There is relatively little known about the distribution of Alzheimer's disease (AD) around the world. Knowledge of high- or low-prevalence foci of disease may aid our understanding of disease mechanisms. Alzheimer's disease occurs less frequently in Asia than in Europe and North America, probably because of lower allele frequency of the apolipoprotein E (apo E) e4 allele. The disease appears to be also less common in India and Africa.
There are few studies of the disease in Arabs, and few in populations with a high level of consanguinity. We have found a remarkably high prevalence of the disease in Arabs residing in Israel.
In a study in Tunisia, unspecified dementia was found to be 3 times less prevalent than in the United States. Treves, Chandra, and Korczyn (1993) found a lower prevalence of presenile AD in Sephardi, as compared with Ashkenazi Jews, but more late-onset disease in Sephardi than Ashkenazi, perhaps because of lower levels of education in Sephardi. The state of Israel is comprised of about 5 million Jews and 1 million non-Jews, mostly Moslem Arabs. This Arab population of Israel is valuable for medical research because of a high level of inbreeding, large family size, high level of smoking exposure, high level of medical care available through the Israeli Health System, excellent demographic databases available from the government, absence of alcohol use because of the religious proscription, and high participation rate (>98%).
Consanguinity increases the prevalence in a population of autosomal recessive genes that may have undesirable characteristics. For example, an additional 1/16 of the variation of DNA is made homozygous by the inbreeding of a marriage of first-cousins. Conversely, the probability of
identifying recessive or quasirecessive susceptibility factors is enhanced by inbreeding. Childhood mortality is increased in offspring of first-cousin marriages by a factor of 1.4 to 1.7, and children born to consanguineous unions have poorer health than the offspring of nonconsanguineous unions (including malignancies, congenital abnormalities, mental retardation,
and physical handicap). Curiously, there are few studies of the effects of inbreeding on the health of adults. We have hypothesized that consanguinity in the Wadi Ara community has increased the prevalence of autosomal recessive genes that are responsible, in part, for the
increased prevalence of the disease.
It has been reported that 44% of all Arab marriages in Israel are consanguineous, with a mean inbreeding coefficient of .0192 (Jaber, Shohat, Rotter, & Shohat, 1997). The inbreeding rates for Israeli Arabs may be particularly high (as compared with Egyptians or Syrians) because mobility
was reduced for centuries by the Turks. At times in Arab communities, it has been required for children to marry into their own family in part to avoid sharing resources with competing family groups.
Linkage studies by the Boston University group and others focused on inbred Arab families have helped to locate genes for several inherited, neurological diseases, including Wilson's disease, spinal muscular atrophy, sensorineural deafness, and autosomal recessive Duchenne-like
muscular dystrophy. Of critical relevance, successes in mapping genes for Wilson's disease and deafness using inbred Arab kindreds facilitated the cloning of these genes, which were subsequently shown to have diseasecausing mutations prevalent in outbred populations from other parts of the world, including the United States.
All of the known Alzheimer-related genes (on chromosomes 21, 14, 1, and 19) are dominant (chromosomes 21,14,1) or codominant (chromosome 19). There are no known genes affecting the development of AD that are recessive, perhaps because there have been few studies of AD in populations with high levels of inbreeding. De Braekeleer et al. (1989) reported an association between inbreeding and the development of AD (inbreeding coefficient 9 times higher in AD cases than in controls) in a rural population in Quebec. Studies in the Old Order Amish have found a low prevalence of disease in this inbred community, also having a low frequency
of the apo E-e4 allele (.037). Inbreeding could be linked to AD through a confounding effect of education, but the association of inbreeding and education is controversial (found for a Saudi population but not for Israeli Arabs). We expect that there are recessive factors for AD Genetic and Environmental Risk Factors 15 because of indirect evidence: genetic modeling studies of AD in apo E-e4 negative families are unable to reject a recessive model (Rao et al., 1996).
However, it is difficult to evaluate recessive models in outbred populations. The high prevalence we have seen in our highly inbred Arab population in Israel might be due to the inculcation of recessive AD susceptibility alleles or to a dominant gene that became frequent by founder effect.
In a population-based study of AD, we have screened all elderly residents of Wadi Ara, an Arab community in northern Israel, and observed an unusually high prevalence (20.5% of those >60 years, 60.5% of those >85 years). This prevalence is higher than that found in other populations in Israel, China, Europe, or the United States, even after adjustment for
age, education, and gender, and is not due to increased frequency of the apo E-e4 allele (Corder, Saunders, Strittmatter, et al., 1993; Saunders, Strittmatter, Schmechel, et al., 1993) which is actually reduced in this community (0.035 for nondemented elders) as compared with other Caucasians.
DNA samples were collected randomly from 256 participants of the Wadi Ara study, aged 75 ± 9, 118 male, and their apo E genotype was determined by a PCR-based method (Chapman, Estupinan, Asherov, & Goldfarb, 1996). Of the 256 cases examined, 22 carried an apo E-e4 allele
(all heterozygous), including 3 of 34 with AD (apo E-e4 allele frequency 0.04), 8 of 128 nondemented elderly participants (apo E-e4 allele frequency 0.03), 7 of 56 with age-associated memory impairment (AAMI; apo E-e4 allele frequency 0.06), and 4 of 38 with other types of dementia and pseudodementia (apo E-e4 allele frequency 0.05). These data suggest that the
apo E-e4 allele is relatively uncommon in Arabs in Wadi Ara. In fact, this is the lowest frequency of apo E-e4 ever recorded. Although the possibility that it is associated with dementia was not excluded, it cannot explain the high AD prevalence in this population.
Pedigree studies showed that more than one of three of the 168 prevalent cases were from one hamula (extended family) of the 14 found in Wadi Ara. A lOcM genome scan showed significant association with a site that has been narrowed to 1.6 cM. Evidence for linkage stemmed primarily from excess homozygosity of one of the alleles for a marker in this region in the total sample of cases (15%) compared with controls (3%). The crude odds ratio of AD associated with this genotype was 5.7 (95% CI = 1.5,21.7).
The odds increased to 10.0 (1.3-75.9) after adjustment for age, sex, and systolic blood pressure. The observation of significant but different patterns of association within multiple hamulas suggests the existence of multiple recombination between the marker and the AD susceptibility locus. This genetic location notably overlaps a region showing evidence for linkage to AD in a genome scan (Kehoe et al., 1999). This location includes several genes, including a gene strongly related to lipid metabolism. We are currently working on the precise identification of the linked gene. We are also investigating the possibility that the high prevalence of AD in Wadi Ara is related to environmental risk factors and medical illness, including a high-fat diet, altered lipid metabolism, thyroid disease, smoking, hypertension, heart disease, and stroke.
Wednesday, March 21, 2012
Thursday, February 23, 2012
DEMENTIA PREVALENCE IN EXTREME OLD AGE
Numerous researchers have extrapolated from dementia and AD prevalence rates in younger people that all centenarians should have at least some degree of cognitive impairment. Yet our studies, as well as those of other centenarian studies, indicate that approximately 20% to 30% are cognitively intact.
Dr. Silver, our lead neuropsychologist, examined a series of 74 centenarians during a 3-year period. Some of their characteristics are noted in Table 2.1, and Table 2.2 lists the neuropsychological tests performed. We are collaborating with other centenarian studies to establish norms for components of the Mattis Dementia Rating Scale and other tests.
The neuropsychological examination, as well as other phenotyping, is performed where the person lives. Specific maneuvers are performed to accommodate for hearing and vision deficits. Multiple visits are performed to prevent fatigue from factoring into the testing, and family is often invited to participate in order to help language barriers.
Table 2.3 summarizes Dr. Silver's neuropsychological test results of 74 subjects. The neuropathological findings for 14 of these participants are summarized in Table 2.4.
It is noteworthy that evidence of microvascular disease was conspicuously absent in the 14 cases found in Table 2.4. We have noted the absence of diagnoses and blood pressure measurements for many of our participants, which would predispose to vascular disease.
We are now in the process of recruiting individuals who are willing to eventually proceed to postmortem autopsy, following them longitudinally with annual detailed neuropsychological examinations. Our aim is to recruit 33 centenarians per year, who live in close enough proximity to the Massachusetts ADRC to ensure that the brain can be obtained within 4 hours of death.
TABLE 2.1 Centenarians Who Have Undergone Neuropsychological Testing
Age range 100-110 years
Gender 86% women, 14% men
Living situation 7% live alone, 26% with family, 67% in nursing homes
Country of origin 50% foreign born
Most frequent birthplaces Italy, Ireland, and Canada Education Mean = 11 years
Range = 1-20 years
TABLE 2.2 Neuropsychological Test Battery
Mini-Mental State Exam
• Mattis Dementia Rating Scale
• Boston Naming Test (CERAD)
• Trail Making Tests
A and B
• Clock Drawing
• Drilled Word Span
• Cowboy Story
(Boston-Rochester)
• Presidents since FDR
Inventory: Self report and Observer report
• Spiers' Calculations
Geriatric Depression Scale
* Telephone Interview for Cognitive Status
• Test for Severe Impairment
• Tactile Naming
• Cognition and Health History (Informant)
• Psychiatry History (Informant)
• Clinical Dementia Rating Scale
• NEO-Five Factor Personality
Dr. Silver, our lead neuropsychologist, examined a series of 74 centenarians during a 3-year period. Some of their characteristics are noted in Table 2.1, and Table 2.2 lists the neuropsychological tests performed. We are collaborating with other centenarian studies to establish norms for components of the Mattis Dementia Rating Scale and other tests.
The neuropsychological examination, as well as other phenotyping, is performed where the person lives. Specific maneuvers are performed to accommodate for hearing and vision deficits. Multiple visits are performed to prevent fatigue from factoring into the testing, and family is often invited to participate in order to help language barriers.
Table 2.3 summarizes Dr. Silver's neuropsychological test results of 74 subjects. The neuropathological findings for 14 of these participants are summarized in Table 2.4.
It is noteworthy that evidence of microvascular disease was conspicuously absent in the 14 cases found in Table 2.4. We have noted the absence of diagnoses and blood pressure measurements for many of our participants, which would predispose to vascular disease.
We are now in the process of recruiting individuals who are willing to eventually proceed to postmortem autopsy, following them longitudinally with annual detailed neuropsychological examinations. Our aim is to recruit 33 centenarians per year, who live in close enough proximity to the Massachusetts ADRC to ensure that the brain can be obtained within 4 hours of death.
TABLE 2.1 Centenarians Who Have Undergone Neuropsychological Testing
Age range 100-110 years
Gender 86% women, 14% men
Living situation 7% live alone, 26% with family, 67% in nursing homes
Country of origin 50% foreign born
Most frequent birthplaces Italy, Ireland, and Canada Education Mean = 11 years
Range = 1-20 years
TABLE 2.2 Neuropsychological Test Battery
Mini-Mental State Exam
• Mattis Dementia Rating Scale
• Boston Naming Test (CERAD)
• Trail Making Tests
A and B
• Clock Drawing
• Drilled Word Span
• Cowboy Story
(Boston-Rochester)
• Presidents since FDR
Inventory: Self report and Observer report
• Spiers' Calculations
Geriatric Depression Scale
* Telephone Interview for Cognitive Status
• Test for Severe Impairment
• Tactile Naming
• Cognition and Health History (Informant)
• Psychiatry History (Informant)
• Clinical Dementia Rating Scale
• NEO-Five Factor Personality
Thursday, February 16, 2012
Intrathecal corticosteroids might slow Alzheimer’s disease progression
Anti-inflammatory drugs for treatment and prevention of Alzheimer’s disease have to date proved disappointing, including a large study of low-dose prednisone, but higher dose steroids significantly reduced amyloid secretion in a small series of nondemented patients. In addition, there is a case report of a patient with amyloid angiopathy who had complete remission from two doses of dexamethasone, and very high dose steroids are already used for systemic amyloidosis. This paper presents the hypothesis that pulse-dosed intrathecal methylprednisolone or dexamethasone will produce detectable slowing of Alzheimer’s progression, additive to that obtained with cholinesterase inhibitors and memantine. A protocol based on treatment regimens for multiple sclerosis and central nervous system lupus is outlined, to serve as a basis for formulating clinical trials. Ultimately intrathecal corticosteroids might become part of a multi-agent regimen for Alzheimer’s disease and also have application for other neurodegenerative disorders.
Epidemiological evidence suggests that drugs which counteract inflammation might have efficacy for the prevention and treatment of Alzheimer’s disease, but up to now clinical trials have failed to show any clear-cut benefits for nonsteroidal anti-inflammatory drugs (NSAIDs), hydroxychloroquine, anti-leprosy agents or prednisone. In the case of prednisone, however, it may be that much higher doses might be effective where lower doses were not. In the largest clinical trial to date, patients were given prednisone starting at 20 mg per day for one month, followed by one year at 10 mg daily and then tapering off over another 4 months. By contrast, in a series of 16 nondemented patients aged 25 to 82 who were given prednisolone 30–60 mg per day for at least month for treatment of various conditions, there was significant reduction in cerebrospinal fluid amyloid beta peptides in 15 out of 16 patients, up to about a 50% decline for patients receiving 50 and 60 mg of prednisolone. If amyloid is indeed a cause of Alzheimer’s disease, the above data suggests high dose steroids could suppress Alzheimer’s disease by reducing amyloid.
If the above line of reasoning is on the right track, it is important to note that high dose corticosteroids are already used clinically for treatment of primary systemic amyloidosis, in amounts orders of magnitude greater than those used in the Alzheimer’s disease trial. For example, in one recently published study of a regimen combining dexamethasone and interferon, patients were given several days of dexamethasone in an amount of 40 mg per day, which would be equivalent to 400 mg of prednisone daily.
Finally, there is a case report of a 64-year-old man with multiple myeloma who had a temporary remission of Alzheimer’s disease while receiving chemotherapy with vincristine, carmustine, melphalan, cyclophosphamide, and prednisone.
Obviously megadose of anabolic steroids or cytotoxic chemotherapy as a treatment for Alzheimer’s disease would be hard to justify, but if one can knock down amyloid production, inflammation or both with corticosteroids alone, there should be at least some therapeutic effects. The key is delivering high enough doses of corticosteroids to have efficacy without devastating or killing patients with steroid-induced side effects in the process. Building on several case reports of patients with central nervous system lupus erythematosus and multiple sclerosis who responded to intrathecal prednisolone, dexamethasone, or triamcinalone after failing oral and intravenous steroids, this paper proposes that a similar therapeutic strategy could be pursued for patients with Alzheimer’s disease. Studies in rhesus monkeys and pigs indicate that that intrathecal steroids maximize biodistribution within the brain and minimize it within the rest of the body.
Epidemiological evidence suggests that drugs which counteract inflammation might have efficacy for the prevention and treatment of Alzheimer’s disease, but up to now clinical trials have failed to show any clear-cut benefits for nonsteroidal anti-inflammatory drugs (NSAIDs), hydroxychloroquine, anti-leprosy agents or prednisone. In the case of prednisone, however, it may be that much higher doses might be effective where lower doses were not. In the largest clinical trial to date, patients were given prednisone starting at 20 mg per day for one month, followed by one year at 10 mg daily and then tapering off over another 4 months. By contrast, in a series of 16 nondemented patients aged 25 to 82 who were given prednisolone 30–60 mg per day for at least month for treatment of various conditions, there was significant reduction in cerebrospinal fluid amyloid beta peptides in 15 out of 16 patients, up to about a 50% decline for patients receiving 50 and 60 mg of prednisolone. If amyloid is indeed a cause of Alzheimer’s disease, the above data suggests high dose steroids could suppress Alzheimer’s disease by reducing amyloid.
If the above line of reasoning is on the right track, it is important to note that high dose corticosteroids are already used clinically for treatment of primary systemic amyloidosis, in amounts orders of magnitude greater than those used in the Alzheimer’s disease trial. For example, in one recently published study of a regimen combining dexamethasone and interferon, patients were given several days of dexamethasone in an amount of 40 mg per day, which would be equivalent to 400 mg of prednisone daily.
Finally, there is a case report of a 64-year-old man with multiple myeloma who had a temporary remission of Alzheimer’s disease while receiving chemotherapy with vincristine, carmustine, melphalan, cyclophosphamide, and prednisone.
Obviously megadose of anabolic steroids or cytotoxic chemotherapy as a treatment for Alzheimer’s disease would be hard to justify, but if one can knock down amyloid production, inflammation or both with corticosteroids alone, there should be at least some therapeutic effects. The key is delivering high enough doses of corticosteroids to have efficacy without devastating or killing patients with steroid-induced side effects in the process. Building on several case reports of patients with central nervous system lupus erythematosus and multiple sclerosis who responded to intrathecal prednisolone, dexamethasone, or triamcinalone after failing oral and intravenous steroids, this paper proposes that a similar therapeutic strategy could be pursued for patients with Alzheimer’s disease. Studies in rhesus monkeys and pigs indicate that that intrathecal steroids maximize biodistribution within the brain and minimize it within the rest of the body.
Thursday, February 9, 2012
Genetic Correlates of Successful Cognitive Aging
IDENTIFYING GENES PREDISPOSING TO SUCCESSFUL COGNITIVE AGING
The hypothesis driving this study is that centenarians are a select group of people who have a history of aging relatively slowly and who have either markedly delayed or entirely escaped diseases normally associated with aging, such as Alzheimer's disease (AD), cancer, stroke, and heart disease.
The ultimate challenge in this area of research is to identify the genes that are associated with such a survival advantage and the ability to age so well for such a long time without cognitive impairment. We have very exciting preliminary results revealing that centenarians can be the
key to discovering these genes.
Primarily because of funding by the Institute for the Study of Aging, continue careful annual neuropsychological testing and eventual neuropathological study of the centenarian subjects.
Approximately 20% of our participants wish to be postmortem brain donors, but we anticipate
increasing this rate to 50%, again, in part, due to the generosity of the Institute. These neuropsychological-neuropathological correlations will help us better understand what disease-free aging of the brain means and what it looks like; if causes of dementia are different in the extremely old compared with younger individuals; and the type and quantity of changes in the brain that correlate with different levels of cognitive impairment.
At the same time, we are studying the centenarians for genes that may play pivotal roles in determining how centenarians markedly delay or, in some cases, escape cognitive impairment. We have obtained the largest collection of centenarian sibships in the world (N ~ 200). Genome-wide scans from these individuals were performed and the data was given to our statistics colleagues at the Whitehead Institute and Rutgers University for linkage analyses. Based upon scans of 308 individuals making up 137 families, currently we have noted statistically significant linkage to a 20 cM region on chromosome 4. A manuscript reporting these results is currently in the review process. Discovery of genes that powerfully affect processes as broad as rates of aging and/or susceptibility to diseases, such as AD and stroke, would have dramatic impact upon understanding the underpinnings of aging and could, ultimately, lead to promising targets for drug discovery.
In our attempts to locate and recruit sibships, we have enrolled five families with many members achieving extreme old age. Such clustering lends itself to linkage studies similar to those performed in families with clustering for rare diseases (such as Tay-Sachs, cystic fibrosis, and sickle-cell anemia).
In this instance, we are not looking for the cause of a disease but rather a fantastic advantage. Four of these families are described in a recent article published in the Journal of the American Geriatrics Society. Unfortunately, because there is likely to be more than one gene (or the lack of a specific mutation) increasing the probability of achieving exceptional old age, we believe that even 10 members of one family being included in a linkage study is unlikely to produce statistically significant results. However, as we include cousins and perhaps children, such studies might prove to be feasible.
In another approach to gene discovery, we have established a collaboration with gene - expression expert Steven Gullens, PhD, from the Brigham and Women's Hospital. Because we are able to obtain brain tissue at postmortem autopsy within 4 hours of death, we will provide Dr. Gullens with ideal brain tissue samples from regions of specific interest regarding AD, as well as regions that play critical roles in cognition (e.g., frontal lobe and its influence upon executive function) for differential gene expression studies. Determining which genes are active in cognitively intact participants versus those with various causes of cognitive impairment versus
other younger controls should be an efficient approach to discovering genes critical to AD pathogenesis.
The hypothesis driving this study is that centenarians are a select group of people who have a history of aging relatively slowly and who have either markedly delayed or entirely escaped diseases normally associated with aging, such as Alzheimer's disease (AD), cancer, stroke, and heart disease.
The ultimate challenge in this area of research is to identify the genes that are associated with such a survival advantage and the ability to age so well for such a long time without cognitive impairment. We have very exciting preliminary results revealing that centenarians can be the
key to discovering these genes.
Primarily because of funding by the Institute for the Study of Aging, continue careful annual neuropsychological testing and eventual neuropathological study of the centenarian subjects.
Approximately 20% of our participants wish to be postmortem brain donors, but we anticipate
increasing this rate to 50%, again, in part, due to the generosity of the Institute. These neuropsychological-neuropathological correlations will help us better understand what disease-free aging of the brain means and what it looks like; if causes of dementia are different in the extremely old compared with younger individuals; and the type and quantity of changes in the brain that correlate with different levels of cognitive impairment.
At the same time, we are studying the centenarians for genes that may play pivotal roles in determining how centenarians markedly delay or, in some cases, escape cognitive impairment. We have obtained the largest collection of centenarian sibships in the world (N ~ 200). Genome-wide scans from these individuals were performed and the data was given to our statistics colleagues at the Whitehead Institute and Rutgers University for linkage analyses. Based upon scans of 308 individuals making up 137 families, currently we have noted statistically significant linkage to a 20 cM region on chromosome 4. A manuscript reporting these results is currently in the review process. Discovery of genes that powerfully affect processes as broad as rates of aging and/or susceptibility to diseases, such as AD and stroke, would have dramatic impact upon understanding the underpinnings of aging and could, ultimately, lead to promising targets for drug discovery.
In our attempts to locate and recruit sibships, we have enrolled five families with many members achieving extreme old age. Such clustering lends itself to linkage studies similar to those performed in families with clustering for rare diseases (such as Tay-Sachs, cystic fibrosis, and sickle-cell anemia).
In this instance, we are not looking for the cause of a disease but rather a fantastic advantage. Four of these families are described in a recent article published in the Journal of the American Geriatrics Society. Unfortunately, because there is likely to be more than one gene (or the lack of a specific mutation) increasing the probability of achieving exceptional old age, we believe that even 10 members of one family being included in a linkage study is unlikely to produce statistically significant results. However, as we include cousins and perhaps children, such studies might prove to be feasible.
In another approach to gene discovery, we have established a collaboration with gene - expression expert Steven Gullens, PhD, from the Brigham and Women's Hospital. Because we are able to obtain brain tissue at postmortem autopsy within 4 hours of death, we will provide Dr. Gullens with ideal brain tissue samples from regions of specific interest regarding AD, as well as regions that play critical roles in cognition (e.g., frontal lobe and its influence upon executive function) for differential gene expression studies. Determining which genes are active in cognitively intact participants versus those with various causes of cognitive impairment versus
other younger controls should be an efficient approach to discovering genes critical to AD pathogenesis.
Monday, November 28, 2011
The benefits of pool
The benefits of pool
Billiards ... It is difficult to find another such game anywhere so to diversify would appear physical and mental capacities player.
In a game of billiards people constantly moving. During one party player can wind up in total around the table, two - three miles, and even more. In fact, playing in the pool - this is long (from one hour up to ...) useful walk without leaving the premises.
Known is the fact that even in pre-revolutionary times many inactive and apathetic doctors advised patients to play billiards, snooker for them was a great way to support reasonable physical condition.
On top, the game of billiards improves eye, sharpens the player coordinate his movements.
In humans who plays billiards, eyes are rests and restores his sight. The game of billiards triggers active ocular muscles, this phenomenon has some similarity with movement exercises for the eyes, which favorably affect the visual acuity. All of that while playing your eyes have to constantly keep track of the same balls at different distances, among other things, the position of the balls are constantly changing ... Note that most of the professional pool players, even in middle age have excellent vision.
Billiards helps to become more balanced, it teaches players to be patient and cold reason, in other words helping people to acquire a number of qualities he needed in everyday life.
Billiards produces in human the will to win, but at the same time learn to accept defeat with dignity, do not despair and do not lose faith in yourself.
We must not forget that the game of billiards is also a great holiday. Starting to play pool in a few minutes to remove the accumulated stress. Playing human almost completely forget about the daily minutiae and the whole is immersed in the exciting action.
Play Pool and Be Healthy!
Some diets may help prevent Alzheimer's disease
Some diets may help prevent Alzheimer's disease, others may increase the risk and according to some studies antioxidant vitamins may be ineffective in the treatment of diseases associated with clouding of the mind.
Some diets that aim to strengthen the heart muscle, also increase the risk of getting Alzheimer's disease ..
Scientists from Columbia University have shown that the use of antioxidants completely ineffective in preventing the disease, tend to think that vitamins do not work on older people, because they are less susceptible to their action, and action is of short duration. This was stated by Dr. Jose Lachsinger Columbia University.
Another study on the effect of fat on the heart and the brain was conducted by Dr. Martha Clare Morris of Chicago Medical Center, Presbyterian St. Luke's. The study involved 815 volunteers aged 65 and older. All were interviewed about diet and eating habits. The subsequent four years later tests showed that in 131 of the test developed Alzheimer's disease.
People who used the saturated fats in large amounts (products of animal origin such as meat, butter) doubled the risk of Alzheimer's disease compared with those who almost never ate food with saturated fats. This risk is particularly increased in those who ate more than 25 grams of saturated fat daily. For comparison, one tablespoon of butter - 7 grams. Those who ate less than 25 grams have a smaller but still significant risk of developing Alzheimer's disease.
Patients who consumed 14.5 grams of polyunsaturated fat daily (polyunsaturated fats found in vegetables, fish and nuts) reduced the risk by 70%, compared with those who ate little of these fats.
Dr. Morris believes that the Diet is the regular consumation of toast with margarine with polyunsaturated fats, peanut butter, nuts and canola salad dressing. The discovery of researchers is that they proved that the products that increase the risk of cardiovascular disease, also increase the risk of Alzheimer's disease.
Study about the effect of antioxidants was carried out in New York. 980 patients aged over 75 also interviewed about their food parcels during the first year of a four-year study.
After research on Alzheimer's disease diagnosed 242 patients. The subjects consumed a variety of foods rich in antioxidants, such as oranges, corn oil margarine on, and carrots. Some take vitamin supplements, but the absence or lack of antioxidants in the diet had no relation to the development of the risk of Alzheimer's disease.
Antioxidants block the effect of oxygen molecules called free radicals that damage cells. But their action does not preclude the possibility of Alzheimer's disease.
Some diets that aim to strengthen the heart muscle, also increase the risk of getting Alzheimer's disease ..
Scientists from Columbia University have shown that the use of antioxidants completely ineffective in preventing the disease, tend to think that vitamins do not work on older people, because they are less susceptible to their action, and action is of short duration. This was stated by Dr. Jose Lachsinger Columbia University.
Another study on the effect of fat on the heart and the brain was conducted by Dr. Martha Clare Morris of Chicago Medical Center, Presbyterian St. Luke's. The study involved 815 volunteers aged 65 and older. All were interviewed about diet and eating habits. The subsequent four years later tests showed that in 131 of the test developed Alzheimer's disease.
People who used the saturated fats in large amounts (products of animal origin such as meat, butter) doubled the risk of Alzheimer's disease compared with those who almost never ate food with saturated fats. This risk is particularly increased in those who ate more than 25 grams of saturated fat daily. For comparison, one tablespoon of butter - 7 grams. Those who ate less than 25 grams have a smaller but still significant risk of developing Alzheimer's disease.
Patients who consumed 14.5 grams of polyunsaturated fat daily (polyunsaturated fats found in vegetables, fish and nuts) reduced the risk by 70%, compared with those who ate little of these fats.
Dr. Morris believes that the Diet is the regular consumation of toast with margarine with polyunsaturated fats, peanut butter, nuts and canola salad dressing. The discovery of researchers is that they proved that the products that increase the risk of cardiovascular disease, also increase the risk of Alzheimer's disease.
Study about the effect of antioxidants was carried out in New York. 980 patients aged over 75 also interviewed about their food parcels during the first year of a four-year study.
After research on Alzheimer's disease diagnosed 242 patients. The subjects consumed a variety of foods rich in antioxidants, such as oranges, corn oil margarine on, and carrots. Some take vitamin supplements, but the absence or lack of antioxidants in the diet had no relation to the development of the risk of Alzheimer's disease.
Antioxidants block the effect of oxygen molecules called free radicals that damage cells. But their action does not preclude the possibility of Alzheimer's disease.
Wednesday, November 9, 2011
Means of preventing Alzheimer's disease
A group of scientists from the University of Minnesota Medical School, "Mount Sinai" (USA) discovered that isolated from grape seed polyphenols are capable of lowering the content in the brain of a substance called "beta-peptide amilodny Aβ». Its toxic effects on brain cells is the reason of memory loss in Alzheimer's disease.
Now the researchers plan to find a biomarker that will enable patients to determine a high probability of developing Alzheimer's disease. This would allow for early prevention of severe illness, even when the symptoms are absent or mild.
Now the researchers plan to find a biomarker that will enable patients to determine a high probability of developing Alzheimer's disease. This would allow for early prevention of severe illness, even when the symptoms are absent or mild.
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