-carriers, heterozygote (prevalence 25%) and homozygote (prevalence 2%) APOE ε4 carriers had increased risk of dementia, sub-distribution hazard ratios 2.19 (95% CI 1.73, 2.77) and 5.97 (95% CI 3.85, 9.28) respectively. Using data spanning 45–85 years with non-ε4 carriers as the reference, ε4 homozygotes had poorer global cognitive score starting from 65 years; ε4 heterozygotes had better scores between 45 and 55 years, then no difference until poorer cognitive scores from 75 years onwards. In analysis of individual cognitive tests, better cognitive performance in the younger ε4 heterozygotes was primarily attributable to executive function.
The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late onset Alzheimer’s disease (AD) [1]. Around 25% of the Caucasian population carries at least one ε4 allele [2], with a 3-fold increased risk of AD for heterozygotes and a nearly 15-fold increased risk for homozygotes compared to the ε3 homozygotes, the most common genotype [3].
The mechanisms underlying the relationship between APOE ε4 and AD are thought to be complex [5], involving, e.g., β-amyloid (Aβ) peptide clearance [6], neuronal death [7], and phosphorylation of tau [8].
In addition to AD, APOE ε4 plays a role in other causes of dementia, including vascular dementia [9], and Lewy Body disease [10]. Although case-control and longitudinal studies have examined the association of APOE with dementia, its association with cognitive decline over the adult life course remains debated [11, 12]. Some studies show accelerated cognitive decline in APOE ε4 homozygotes but not heterozygotes [13,14,15].
Furthermore, the association between APOE ε4 and cognition is thought to be modified by age; some [16,17,18] but not all studies [19, 20] report better cognitive performance among ε4 carriers at younger ages. The antagonistic pleiotropy hypothesis [21, 22], whereby a gene is thought to have different effects on health during different life stages, is a possible explanation for the age-varying association of APOE ε4 with cognitive performance over the life course [18, 22, 23].
However, much of the research on APOE is based on adults older than 65 years, followed for less than 10 years, making it difficult to ascertain how APOE shapes cognitive performance over the life course.
Link - https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00740-0#Sec2
BioMed Central
The association of APOE ε4 with cognitive function over the adult life course and incidence of dementia: 20 years follow-up of…
Background Approximately 25% of the general population carries at least one ε4 allele of the Apolipoprotein E (APOE ε4), the strongest genetic risk factor for late onset Alzheimer’s disease. Beyond its association with late-onset dementia, the association…
Combining berberine, quercetin, and piperine (black pepper extract) in a single supplement is relatively uncommon.
However, some formulations include these ingredients to enhance absorption and efficacy.
For instance, Pure Encapsulations offers a supplement called "Curcumin with Bioperine," which contains curcumin and piperine to improve bioavailability.
While this product doesn't include berberine or quercetin, it exemplifies the use of piperine to enhance nutrient absorption. (https://www.health.com/best-joint-supplements-8683190?utm_source=chatgpt.com))
If you're interested in a supplement that combines berberine, quercetin, and piperine, you might consider taking them separately or consulting with a healthcare provider to ensure appropriate dosing and to avoid potential interactions.
It's important to note that while piperine can enhance the absorption of certain compounds, it may also affect the metabolism of various medications, so professional guidance is recommended.
https://www.verywellhealth.com/best-berberine-supplements-8704634
However, some formulations include these ingredients to enhance absorption and efficacy.
For instance, Pure Encapsulations offers a supplement called "Curcumin with Bioperine," which contains curcumin and piperine to improve bioavailability.
While this product doesn't include berberine or quercetin, it exemplifies the use of piperine to enhance nutrient absorption. (https://www.health.com/best-joint-supplements-8683190?utm_source=chatgpt.com))
If you're interested in a supplement that combines berberine, quercetin, and piperine, you might consider taking them separately or consulting with a healthcare provider to ensure appropriate dosing and to avoid potential interactions.
It's important to note that while piperine can enhance the absorption of certain compounds, it may also affect the metabolism of various medications, so professional guidance is recommended.
https://www.verywellhealth.com/best-berberine-supplements-8704634
Health
Stiff and Achy? Experts Recommend These Top Joint Supplements to Get You Moving
The best joint supplements to keep your joints healthy and relieve the aches and pains associated with arthritis and overuse.
If you are in the your 30-40 years old you should know, that you have about 350,000 hours left, unless you help yourself by investing anything you have (time, efforts, money & etc) into any longevity company or research
Spices for Longevity: Turmeric’s Anti-Aging Properties 🌱
Turmeric, known for its bright yellow color, contains curcumin, a compound with powerful anti-inflammatory and antioxidant effects. Studies suggest that curcumin can help reduce the risk of chronic diseases like heart disease, Alzheimer's, and cancer. Regular consumption of turmeric may contribute to longevity by protecting cells from damage.
Learn more about turmeric’s benefits [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664031/).
---
How Green Spaces Impact Longevity 🌳
Living near green spaces, like parks or forests, has been shown to reduce stress, lower blood pressure, and improve mental health. A study from *Environmental Health Perspectives* found that people living close to nature had a lower risk of mortality from chronic diseases. Spending time in green spaces may be a natural way to extend lifespan.
Discover more about the impact of green spaces on longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7851085/).
---
Mindfulness for Healthy Aging: Slowing Down the Clock 🧘
Practicing mindfulness has been linked to lower levels of stress and improved emotional well-being. Research shows that mindfulness can reduce inflammation, improve immune function, and even slow cellular aging. A study from *Biobehavioral Medicine* found that mindfulness practices positively influence telomere length, a marker of biological aging.
Read more about mindfulness and aging [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6189422/).
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Fiber-Rich Diet for a Longer Life 🌾
A diet high in fiber, particularly from whole grains, fruits, and vegetables, is linked to lower risks of heart disease, diabetes, and even cancer. Fiber supports digestive health, reduces inflammation, and helps regulate blood sugar. Research from *The Lancet* suggests that people with high fiber intake have a reduced risk of early death.
Learn more about the longevity benefits of fiber [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6647660/).
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How Proper Sleep Hygiene Extends Lifespan 🛌
Quality sleep is crucial for your health and longevity. Studies show that poor sleep is linked to an increased risk of diseases like heart disease and diabetes. Practicing good sleep hygiene—like maintaining a consistent sleep schedule and avoiding screens before bed—can help improve sleep quality and support a longer, healthier life.
Find out more about the link between sleep hygiene and longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449130/).
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Vitamin E: An Antioxidant for Anti-Aging 🥜
Vitamin E is a powerful antioxidant that helps protect cells from oxidative damage, which can accelerate aging. It also supports immune function and skin health. Studies suggest that regular intake of vitamin E through foods like nuts and seeds may slow aging and reduce the risk of chronic diseases.
Discover the benefits of vitamin E for aging well [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7766596/).
Turmeric, known for its bright yellow color, contains curcumin, a compound with powerful anti-inflammatory and antioxidant effects. Studies suggest that curcumin can help reduce the risk of chronic diseases like heart disease, Alzheimer's, and cancer. Regular consumption of turmeric may contribute to longevity by protecting cells from damage.
Learn more about turmeric’s benefits [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664031/).
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How Green Spaces Impact Longevity 🌳
Living near green spaces, like parks or forests, has been shown to reduce stress, lower blood pressure, and improve mental health. A study from *Environmental Health Perspectives* found that people living close to nature had a lower risk of mortality from chronic diseases. Spending time in green spaces may be a natural way to extend lifespan.
Discover more about the impact of green spaces on longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7851085/).
---
Mindfulness for Healthy Aging: Slowing Down the Clock 🧘
Practicing mindfulness has been linked to lower levels of stress and improved emotional well-being. Research shows that mindfulness can reduce inflammation, improve immune function, and even slow cellular aging. A study from *Biobehavioral Medicine* found that mindfulness practices positively influence telomere length, a marker of biological aging.
Read more about mindfulness and aging [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6189422/).
---
Fiber-Rich Diet for a Longer Life 🌾
A diet high in fiber, particularly from whole grains, fruits, and vegetables, is linked to lower risks of heart disease, diabetes, and even cancer. Fiber supports digestive health, reduces inflammation, and helps regulate blood sugar. Research from *The Lancet* suggests that people with high fiber intake have a reduced risk of early death.
Learn more about the longevity benefits of fiber [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6647660/).
---
How Proper Sleep Hygiene Extends Lifespan 🛌
Quality sleep is crucial for your health and longevity. Studies show that poor sleep is linked to an increased risk of diseases like heart disease and diabetes. Practicing good sleep hygiene—like maintaining a consistent sleep schedule and avoiding screens before bed—can help improve sleep quality and support a longer, healthier life.
Find out more about the link between sleep hygiene and longevity [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449130/).
---
Vitamin E: An Antioxidant for Anti-Aging 🥜
Vitamin E is a powerful antioxidant that helps protect cells from oxidative damage, which can accelerate aging. It also supports immune function and skin health. Studies suggest that regular intake of vitamin E through foods like nuts and seeds may slow aging and reduce the risk of chronic diseases.
Discover the benefits of vitamin E for aging well [here](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7766596/).
PubMed Central (PMC)
Curcumin: A Review of Its’ Effects on Human Health
Turmeric, a spice that has long been recognized for its medicinal properties, has received interest from both the medical/scientific world and from culinary enthusiasts, as it is the major source of the polyphenol curcumin. It aids in the management of ...
Incorporation of photosynthetically active algal chloroplasts in cultured mammalian cells towards photosynthesis in animals
https://www.jstage.jst.go.jp/article/pjab/advpub/0/advpub_pjab.100.035/_article
https://www.jstage.jst.go.jp/article/pjab/advpub/0/advpub_pjab.100.035/_article
J-STAGE
Incorporation of photosynthetically active algal chloroplasts in cultured mammalian cells towards photosynthesis in animals
Chloroplasts are photosynthetic organelles that evolved through the endosymbiosis between cyanobacteria-like symbionts and hosts. Many studies have at …
If u r 30+ years old, you have 350K hours left! Everyday 166K people die due to premature death causes. You can help to stop this: https://gogetfunding.com/track-earky-live-longer/
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Elon Musk fight the Death
Hi fellows!
Yesterday had a chance to introduce AI simulations of clinical trials in online symposium in Brussels. Will share the video soon.
Thanks to Didier Couernelle the organizer!
We have about 350,000 hours (40 years) left and we don’t have up to 15 years (38% of the time left) to wait for all stages of clinical trials to pass to bring fundamental scientific interventions to market, with about 8% chance that they will succeed!
AI simulations one of the solutions
Here is the link to presentation.
https://docs.google.com/file/d/1ktbWxv_CKLysHtKkmanmhIdOm8-9udtt/edit?usp=docslist_api&filetype=mspresentation
Maybe it’s not the best and not the only solution, but we all need to diversify our approach and use ALL options.
If you are interested to donate to our work, use a link for a donation platform or contact me directly.
https://gogetfunding.com/track-earky-live-longer/
Please note, that you leave tips in restaurants every day more than you donated to this kind of research!
Thanks
Oleg Teterin
Yesterday had a chance to introduce AI simulations of clinical trials in online symposium in Brussels. Will share the video soon.
Thanks to Didier Couernelle the organizer!
We have about 350,000 hours (40 years) left and we don’t have up to 15 years (38% of the time left) to wait for all stages of clinical trials to pass to bring fundamental scientific interventions to market, with about 8% chance that they will succeed!
AI simulations one of the solutions
Here is the link to presentation.
https://docs.google.com/file/d/1ktbWxv_CKLysHtKkmanmhIdOm8-9udtt/edit?usp=docslist_api&filetype=mspresentation
Maybe it’s not the best and not the only solution, but we all need to diversify our approach and use ALL options.
If you are interested to donate to our work, use a link for a donation platform or contact me directly.
https://gogetfunding.com/track-earky-live-longer/
Please note, that you leave tips in restaurants every day more than you donated to this kind of research!
Thanks
Oleg Teterin
GoGetFunding
Track Early Live Longer
I am raising for AI simulations of clinical trials that can save up to 166,000 people every day! And one day you & your loved ones. In 2018 I founded one of the promising AI powered longevity technologies. All my money from the previous achievements were…
Check out our @DiseaseTrackerBot
Check our Disease Tracker app simulation. More complexed than a bot: @DiseaseTrackerBot
If you liked the app flow, please participate in the quick poll (less than 1 minute):
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