11 July 2012
Last updated at 22:43 GMT
Showing posts with label Alzheimer's. Show all posts
Showing posts with label Alzheimer's. Show all posts
Friday, June 20, 2014
Glen Campbell Needs Care for Alzheimers
http://bigstory.ap.org/article/ap-exclusive-campbells-wife-defends-his-care#overlay-context=users/mstewart
Tuesday, December 17, 2013
BBC News - Could diabetes drug slow Alzheimer's?
BBC News - Could diabetes drug slow Alzheimer's?
PET+BLOGSPOT is the ONLINE BLOG of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association or Petpositive.Our stories are CURRENT, ACCURATE and RELIABLE. We offer both local and foreign news on animals, disability and the elderly. PET+BLOGSPOT was first established in October 2007. Our hits since then are now 250,000 and ever increasing! PET+BLOGSPOT is updated daily. Kindly note that views expressed in PET+BLOGSPOT are not necessarily those of PETPOSITIVE.You may also visit our Webpage by browsing: www.petpositive.orgYou can also find us in Facebook under PETPOSITIVE EMPOWERMENT.Please sign up as a FOLLOWER of this Blog if you haven't done so already in order to show us your kind support for our work. Thank you!
PET+BLOGSPOT is the ONLINE BLOG of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association or Petpositive.Our stories are CURRENT, ACCURATE and RELIABLE. We offer both local and foreign news on animals, disability and the elderly. PET+BLOGSPOT was first established in October 2007. Our hits since then are now 250,000 and ever increasing! PET+BLOGSPOT is updated daily. Kindly note that views expressed in PET+BLOGSPOT are not necessarily those of PETPOSITIVE.You may also visit our Webpage by browsing: www.petpositive.orgYou can also find us in Facebook under PETPOSITIVE EMPOWERMENT.Please sign up as a FOLLOWER of this Blog if you haven't done so already in order to show us your kind support for our work. Thank you!
Monday, July 23, 2012
Early Timeline Signs Of Alzheimer's Developed
Alzheimer's 'early signs timeline developed'
Protein plaques in the brain indicate Alzheimer's disease
Scientists have assembled a "timeline" of the unseen progress of Alzheimer's before symptoms appear.
A team at Washington University School of Medicine looked at families with a genetic risk of the disease.
Writing in the New England Journal of Medicine, they say signs appeared up to 25 years before the expected onset of the disease.
UK experts said the ability to detect Alzheimer's early would give the best chance of successful treatment.
'Key changes' The 128 people in the study, from the UK, US and Australia, had a 50% chance of inheriting one of three mutations that are certain to cause early Alzheimer's, which often develops in people's 30s and 40s - much earlier than the more common form of Alzheimer's which generally affects people in their 60s.
Those who carry the mutations will go on to develop the disease.
The researchers looked at the age the participants' parents were when they developed the disease - and therefore how many years it was likely to be before they too showed symptoms.
At 15 years, raised levels of tau, a structural protein in brain cells can be seen in spinal fluid - and shrinkage can also be detected within parts of the brain.
Changes in the brain's use of the sugar glucose and slight memory problems become apparent 10 years before symptoms would appear, they suggest.
Researchers also tested other members of the families without the inherited mutations - and found no changes in the markers they tested for.
Prof Clive Ballard, director of research at the Alzheimer's Society, said: "This important research highlights that key changes in the brain, linked to the inherited form of Alzheimer's disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future.
"These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimer's disease, but we can't be sure. Further research into this complex condition is needed to confirm a definite link."
And Dr Eric Karran, director of Research at Alzheimer's Research UK, said: "These results from people with the inherited form of Alzheimer's seem to be very similar to the changes in the non-genetic, common form of the disease.
"It's likely that any new treatment for Alzheimer's would need to be given early to have the best chance of success.
"The ability to detect the very earliest stages of Alzheimer's would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialled in the right people, at the right time."
Protein plaques in the brain indicate Alzheimer's disease
Scientists have assembled a "timeline" of the unseen progress of Alzheimer's before symptoms appear.
A team at Washington University School of Medicine looked at families with a genetic risk of the disease.
Writing in the New England Journal of Medicine, they say signs appeared up to 25 years before the expected onset of the disease.
UK experts said the ability to detect Alzheimer's early would give the best chance of successful treatment.
'Key changes' The 128 people in the study, from the UK, US and Australia, had a 50% chance of inheriting one of three mutations that are certain to cause early Alzheimer's, which often develops in people's 30s and 40s - much earlier than the more common form of Alzheimer's which generally affects people in their 60s.
Those who carry the mutations will go on to develop the disease.
The researchers looked at the age the participants' parents were when they developed the disease - and therefore how many years it was likely to be before they too showed symptoms.
They underwent blood and spinal fluid tests as well as brain scans and mental ability assessments.
The earliest change - a drop in spinal fluid levels of the
key ingredient of Alzheimer's brain plaques - can be detected 25 years
before the anticipated age of disease onset, they suggest.At 15 years, raised levels of tau, a structural protein in brain cells can be seen in spinal fluid - and shrinkage can also be detected within parts of the brain.
Changes in the brain's use of the sugar glucose and slight memory problems become apparent 10 years before symptoms would appear, they suggest.
Researchers also tested other members of the families without the inherited mutations - and found no changes in the markers they tested for.
Prof Clive Ballard, director of research at the Alzheimer's Society, said: "This important research highlights that key changes in the brain, linked to the inherited form of Alzheimer's disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future.
"These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimer's disease, but we can't be sure. Further research into this complex condition is needed to confirm a definite link."
And Dr Eric Karran, director of Research at Alzheimer's Research UK, said: "These results from people with the inherited form of Alzheimer's seem to be very similar to the changes in the non-genetic, common form of the disease.
"It's likely that any new treatment for Alzheimer's would need to be given early to have the best chance of success.
"The ability to detect the very earliest stages of Alzheimer's would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialled in the right people, at the right time."
Friday, July 13, 2012
Alzheimers Early Warning Signs Found
11 July 2012
Last updated at 22:43 GMT
Protein plaques in the brain indicate Alzheimer's disease
Alzheimer's 'early signs timeline developed'
Protein plaques in the brain indicate Alzheimer's disease
Scientists have assembled a "timeline" of the unseen progress of Alzheimer's before symptoms appear.
A team at Washington University School of Medicine looked at families with a genetic risk of the disease.
Writing in the New England Journal of Medicine, they say signs appeared up to 25 years before the expected onset of the disease.
UK experts said the ability to detect Alzheimer's early would give the best chance of successful treatment.
A team at Washington University School of Medicine looked at families with a genetic risk of the disease.
Writing in the New England Journal of Medicine, they say signs appeared up to 25 years before the expected onset of the disease.
UK experts said the ability to detect Alzheimer's early would give the best chance of successful treatment.
'Key changes'
The 128 people in the study, from the UK, US and Australia, had a 50% chance of inheriting one of three mutations that are certain to cause early Alzheimer's, which often develops in people's 30s and 40s - much earlier than the more common form of Alzheimer's which generally affects people in their 60s.
Those who carry the mutations will go on to develop the disease.
The researchers looked at the age the participants' parents were when they developed the disease - and therefore how many years it was likely to be before they too showed symptoms.
The 128 people in the study, from the UK, US and Australia, had a 50% chance of inheriting one of three mutations that are certain to cause early Alzheimer's, which often develops in people's 30s and 40s - much earlier than the more common form of Alzheimer's which generally affects people in their 60s.
Those who carry the mutations will go on to develop the disease.
The researchers looked at the age the participants' parents were when they developed the disease - and therefore how many years it was likely to be before they too showed symptoms.
They underwent blood and spinal fluid tests as well as brain scans and mental ability assessments.
The earliest change - a drop in spinal fluid levels of the key ingredient of Alzheimer's brain plaques - can be detected 25 years before the anticipated age of disease onset, they suggest.
At 15 years, raised levels of tau, a structural protein in brain cells can be seen in spinal fluid - and shrinkage can also be detected within parts of the brain.
Changes in the brain's use of the sugar glucose and slight memory problems become apparent 10 years before symptoms would appear, they suggest.
Researchers also tested other members of the families without the inherited mutations - and found no changes in the markers they tested for.
Prof Clive Ballard, director of research at the Alzheimer's Society, said: "This important research highlights that key changes in the brain, linked to the inherited form of Alzheimer's disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future.
"These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimer's disease, but we can't be sure. Further research into this complex condition is needed to confirm a definite link."
And Dr Eric Karran, director of Research at Alzheimer's Research UK, said: "These results from people with the inherited form of Alzheimer's seem to be very similar to the changes in the non-genetic, common form of the disease.
"It's likely that any new treatment for Alzheimer's would need to be given early to have the best chance of success.
"The ability to detect the very earliest stages of Alzheimer's would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialled in the right people, at the right time."
The earliest change - a drop in spinal fluid levels of the key ingredient of Alzheimer's brain plaques - can be detected 25 years before the anticipated age of disease onset, they suggest.
At 15 years, raised levels of tau, a structural protein in brain cells can be seen in spinal fluid - and shrinkage can also be detected within parts of the brain.
Changes in the brain's use of the sugar glucose and slight memory problems become apparent 10 years before symptoms would appear, they suggest.
Researchers also tested other members of the families without the inherited mutations - and found no changes in the markers they tested for.
Prof Clive Ballard, director of research at the Alzheimer's Society, said: "This important research highlights that key changes in the brain, linked to the inherited form of Alzheimer's disease, happen decades before symptoms show, which may have major implications for diagnosis and treatment in the future.
"These findings are a good indicator that there may be key changes in the brain happening early in people who develop non-hereditary Alzheimer's disease, but we can't be sure. Further research into this complex condition is needed to confirm a definite link."
And Dr Eric Karran, director of Research at Alzheimer's Research UK, said: "These results from people with the inherited form of Alzheimer's seem to be very similar to the changes in the non-genetic, common form of the disease.
"It's likely that any new treatment for Alzheimer's would need to be given early to have the best chance of success.
"The ability to detect the very earliest stages of Alzheimer's would not only allow people to plan and access care and existing treatments far sooner, but would also enable new drugs to be trialled in the right people, at the right time."
Tuesday, May 29, 2012
US All Out To Tame Alzheimer's by 2025
15 May 2012
Last updated at 18:49 GMT
A PET scan of a patient with Alzheimer's (right) shows reduced function and blood flow to the brain
Health Secretary Kathleen Sebelius announced the goal as part of the first National Alzheimer's Plan.
An additional $50m will be added to research funding during 2012.
About 5.4 million Americans have Alzheimer's or related dementias, a number expected to reach 16 million by 2050, at a cost of $1tn (£625m).
In addition, the plan calls for better training of doctors in a bid to better recognise the symptoms of the disease, increased support for care-givers and public awareness of the disease, as well as better data tracking.
President Barack Obama has earmarked an additional $80m in his 2013 budget plan for Alzheimer's research in what was described as an effort to "jumpstart" efforts to reach the 2025 goal.
New research As part of the plan, the Department of Health and Human Services also launched a website to provide information and resources to care-givers.
Mrs Sebelius said the Alzheimer's plan was a "national" effort and not a centralised push by the federal government.
"Reducing the burden of Alzheimer's will require the active engagement of both the public and private sectors," she said.
The plan was unveiled as part of a two-day National Institutes for Health (NIH) symposium focused on the fight against the disease, held as researchers prepared to announce two clinical trials designed to treat Alzheimer's.
"We are at an exceptional moment," said Francis Collins, director of the National Institutes of Health.
One trial tests the use of a drug that attacks amyloid - a protein thought to be a cause of Alzheimer's. The trial will involve 300 patients from an extended family who show no symptoms but are genetically likely to have the disease earlier in life.
The trial will be funded through the National Institutes of Health as well as the Banner Alzheimer's Institute in Phoenix, but with most of the funding from Genetech, the drug's US manufacturer.
The second trial will test an insulin nasal spray's ability to restore memory for those with the disease.
Previous research has linked Alzheimer's to diabetes, especially to the adult-onset form of the disease.
The plan comes as the US moves to implement its healthcare reform law, which currently faces scrutiny and possible repeal by the Supreme Court.
Research and advocacy group the Alzheimer's Association estimates that treating the disease would carry a $200bn price tag in 2012 and a cost of $1tn by 2050, including $140 billion in costs to government healthcare programmes Medicare and Medicaid.
US sets 2025 goal to tame Alzheimer's
A PET scan of a patient with Alzheimer's (right) shows reduced function and blood flow to the brain
Health Secretary Kathleen Sebelius announced the goal as part of the first National Alzheimer's Plan.
An additional $50m will be added to research funding during 2012.
About 5.4 million Americans have Alzheimer's or related dementias, a number expected to reach 16 million by 2050, at a cost of $1tn (£625m).
In addition, the plan calls for better training of doctors in a bid to better recognise the symptoms of the disease, increased support for care-givers and public awareness of the disease, as well as better data tracking.
President Barack Obama has earmarked an additional $80m in his 2013 budget plan for Alzheimer's research in what was described as an effort to "jumpstart" efforts to reach the 2025 goal.
New research As part of the plan, the Department of Health and Human Services also launched a website to provide information and resources to care-givers.
Mrs Sebelius said the Alzheimer's plan was a "national" effort and not a centralised push by the federal government.
"Reducing the burden of Alzheimer's will require the active engagement of both the public and private sectors," she said.
The plan was unveiled as part of a two-day National Institutes for Health (NIH) symposium focused on the fight against the disease, held as researchers prepared to announce two clinical trials designed to treat Alzheimer's.
"We are at an exceptional moment," said Francis Collins, director of the National Institutes of Health.
One trial tests the use of a drug that attacks amyloid - a protein thought to be a cause of Alzheimer's. The trial will involve 300 patients from an extended family who show no symptoms but are genetically likely to have the disease earlier in life.
The trial will be funded through the National Institutes of Health as well as the Banner Alzheimer's Institute in Phoenix, but with most of the funding from Genetech, the drug's US manufacturer.
The second trial will test an insulin nasal spray's ability to restore memory for those with the disease.
Previous research has linked Alzheimer's to diabetes, especially to the adult-onset form of the disease.
The plan comes as the US moves to implement its healthcare reform law, which currently faces scrutiny and possible repeal by the Supreme Court.
Research and advocacy group the Alzheimer's Association estimates that treating the disease would carry a $200bn price tag in 2012 and a cost of $1tn by 2050, including $140 billion in costs to government healthcare programmes Medicare and Medicaid.
PET+BLOGSPOT is the ONLINE BLOG of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association or Petpositive. Our stories are CURRENT, ACCURATE and RELIABLE. We offer both local and foreign news on animals, disability and the elderly. PET+BLOGSPOT was first established in October 2007. Our hits since then are now 150,000 and ever increasing! PET+BLOGSPOT is updated daily. Kindly note that views expressed in PET+BLOGSPOT are not necessarily those of PETPOSITIVE. You may also visit our Webpage by browsing: www.petpositive.com.my You can also find us in Facebook under PETPOSITIVE EMPOWERMENT. Please sign up as a FOLLOWER of this Blog if you haven't done so already in order to show us your kind support for our work. Thank you!
Sunday, September 12, 2010
Another Plus Point For Vitamins - B Keeps Alzheimer's Away
8 September 2010 Last updated at 21:05 GMT
Vitamin B 'puts off Alzheimer's'
Brain scan of a person with Alzheimer's
Brain shrinkage is one of the symptoms of mild cognitive impairment, which often leads to dementia.
Researchers say this could be the first step towards finding a way to delay the onset of Alzheimer's.
Experts said the findings were important but more research was needed.
The study, published in the journal Public Library of Science One, looked at 168 elderly people experiencing levels of mental decline known as mild cognitive impairment.
This condition, marked by mild memory lapses and language problems, is beyond what can be explained by normal ageing and can be a precursor to Alzheimer's and other forms of dementia.
After two years, the rate at which their brains had shrunk was measured.
The average brain shrinks at a rate of 0.5% a year after the age of 60. The brains of those with mild cognitive impairment shrink twice as fast. Alzheimer's patients have brain shrinkage of 2.5% a year.
The team, from the Oxford Project to investigate Memory and Ageing (Optima), found that on average, in those taking vitamin supplements, brain shrinkage slowed by 30%.
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In some cases it slowed by more than 50%, making their brain atrophy no worse than that of people without cognitive impairment.
'Protecting' the brain Certain B vitamins - folic acid, vitamin B6 and B12 - control levels of a substance known as homocysteine in the blood. High levels of homocysteine are associated with faster brain shrinkage and Alzheimer's disease.
Brain scan of a person with Alzheimer's A new study suggests high doses of B vitamins may halve the rate of brain shrinkage in older people experiencing some of the warning signs of Alzheimer's disease.
Brain shrinkage is one of the symptoms of mild cognitive impairment, which often leads to dementia.
Researchers say this could be the first step towards finding a way to delay the onset of Alzheimer's.
Experts said the findings were important but more research was needed.
The study, published in the journal Public Library of Science One, looked at 168 elderly people experiencing levels of mental decline known as mild cognitive impairment.
This condition, marked by mild memory lapses and language problems, is beyond what can be explained by normal ageing and can be a precursor to Alzheimer's and other forms of dementia.
Half of the volunteers were given a daily tablet containing levels of the B vitamins folate, B6 and B12 well above the recommended daily amount. The other half were given a placebo.
After two years, the rate at which their brains had shrunk was measured.
The average brain shrinks at a rate of 0.5% a year after the age of 60. The brains of those with mild cognitive impairment shrink twice as fast. Alzheimer's patients have brain shrinkage of 2.5% a year.
The team, from the Oxford Project to investigate Memory and Ageing (Optima), found that on average, in those taking vitamin supplements, brain shrinkage slowed by 30%.
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John Hough: "You become more forgetful and annoyed with yourself"
'Protecting' the brain Certain B vitamins - folic acid, vitamin B6 and B12 - control levels of a substance known as homocysteine in the blood. High levels of homocysteine are associated with faster brain shrinkage and Alzheimer's disease.
The study authors believe it was the B vitamins' effect on levels of homocysteine that helped slow the rate of brain shrinkage. The study author, Professor David Smith, said the results were more significant than he had expected.
"It's a bigger effect than anyone could have predicted," he said, "and it's telling us something biological.
"These vitamins are doing something to the brain structure - they're protecting it, and that's very important because we need to protect the brain to prevent Alzheimer's."
He said more research was now needed to see whether high doses of B vitamins actually prevented the development of Alzheimer's in people with mild cognitive impairment.
The Alzheimer's Research Trust, which co-funded the study, also called for further investigation.
"These are very important results, with B vitamins now showing a prospect of protecting some people from Alzheimer's in old age," said chief executive Rebecca Wood.
"The strong findings must inspire an expanded trial to follow people expected to develop Alzheimer's."
B vitamins are found naturally in many foods, including meat, fish, eggs and green vegetables.
Experts are advising against taking higher than recommended levels in the light of these findings.
Chris Kennard, chair of the Medical Research Council's Neurosciences and Mental Health Board, said: "We must be cautious when recommending supplements like vitamin B as there are separate health risks if taken in too high doses.
"Further research is required before we can recommend the supplement as a treatment for neurodegenerative diseases, such as Alzheimer's."
"It's a bigger effect than anyone could have predicted," he said, "and it's telling us something biological.
"These vitamins are doing something to the brain structure - they're protecting it, and that's very important because we need to protect the brain to prevent Alzheimer's."
He said more research was now needed to see whether high doses of B vitamins actually prevented the development of Alzheimer's in people with mild cognitive impairment.
The Alzheimer's Research Trust, which co-funded the study, also called for further investigation.
"These are very important results, with B vitamins now showing a prospect of protecting some people from Alzheimer's in old age," said chief executive Rebecca Wood.
"The strong findings must inspire an expanded trial to follow people expected to develop Alzheimer's."
B vitamins are found naturally in many foods, including meat, fish, eggs and green vegetables.
Experts are advising against taking higher than recommended levels in the light of these findings.
Chris Kennard, chair of the Medical Research Council's Neurosciences and Mental Health Board, said: "We must be cautious when recommending supplements like vitamin B as there are separate health risks if taken in too high doses.
"Further research is required before we can recommend the supplement as a treatment for neurodegenerative diseases, such as Alzheimer's."
PET+BLOGSPOT is an ACTIVE ONLINE BLOG of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association (Petpositive). We strive to keep our reports and stories CURRENT, ACCURATE and RELIABLE. We offer both local and foreign news on animals, disability and the elderly. PET+BLOGSPOT was first established in October 2007. Our hits since then is now 55,000 and counting. PET+BLOGSPOT is updated daily. Sometimes even twice and three times a day. Kindly take note that views expressed in this blog are not necessarily those of PETPOSITIVE. You may also visit our Webpage by browsing: www.petpositive.com.my You can also find us in Facebook as PETPOSITIVE EMPOWERMENT. Thank you for your support.
Tuesday, August 24, 2010
Arthritis Cuts Alzheimer's Risk
22 August 2010 Last updated at 23:04 GMT BBC Online 
Rheumatoid arthritis is caused by the immune system attacking the body's own tissues
In the Journal of Alzheimer's Research study, mice with memory loss given the protein fared better in tests.
A synthetic version of GM-CSF protein is already used as a cancer treatment.
UK experts said the study was "an important first step" and tests were needed to see if the drug worked for people with Alzheimer's.
In people with rheumatoid arthritis, the immune system goes into "overdrive" and produces attacking proteins - including GM-CSF.
Arthritis protein 'guards against Alzheimer's disease'
Rheumatoid arthritis is caused by the immune system attacking the body's own tissuesA protein produced in cases of rheumatoid arthritis appears to protect against the development of Alzheimer's disease, US scientists have said.
In the Journal of Alzheimer's Research study, mice with memory loss given the protein fared better in tests.
A synthetic version of GM-CSF protein is already used as a cancer treatment.
UK experts said the study was "an important first step" and tests were needed to see if the drug worked for people with Alzheimer's.
In people with rheumatoid arthritis, the immune system goes into "overdrive" and produces attacking proteins - including GM-CSF.
Rubbish collectors It had already been recognised that people with rheumatoid arthritis were less likely to develop Alzheimer's, but the protective link had been thought to be due to non-steroidal anti-inflammatory drugs (NSAIDs) taken by people with the condition.
However tests showed this was not the case.
In this study, University of South Florida researchers genetically altered mice to have memory problems similar to those seen in Alzheimer's disease, which is a form of dementia.
They then treated them - and some healthy mice - with the protein. Other mice - both healthy ones and those with Alzheimer's symptoms - were given a dummy (placebo) treatment.
Even the healthy mice treated with GM-CSF performed slightly better than their untreated peers.
Mice with Alzheimer's that were given the placebo continued to do poorly in the tests.
The researchers have suggested the protein may attract an influx of cells called microglia from the peripheral blood supply around the brain, which then attack the characteristic plaques that form in people with Alzheimer's.
Microglia are like the body's natural "rubbish collectors" that go to damaged or inflamed areas to get rid of toxic substances.
The brains of GM-CSF-treated Alzheimer's mice showed more than a 50% decrease in beta amyloid, the substance which forms Alzheimer's plaques.
The researchers also observed an apparent increase in nerve cell connections in the brains of the GM-CSF-treated mice, which they say could be a reason memory decline was reversed.
However tests showed this was not the case.
In this study, University of South Florida researchers genetically altered mice to have memory problems similar to those seen in Alzheimer's disease, which is a form of dementia.
They then treated them - and some healthy mice - with the protein. Other mice - both healthy ones and those with Alzheimer's symptoms - were given a dummy (placebo) treatment.
At the end of the 20-day study, the Alzheimer's mice treated with GM-CSF fared substantially better on tests measuring memory and learning, and performed at a similar level to mice of the same age without the condition.
Even the healthy mice treated with GM-CSF performed slightly better than their untreated peers.
Mice with Alzheimer's that were given the placebo continued to do poorly in the tests.
The researchers have suggested the protein may attract an influx of cells called microglia from the peripheral blood supply around the brain, which then attack the characteristic plaques that form in people with Alzheimer's.
Microglia are like the body's natural "rubbish collectors" that go to damaged or inflamed areas to get rid of toxic substances.
The brains of GM-CSF-treated Alzheimer's mice showed more than a 50% decrease in beta amyloid, the substance which forms Alzheimer's plaques.
The researchers also observed an apparent increase in nerve cell connections in the brains of the GM-CSF-treated mice, which they say could be a reason memory decline was reversed.
'Crucial next stage' Dr Huntington Potter, who led the research at the University of South Florida's Health Byrd Alzheimer's Institute, said: "Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer's disease."
An artificial version of GM-CSF, a drug called Leukine, is already approved by the US Food and Drug Administration and has been used to treat cancer patients who need to generate more immune cells.
Dr Potter added. "Our study, along with the drug's track record for safety, suggests Leukine should be tested in humans as a potential treatment for Alzheimer's disease."
Dr Simon Ridley, head of research at the UK's Alzheimer's Research Trust, said: "Positive results in mice can be an important first step for any new treatment, and it's encouraging the team is already planning the crucial next stage of a trial in people.
"We won't know whether GM-CSF can help people with Alzheimer's until clinical trials are completed".
Dr Susanne Sorensen, head of research at the Alzheimer's Society, said: "This exciting research provides a possible answer to the long, unexplained question of why rheumatoid arthritis could reduce the risk of Alzheimer's disease.
"Given the identified protein is already available as a drug that is proven to be safe in humans, the time taken to develop an Alzheimer's disease treatment could be substantially reduced.
"However, we must not jump the gun. Much more research is needed before we can say for certain that the findings demonstrated in mice would also occur in humans."
An artificial version of GM-CSF, a drug called Leukine, is already approved by the US Food and Drug Administration and has been used to treat cancer patients who need to generate more immune cells.
Dr Potter added. "Our study, along with the drug's track record for safety, suggests Leukine should be tested in humans as a potential treatment for Alzheimer's disease."
Dr Simon Ridley, head of research at the UK's Alzheimer's Research Trust, said: "Positive results in mice can be an important first step for any new treatment, and it's encouraging the team is already planning the crucial next stage of a trial in people.
"We won't know whether GM-CSF can help people with Alzheimer's until clinical trials are completed".
Dr Susanne Sorensen, head of research at the Alzheimer's Society, said: "This exciting research provides a possible answer to the long, unexplained question of why rheumatoid arthritis could reduce the risk of Alzheimer's disease.
"Given the identified protein is already available as a drug that is proven to be safe in humans, the time taken to develop an Alzheimer's disease treatment could be substantially reduced.
"However, we must not jump the gun. Much more research is needed before we can say for certain that the findings demonstrated in mice would also occur in humans."
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PET+BLOGSPOT is an ACTIVE ONLINE BLOG of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association (Petpositive). We strive to keep our reports and stories CURRENT, ACCURATE and RELIABLE. We offer both local and foreign news on animals, disability and the elderly. PET+BLOGSPOT was first established in October 2007. Our hits since then is now 55,000 and counting. PET+BLOGSPOT is updated daily. Sometimes even twice and three times a day. Kindly take note that views expressed in this blog are not necessarily those of PETPOSITIVE. You may also visit our Webpage by browsing: www.petpositive.com.my You can also find us in Facebook as PETPOSITIVE EMPOWERMENT. Thank you for your support.
Tuesday, November 10, 2009
Dementia and Alzheimer's - What Are They? From BBC Online
Alzheimer's and dementia
Aricept
Aricept is used to treat Alzheimer's disease
Alzheimer's disease is a progressive, degenerative and irreversible brain disorder that causes intellectual impairment, disorientation and eventually death and the most common cause of dementia.
There is no cure. It is estimated that 2-5% of people over 65 years of age and up to 20% of those over 85 years of age suffer from the disease.
What is dementia?
Dementia is an umbrella term which describes a serious deterioration in mental functions, such as memory, language, orientation and judgement.
Alzheimer's disease is one cause of dementia, but several other diseases can cause it too, including vascular disease. Alzheimer's disease is the most common cause of dementia, accounting for around two thirds of cases in the elderly.
What causes Alzheimer's?
The causes of Alzheimer's disease are not yet fully understood.
There are some very rare inherited cases caused by genetic mutations, but these account for around 1% of people with Alzheimer's.
For most cases, there is a complex interaction of many genetic, environmental and life-style risk factors, with age and genetics playing the largest part.
Some factors, such as a well-balanced diet and regular physical and mental exercise can reduce the risk of developing Alzheimer's.
Protein deposits, known as amyloid plaques and tau tangles, appear and spread in the brain, particularly in the cortex and the hippocampus.
The levels of important chemical transmitters, such as acetylcholine, are reduced. Many of the blood vessels of the brain are also damaged.
These processes are made worse by chronic inflammation in the brain and by an excess of highly reactive molecules known as free radicals, which damage brain tissue.
Gradually the connections between brain cells are lost and eventually many of the cells themselves die.
It is particularly the loss of connections between brain cells that is thought to cause the devastating symptoms of the disease.
What are the symptoms?
Alzheimer's disease has a gradual onset. The early stages of Alzheimer's disease and other dementias can be difficult to diagnose because many of the symptoms are initially subtle or common to other illnesses.
Well established features of the disease include:
* Problems with memory
* Poor or decreased judgement
* Difficulty in performing everyday tasks
* Problems with language
* Disorientation in time and place
* Problems with abstract thinking
* Change in mood and behaviour
* Change in personality
* Loss of initiative
The disease is often associated with depression, anxiety and sleep disturbance.
The rate of decline varies from patient to patient. The disease course runs anywhere from three to twenty years, with eight years being the average life span after diagnosis.
How is the disease diagnosed?
There is no single diagnostic test for Alzheimer's disease. Experts are able to observe the pattern of symptoms and perform a few simple tests over a period of time to measure any change.
Although the tests currently performed are fairly accurate, a definitive diagnosis can still only be made after death by examining the brain tissue at post mortem.
Early diagnosis is important because it helps a doctor to rule out other illnesses with similar symptoms to dementia, such as depression. It also enables new drugs to be prescribed which can improve the quality of life for both patient and carer.
Many other disease processes can mimic Alzheimer's such as thyroid imbalances, vitamin B12 deficiency, brain injuries, tumours, and severe depression.
What are memory clinics?
Specialist memory clinics operate throughout the county and offer assessment, support, information and advice to those with memory problems and their carers.
The assessment includes formal neuropsychological testing in the form of structured questions and tasks. The experts may also carry out blood tests to look for medical causes.
The staff can offer counselling and support as well as treatment.
Are there other types of dementia?
Yes. These include Dementia with Lewy bodies, which gets its name from tiny structures that develop inside nerve cells, and which trigger the degeneration of brain tissue.
Other rarer causes of dementia include progressive supranuclear palsy, Korsakoff's syndrome, Binswanger's disease, HIV and Creutzfeldt-Jakob disease (CJD).
People with multiple sclerosis, motor neurone disease, Parkinson's disease and Huntington's disease can also be at an increased risk.
What treatment is available?
Various types of therapy are used to try to stimulate Alzheimer's patients.
These include: psychological methods, art therapy, music therapy, playing with toys.
Some health professionals try to encourage patients to reminisce about past memories as a way to reduce depression without the use of drugs.
A variety of drug treatments have been shown to benefit patients. None are a cure, but they can temporarily relieve some of the symptoms in some patients:
* Cholinesterase inhibitors including donepezil (Aricept), galantamine (Reminyl) and rivastigmine (Exelon)
* NMDA receptor antagonist, namely memantine (Ebixa)
* Neuroleptics, also known as anti-psychotics or major tranquillisers - although these drugs are only used as a last resort when other methods have failed
* Antidepressants and anti-anxiety drugs
Is there controversy over availability of drugs?
Most certainly. The National Institute for Health and Clinical Excellence (NICE) says that donepezil, rivastigmine and galantamine should only be used to treat Alzheimer's once it has progressed to its moderate stages. Memantine is not recommended as an option for people with moderately severe to severe Alzheimer's disease unless it is being used as part of a clinical trial.
Campaigners argue patients in the early stages of Alzheimer's should also have access to the drugs.
This page contains basic information. If you are concerned about your health, you should consult a doctor. The Alzheimer's Society runs a helpline on 0845 300 0336 and further information is also available free from the Alzheimer's Research Trust on 01223 843899.
PET+BLOGSPOT is the official online blog of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association (Petpositive).
Our blog which was first established in October 2007 currently has more than 30,000 hits. Kindly take note that views expressed in this blog are not necessarily those of Petpositive.
You may also visit our Webpage by browsing: www.petpositive.com.my
Aricept
Aricept is used to treat Alzheimer's disease
Alzheimer's disease is a progressive, degenerative and irreversible brain disorder that causes intellectual impairment, disorientation and eventually death and the most common cause of dementia.
There is no cure. It is estimated that 2-5% of people over 65 years of age and up to 20% of those over 85 years of age suffer from the disease.
What is dementia?
Dementia is an umbrella term which describes a serious deterioration in mental functions, such as memory, language, orientation and judgement.
Alzheimer's disease is one cause of dementia, but several other diseases can cause it too, including vascular disease. Alzheimer's disease is the most common cause of dementia, accounting for around two thirds of cases in the elderly.
What causes Alzheimer's?
The causes of Alzheimer's disease are not yet fully understood.
There are some very rare inherited cases caused by genetic mutations, but these account for around 1% of people with Alzheimer's.
For most cases, there is a complex interaction of many genetic, environmental and life-style risk factors, with age and genetics playing the largest part.
Some factors, such as a well-balanced diet and regular physical and mental exercise can reduce the risk of developing Alzheimer's.
Protein deposits, known as amyloid plaques and tau tangles, appear and spread in the brain, particularly in the cortex and the hippocampus.
The levels of important chemical transmitters, such as acetylcholine, are reduced. Many of the blood vessels of the brain are also damaged.
These processes are made worse by chronic inflammation in the brain and by an excess of highly reactive molecules known as free radicals, which damage brain tissue.
Gradually the connections between brain cells are lost and eventually many of the cells themselves die.
It is particularly the loss of connections between brain cells that is thought to cause the devastating symptoms of the disease.
What are the symptoms?
Alzheimer's disease has a gradual onset. The early stages of Alzheimer's disease and other dementias can be difficult to diagnose because many of the symptoms are initially subtle or common to other illnesses.
Well established features of the disease include:
* Problems with memory
* Poor or decreased judgement
* Difficulty in performing everyday tasks
* Problems with language
* Disorientation in time and place
* Problems with abstract thinking
* Change in mood and behaviour
* Change in personality
* Loss of initiative
The disease is often associated with depression, anxiety and sleep disturbance.
The rate of decline varies from patient to patient. The disease course runs anywhere from three to twenty years, with eight years being the average life span after diagnosis.
How is the disease diagnosed?
There is no single diagnostic test for Alzheimer's disease. Experts are able to observe the pattern of symptoms and perform a few simple tests over a period of time to measure any change.
Although the tests currently performed are fairly accurate, a definitive diagnosis can still only be made after death by examining the brain tissue at post mortem.
Early diagnosis is important because it helps a doctor to rule out other illnesses with similar symptoms to dementia, such as depression. It also enables new drugs to be prescribed which can improve the quality of life for both patient and carer.
Many other disease processes can mimic Alzheimer's such as thyroid imbalances, vitamin B12 deficiency, brain injuries, tumours, and severe depression.
What are memory clinics?
Specialist memory clinics operate throughout the county and offer assessment, support, information and advice to those with memory problems and their carers.
The assessment includes formal neuropsychological testing in the form of structured questions and tasks. The experts may also carry out blood tests to look for medical causes.
The staff can offer counselling and support as well as treatment.
Are there other types of dementia?
Yes. These include Dementia with Lewy bodies, which gets its name from tiny structures that develop inside nerve cells, and which trigger the degeneration of brain tissue.
Other rarer causes of dementia include progressive supranuclear palsy, Korsakoff's syndrome, Binswanger's disease, HIV and Creutzfeldt-Jakob disease (CJD).
People with multiple sclerosis, motor neurone disease, Parkinson's disease and Huntington's disease can also be at an increased risk.
What treatment is available?
Various types of therapy are used to try to stimulate Alzheimer's patients.
These include: psychological methods, art therapy, music therapy, playing with toys.
Some health professionals try to encourage patients to reminisce about past memories as a way to reduce depression without the use of drugs.
A variety of drug treatments have been shown to benefit patients. None are a cure, but they can temporarily relieve some of the symptoms in some patients:
* Cholinesterase inhibitors including donepezil (Aricept), galantamine (Reminyl) and rivastigmine (Exelon)
* NMDA receptor antagonist, namely memantine (Ebixa)
* Neuroleptics, also known as anti-psychotics or major tranquillisers - although these drugs are only used as a last resort when other methods have failed
* Antidepressants and anti-anxiety drugs
Is there controversy over availability of drugs?
Most certainly. The National Institute for Health and Clinical Excellence (NICE) says that donepezil, rivastigmine and galantamine should only be used to treat Alzheimer's once it has progressed to its moderate stages. Memantine is not recommended as an option for people with moderately severe to severe Alzheimer's disease unless it is being used as part of a clinical trial.
Campaigners argue patients in the early stages of Alzheimer's should also have access to the drugs.
This page contains basic information. If you are concerned about your health, you should consult a doctor. The Alzheimer's Society runs a helpline on 0845 300 0336 and further information is also available free from the Alzheimer's Research Trust on 01223 843899.
PET+BLOGSPOT is the official online blog of the Malaysian Animal-Assisted Therapy for the Disabled and Elderly Association (Petpositive).
Our blog which was first established in October 2007 currently has more than 30,000 hits. Kindly take note that views expressed in this blog are not necessarily those of Petpositive.
You may also visit our Webpage by browsing: www.petpositive.com.my
Tuesday, May 20, 2008
BBC ONLINE: Alzheimers; Laughter The Best Medicine
Page last updated at 08:14 GMT, Thursday, 15 May 2008 09:14 UK
'Alzheimer's and my bizarre tennis' | |||
Yet as Heather, who was diagnosed aged 50, an ambassador for the Alzheimer's Society, tells The One Show, she is determined to live a normal life for as long as possible especially her regular games of tennis. Everything coordinates together and everything works and I can get the shot in. But a lot of the time it's sort of all over the place or the racket goes all over the court or I miss the ball or the timings wrong and I have been known to fall over; that's all part of the Alzheimer's and the way it affects me. Tennis is about getting all the factors right and getting the bits and pieces right, but most of the time I can't manage that. My brain is too busy trying to get all of the bits right and quite often I miss the shot all together. I think most people have spotted that something is wrong when I hit the ball astray.
Laughter is the key to coping with Alzheimer's disease, being able to laugh at myself and at the situation makes life more bearable and gives me a better quality of life. I have been known to lose track of money and not to understand the value of money this is something I'll check with my daughter Frances, is this the right amount of money for this thing? Because I've lost the ability to deal with that. We've got to talk about this, we've got to bring it out from cupboards and behind doors where it's all been hidden and we've got to talk about it. I'm going to fight this all the way down, but some days you can't fight this, you've got to give in gracefully. But most of the time I'm going to fight it all the way. | |||
I used to be a good player and it's only occasionally that you see glimpses of this. 
Thursday, May 08, 2008
BBC ONLINE: Depression Linked To Alzheimer's
Depression linked to Alzheimer's
 Depression has been linked to loss of brain cells |
People who have had depression may be more prone to Alzheimer's disease, two studies suggest.
Dutch researchers found Alzheimer's was 2.5 times more likely in people with a history of depression.
Similarly, US researchers, examining Catholic clergy, found those with signs of depression were more likely to go on to develop Alzheimer's.
The Dutch appears in the journal Neurology and the US study in Archives of General Psychiatry.
The Dutch study was small - 486 people over an average of six years, with just 33 people developing Alzheimer's.
But it found that people who showed signs of depression before the age of 60 were four times more likely to develop Alzheimer's.
 |  We don't know yet whether depression contributes to the development of Alzheimer's disease, or whether another unknown factor causes both depression and dementia  Dr Monique Breteler Erasmus University Medical Center |
The researchers, from the Erasmus University Medical Center in Rotterdam, said more work was needed to fully understand the link between Alzheimer's and depression.
Lead researcher Dr Monique Breteler said: "We don't know yet whether depression contributes to the development of Alzheimer's disease, or whether another unknown factor causes both depression and dementia."
One theory is that depression leads to the loss of cells in two areas of the brain, the hippocampus and the amygdala, which then contributes to Alzheimer's disease.
However, the latest study found no difference in the size of these two brain areas in people with depression and people who had never developed the condition.
Second study
The findings were echoed in a second study by Rush University in the US published in Archives of General Psychiatry.
The researchers followed more than 900 members of the Catholic clergy for up to 13 years during which time 190 developed Alzheimer's.
They found that those with more signs of depression at the start of the study were more likely to develop Alzheimer's.
But there was little evidence of an increase in depressive symptoms during the early stages of disease.
Even after the diagnosis of Alzheimer's was made there was no general increase in depression, but rather an increase that was confined to individuals with certain personality traits.
The researchers said their findings suggested that depression was a risk factor for Alzheimer's disease - rather than a subtle early sign of its underlying pathology.
Researcher Dr Robert Wilson said: "Depressive symptoms may be associated with distinctive changes in the brain that somehow reduce neural reserve, which is the brain's ability to tolerate the pathology associated with Alzheimer's disease."
Rebecca Wood, of the Alzheimer's Research Trust, said the research was interesting, and potentially useful.
She said: "Identifying people at higher risk could lead to ways to reduce the number of people who develop dementia, help researchers to understand more about dementia and create new avenues of research."
Dr Susanne Sorensen, head of research at the Alzheimer's Society, said: "More research is needed to clarify the relationship between dementia and depression and determine whether depression causes changes in the brain that make dementia more likely."
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