Ketones or therapeutic methods for AD treatment
[China Pharmaceutical Network Technology News] Alzheimers disease (AD) is the most common form of dementia that afflicts the elderly. So far, the methods and drugs for treating this type of dementia have not been found. However, studies have found that the use of ketones can treat Alzheimer's disease.
A growing body of research suggests that such a specific treatment may already exist, but not in the form of pills, but simply dietary changes. And more and more studies report that interventional approaches to improve metabolic health can alleviate symptoms and reduce brain lesions associated with AD.
A popular theory is that AD has multiple causes, but what they have in common may be metabolic dysfunction. Indeed, poor metabolic health markers such as diabetes, inflammation and high cholesterol levels are major risk factors for AD.
Just like our muscles, the brain needs energy to function properly. But unlike muscle cells, when there is a shortage of glucose, such as during a meal or a low-carbohydrate diet, neurons in the brain have a unique ability to metabolize ketones as a source of alternative energy.
As early as the 1920s, scientists have found that high-fat diets that promote ketogenesis control epilepsy, and ketone production remains one of the most effective ways to treat this disease. This increases the likelihood that ketones will also provide neuroprotective effects against other diseases derived from abnormal neurological metabolism, such as AD. Since then, studies have confirmed that ketones do actually alter brain metabolism, reduce neuropathy and relieve behavioral symptoms.
Ketones relieve AD symptoms
In the past 10 years, several studies have supported the clinical value of ketone production in patients with cognitive impairment. In a 2004 study, 20 patients with AD or Mild Cognitive Impairment (MCI) received placebo or medium chain triglycerides—a type of saturation found in coconut oil and palm oil. Fat can promote the production of ketones - treatment. Ketone levels were increased after 90 minutes of treatment with medium chain triglycerides, and these higher levels of ketones corresponded to better memory improvement. Five years after these initial short-term findings, a larger, longer-term study of 152 patients with mild AD was conducted. After 45 days, those receiving treatment with a ketogenic compound showed cognitive improvement compared to patients receiving placebo treatment. However, both studies suggest that the benefits of ketone production to the brain may depend on genetic factors.
In the previous study, medium-chain triglycerides played a role in improving cognitive function only in participants who lacked the ApoE4 allele, a genetic risk factor for AD. Similarly, in the latter study, cognitive improvement was stronger and more persistent in those patients who lacked the ApoE4 allele—sustained for 90 days.
A new study published in the journal PLoS ONE confirms that the different responses of mice to diet depend on its genetic factors: a high-fat diet only reduces ApoE levels in the brains of mice lacking the ApoE4 gene.
These promising early discoveries about ketogenic compounds provide hope that dietary interventions may similarly benefit brain health. A 2012 study tested whether memory can be improved simply by choosing a low-carbohydrate diet without the use of supplements used in previous studies. Among the 23 MCI patients, patients who underwent a low-carbohydrate diet within 6 weeks showed improved memory compared to those who received a high-carbohydrate diet. These memory improvements are associated with ketone levels, but not with calories burned (in energy units), insulin levels, or body weight, suggesting that increased ketone production is likely to be the cause of cognitive improvement due to low-carbohydrate diets. .
Other potential treatments have shown similar short-term effects in early AD, but failed in long-term treatment of more advanced AD cases.
Although ketone production has not been rigorously tested in formal clinical trials, a recent case study provides persuasive evidence that ketones may actually maintain efficacy in clinical cases.
A 63-year-old male with advanced AD began to eat coconut oil and medium-chain triglycerides, both of which are known to increase ketone levels. After only 2.5 months, he scored from a minimum of 12 to 20 (up to 30) in a Mini Mental State Exam that is widely used at home and abroad.
After two years, his cognitive and daily life functions improved, and his magnetic resonance imaging (MRI) results showed no further brain atrophy. After adding a ketoester supplement to the patient's dietary regimen, he showed further improvement in his mood, self-satisfaction and memory.
Significantly, he carries the ApoE4 gene. Therefore, ketone production appears to be highly beneficial for patients carrying the ApoE4 gene, even though earlier studies have shown that it is more beneficial for patients who lack this risk factor.
How ketones protect the brain
Scientists are looking for AD-mode animals to better understand how ketone production may protect the human brain from neurodegeneration. In AD mode mice, increased levels of toxic beta-amyloid decreased in the brains of mice receiving a high fat/low carbohydrate diet compared to those on a standard diet.
A recent study has helped reveal the metabolic benefits of ketones, the association between lower beta-amyloid and improved cognitive function. This study tested the effects of ketones in AD-mode mice and in beta-amyloid-treated neurons. Although beta-amyloid increases the oxidation reaction and disrupts the function of a mitochondrial enzyme complex, ketones are able to reverse these effects, confirming their neuronal metabolic benefits.
Furthermore, ketones reduce beta-amyloid levels and block beta-amyloid-induced pore formation in cell membranes, suggesting that ketones are resistant to neuronal damage associated with beta-amyloid.
Finally, after being destroyed by β-amyloid, ketones restored normal synaptic plasticity and memory performance.
Treatment of diseases with ketones
If ketone production is shown to be effective in treating AD, further studies are needed to determine the appropriate method of administration because high fat diets, medium chain triglycerides or ketone-producing compounds may differ in efficacy. Patient adherence to a strict diet or supplements may also present potential challenges. Identifying the minimum effective dose will help to develop guidelines for the extent to which a treatment needs to be rigorous.
Although there are still some problems, strong evidence for the potential of ketone-producing treatment supports the possibility that a powerful weapon in our battle against AD may already exist and that this therapeutic agent may be as tasty as a spoonful of coconut oil - providing hope .
A growing body of research suggests that such a specific treatment may already exist, but not in the form of pills, but simply dietary changes. And more and more studies report that interventional approaches to improve metabolic health can alleviate symptoms and reduce brain lesions associated with AD.
A popular theory is that AD has multiple causes, but what they have in common may be metabolic dysfunction. Indeed, poor metabolic health markers such as diabetes, inflammation and high cholesterol levels are major risk factors for AD.
Just like our muscles, the brain needs energy to function properly. But unlike muscle cells, when there is a shortage of glucose, such as during a meal or a low-carbohydrate diet, neurons in the brain have a unique ability to metabolize ketones as a source of alternative energy.
As early as the 1920s, scientists have found that high-fat diets that promote ketogenesis control epilepsy, and ketone production remains one of the most effective ways to treat this disease. This increases the likelihood that ketones will also provide neuroprotective effects against other diseases derived from abnormal neurological metabolism, such as AD. Since then, studies have confirmed that ketones do actually alter brain metabolism, reduce neuropathy and relieve behavioral symptoms.
Ketones relieve AD symptoms
In the past 10 years, several studies have supported the clinical value of ketone production in patients with cognitive impairment. In a 2004 study, 20 patients with AD or Mild Cognitive Impairment (MCI) received placebo or medium chain triglycerides—a type of saturation found in coconut oil and palm oil. Fat can promote the production of ketones - treatment. Ketone levels were increased after 90 minutes of treatment with medium chain triglycerides, and these higher levels of ketones corresponded to better memory improvement. Five years after these initial short-term findings, a larger, longer-term study of 152 patients with mild AD was conducted. After 45 days, those receiving treatment with a ketogenic compound showed cognitive improvement compared to patients receiving placebo treatment. However, both studies suggest that the benefits of ketone production to the brain may depend on genetic factors.
In the previous study, medium-chain triglycerides played a role in improving cognitive function only in participants who lacked the ApoE4 allele, a genetic risk factor for AD. Similarly, in the latter study, cognitive improvement was stronger and more persistent in those patients who lacked the ApoE4 allele—sustained for 90 days.
A new study published in the journal PLoS ONE confirms that the different responses of mice to diet depend on its genetic factors: a high-fat diet only reduces ApoE levels in the brains of mice lacking the ApoE4 gene.
These promising early discoveries about ketogenic compounds provide hope that dietary interventions may similarly benefit brain health. A 2012 study tested whether memory can be improved simply by choosing a low-carbohydrate diet without the use of supplements used in previous studies. Among the 23 MCI patients, patients who underwent a low-carbohydrate diet within 6 weeks showed improved memory compared to those who received a high-carbohydrate diet. These memory improvements are associated with ketone levels, but not with calories burned (in energy units), insulin levels, or body weight, suggesting that increased ketone production is likely to be the cause of cognitive improvement due to low-carbohydrate diets. .
Other potential treatments have shown similar short-term effects in early AD, but failed in long-term treatment of more advanced AD cases.
Although ketone production has not been rigorously tested in formal clinical trials, a recent case study provides persuasive evidence that ketones may actually maintain efficacy in clinical cases.
A 63-year-old male with advanced AD began to eat coconut oil and medium-chain triglycerides, both of which are known to increase ketone levels. After only 2.5 months, he scored from a minimum of 12 to 20 (up to 30) in a Mini Mental State Exam that is widely used at home and abroad.
After two years, his cognitive and daily life functions improved, and his magnetic resonance imaging (MRI) results showed no further brain atrophy. After adding a ketoester supplement to the patient's dietary regimen, he showed further improvement in his mood, self-satisfaction and memory.
Significantly, he carries the ApoE4 gene. Therefore, ketone production appears to be highly beneficial for patients carrying the ApoE4 gene, even though earlier studies have shown that it is more beneficial for patients who lack this risk factor.
How ketones protect the brain
Scientists are looking for AD-mode animals to better understand how ketone production may protect the human brain from neurodegeneration. In AD mode mice, increased levels of toxic beta-amyloid decreased in the brains of mice receiving a high fat/low carbohydrate diet compared to those on a standard diet.
A recent study has helped reveal the metabolic benefits of ketones, the association between lower beta-amyloid and improved cognitive function. This study tested the effects of ketones in AD-mode mice and in beta-amyloid-treated neurons. Although beta-amyloid increases the oxidation reaction and disrupts the function of a mitochondrial enzyme complex, ketones are able to reverse these effects, confirming their neuronal metabolic benefits.
Furthermore, ketones reduce beta-amyloid levels and block beta-amyloid-induced pore formation in cell membranes, suggesting that ketones are resistant to neuronal damage associated with beta-amyloid.
Finally, after being destroyed by β-amyloid, ketones restored normal synaptic plasticity and memory performance.
Treatment of diseases with ketones
If ketone production is shown to be effective in treating AD, further studies are needed to determine the appropriate method of administration because high fat diets, medium chain triglycerides or ketone-producing compounds may differ in efficacy. Patient adherence to a strict diet or supplements may also present potential challenges. Identifying the minimum effective dose will help to develop guidelines for the extent to which a treatment needs to be rigorous.
Although there are still some problems, strong evidence for the potential of ketone-producing treatment supports the possibility that a powerful weapon in our battle against AD may already exist and that this therapeutic agent may be as tasty as a spoonful of coconut oil - providing hope .
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