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Category Archives: alzheimers disease

NovelistTerry Pratchett angry with NHS for failing to provide Aricept for Alzheimer’s patients

Bestselling author, Terry Pratchett, who suffers from posterior cortical atrophy –a rare form of Alzheimer’s– is questioning why he and other sufferers of Alzheimer’s are being denied free access to the drug Aricept in the UK.

Pratchett a millionaire who can afford the drug is speaking up on behalf of those that cannot (about 400,000 are being denied). He points to a flawed system that provides Viagra on the NHS while rejecting Aricept.

“My wife and PA both noticed real changes in me after two or three months on it. I used to fumble with buttons and needed help with seat belts. Now, I get dressed normally and seat belts slide in first time. Mentally, it’s the difference between a sunny day and an overcast day. Ye Gods, that’s worth it!”



The National Institute for Clinical Excellence in the UK, which advises the National Health Service (NHS), ruled that Aricept, along with Reminyl and Exelon, should be prescribed only to those with more severe forms of Alzheimer’s. Aricept cost about $5 a day in the UK.

Prachett says that he derived great benefit from Aricept within two or three months of taking the drug.

“My wife and PA both noticed real changes in me after two or three months on it. I used to fumble with buttons and needed help with seatbelts. Now, I get dressed normally and seatbelts slide in first time. Mentally, it’s the difference between a sunny day and an overcast day. Ye Gods, that’s worth it!”

Questioning how the National Institute for Health and Clinical Excellence rules on the cost effectiveness of drugs, he said: ‘I would very much like to know the basis on which these decisions are made because some of them don’t seem to make very much sense.

More on this story

Terry Pratchett’s anger over the life-changing Alzheimer’s drug not available on the NHS

Terry Pratchett launches attack on NHS

 

NovelistTerry Pratchett angry with NHS for failing to provide Aricept for Alzheimer’s patients

Bestselling author, Terry Pratchett, who suffers from posterior cortical atrophy –a rare form of Alzheimer’s– is questioning why he and other sufferers of Alzheimer’s are being denied free access to the drug Aricept in the UK.

Pratchett a millionaire who can afford the drug is speaking up on behalf of those that cannot (about 400,000 are being denied). He points to a flawed system that provides Viagra on the NHS while rejecting Aricept.

“My wife and PA both noticed real changes in me after two or three months on it. I used to fumble with buttons and needed help with seat belts. Now, I get dressed normally and seat belts slide in first time. Mentally, it’s the difference between a sunny day and an overcast day. Ye Gods, that’s worth it!”



The National Institute for Clinical Excellence in the UK, which advises the National Health Service (NHS), ruled that Aricept, along with Reminyl and Exelon, should be prescribed only to those with more severe forms of Alzheimer’s. Aricept cost about $5 a day in the UK.

Prachett says that he derived great benefit from Aricept within two or three months of taking the drug.

“My wife and PA both noticed real changes in me after two or three months on it. I used to fumble with buttons and needed help with seatbelts. Now, I get dressed normally and seatbelts slide in first time. Mentally, it’s the difference between a sunny day and an overcast day. Ye Gods, that’s worth it!”

Questioning how the National Institute for Health and Clinical Excellence rules on the cost effectiveness of drugs, he said: ‘I would very much like to know the basis on which these decisions are made because some of them don’t seem to make very much sense.

More on this story

Terry Pratchett’s anger over the life-changing Alzheimer’s drug not available on the NHS

Terry Pratchett launches attack on NHS

 

rember and TauRx Therapeutics

I am getting emails asking me about rember. People want to know more about the drug and the phase 3 clinical trial. They are also asking how they can contact the company direct.

To learn more about the drug and get answers to your question use this link:

FAQ (Frequently Asked Questions) about TauRx Therapeutics and rember™

To contact the company use this link:

TauRx Therapeutics Ltd & University of Aberdeen – New treatment halts progress of Alzheimer’s disease

 

Diverse Approaches to Alzheimer’s Therapies Continue to Show Progress at ICAD

A lot of good and encouraging news continues to come out of this week’s Alzheimer’s Association International Conference on Alzheimer’s Disease 2008.

–18-Month Data from an Extension of a Pivotal Trial of Dimebon in Alzheimer’s

–First U.S. Double-Blind Phase II Clinical Trial of IVIg (Immunotherapy) in Alzheimer’s

–Phase II Immunotherapy Trial with LY2062430 in Mild to Moderate Alzheimer’s

–Antidementia Drugs Contribute to Longer Life in People with Alzheimer’s

Diverse Approaches to Alzheimer’s Therapies Continue to Show Progress at ICAD

Results from clinical trials of three potential Alzheimer’s therapies raise hope for new and better treatments of the disease, according to data reported today at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) in Chicago.

A related study showed that taking antidementia drugs appears to have a positive impact on extending lifespan in those with Alzheimer’s.

These reports included:

* Eighteen-month data from an open-label extension of a pivotal trial of Dimebon (Medivation) in mild to moderate Alzheimer’s.
* Nine-month data from an interim analysis of the first U.S. Phase II trial of intravenous immunoglobulin, or IVIg (Baxter), in Alzheimer’s.
* Results of a Phase II study of a monoclonal antibody (LY2062430, Lilly) in mild to moderate Alzheimer’s.
* Research suggesting that persistent antidementia drug use increases survival in people with Alzheimer’s.

“Therapies targeting amyloid in Alzheimer’s disease must continue to be thoroughly tested,” said William Thies, PhD, Alzheimer’s Association vice president for Medical and Scientific Relations. “At the same time, we know that Alzheimer’s is a complex disease and that better treatments and preventions will likely also be complex, so we must investigate every promising drug target looking eventually towards the possibility of a multi-strategy approach.”

18-Month Data from an Extension of a Pivotal Trial of Dimebon in Alzheimer’s

In a study recently reported, Dimebon (Medivation) improved cognition and memory, activities of daily living, and behavior in a one-year placebo-controlled trial of patients with mild to moderate Alzheimer’s. At ICAD 2008, Jeffrey L. Cummings, M.D., the Augustus S. Rose Professor of Neurology, and Professor of Psychiatry and Biobehavioral Sciences, at UCLA, and colleagues reported on an open-label extension of the trial to 18 months.

One hundred eighty-three (183) people with mild-to-moderate Alzheimer’s were initially randomized into a six-month placebo-controlled study of Dimebon. Patients completing six months of treatment were offered the opportunity to re-consent for an additional six months of controlled treatment in their originally randomized group, followed by an open-label extension (OLE). Data presented at ICAD 2008 include only the 104 OLE participants (54 Dimebon, 50 placebo). All were given Dimebon for the OLE, not placebo, at a dose of 20 mg three times per day. Ninety-two (92) (88.5%) patients enrolling into OLE completed six months of treatment.

Patients originally receiving Dimebon for 12 months who continued on Dimebon for an additional six months in the OLE phase had preservation of function close to their starting baselines on the key signs and symptoms of Alzheimer’s disease 18 months after starting the study. Patients originally on placebo for 12 months who were then crossed over to Dimebon on the OLE phase also stabilized across all key measures tested. Since these patients had declined over the previous 12 months while on placebo, they stabilized at a lower level of function than those treated with Dimebon for the full 18 months.

Dimebon was well-tolerated through 18 months. Adverse events that occurred more often with dimebon compared to placebo were dry mouth, sweating and depressed mood/sadness.

“People initially treated with placebo and then crossed over to Dimebon did not show the same level of benefit as those people who took Dimebon for the full 18 months,” Cummings said. “This emphasizes the benefit of earlier treatment, and suggests the possibility that Dimebon may slow of the progression of Alzheimer’s. However, open-label extensions are not that same as placebo-controlled trials, and extrapolation of the treatment results should be done with caution. Patients are being screened now for the Phase III clinical trials.”

“Dimebon appears to work through a mechanism of action that is distinct from currently marketed Alzheimer’s drugs. Dimebon improves impaired mitochondrial function. Mitochondria are the central energy source of all cells and impaired mitochondrial function may play a significant role in the loss of brain cell function in Alzheimer’s,” Cummings added.

First U.S. Double-Blind Phase II Clinical Trial of IVIg (Immunotherapy) in Alzheimer’s

IVIg is under investigation by Baxter International as a potential anti-amyloid immunotherapy for Alzheimer’s. It contains a broad spectrum of antibodies, and is currently indicated as a therapy for people with primary immunodeficiency disorders. IVIg contains antibodies that bind to the beta amyloid aggregates that are thought to be central to Alzheimer’s. In two previous open-label studies, patients with mild to moderate Alzheimer’s showed cognitive improvement when treated with IVIg for six months.

Diamanto Tsakanikas, PhD, Norman Relkin, MD, PhD, and colleagues at Well Cornell Medical College carried out a six-month Phase II double-blind, placebo-controlled study of IVIg for Alzheimer’s followed by a 12-month, rater-blinded extension study. At ICAD 2008, they reported an interim analysis of uninterrupted IVIg treatment for 9 months.

Twenty-four people with mild to moderate Alzheimer’s (MMSE 14-26) participated in the trial. For the first six months, eight participants received placebo and 16 received IVIg at four doses ranging from 0.2 grams IVIg per kilogram of body weight every two weeks to 0.8 grams IVIg per kilogram of body weight given once per month (four people each at the four different doses). After six months, all subjects were given IVIg with the raters blinded to dose. The primary outcome measures were two standard measures of cognition and the clinician’s observation of change (a seven point scale from “markedly improved”=+3 to “marked worsening”=-3), respectively the ADAS-cog and the ADCS-CGIC, which were administered at baseline and three-month intervals thereafter.

In the total group, the researchers found statistically significant differences favoring IVIg treatment on the CGIC at three, six and nine months. At nine months, the IVIg group averaged 1.5 points higher on the CGIC. On the ADAS-cog, scores favoring IVIg reached statistical significance at nine months. The average change in ADAS-Cog score at nine months favored IVIg treatment by 5.4 ADAS points. Uninterrupted IVIg treatment also produced sustained benefits relative to initial placebo treatment in activities of daily living.

When the results for each dose were analyzed individually, subjects receiving 0.4 grams of IVIg per kilogram of body weight given every two weeks improved over baseline on ADAS-Cog, ADCS-CGIC, and a measure of daily functioning. The researchers identified this as the best dose. None of the subjects given placebo showed comparable improvements.

Treatment-related adverse events that occurred at a greater frequency with IVIg treatment as compared to placebo were rash and a transient drop in blood count. In contrast, there were more behavioral disturbances in placebo-treated patients than those who received IVIg.

“While there were relatively small numbers of participants in this study, we were nonetheless able to demonstrate that people with Alzheimer’s who get uninterrupted treatment with IVIg for nine months have statistically significant and clinically relevant improvements on both cognitive and global clinical measures,” Tsakanikas said. “A large-scale, 18-month, multicenter Phase III clinical trial of IVIg in Alzheimer’s is now getting underway, sponsored by Baxter and the National Institutes of Health, that will test whether IVIg immunotherapy provides long-term benefits and has a disease-modifying effect.”

Phase II Immunotherapy Trial with LY2062430 in Mild to Moderate Alzheimer’s

Previous research has shown that antibodies that bind to beta amyloid can be given intravenously. By binding to beta amyloid and increasing the rate of its removal from the body, these antibody infusions may slow the progression of Alzheimer’s.

Eric Siemers, MD, Medical Director of the Alzheimer’s Disease Research Team at Eli Lilly and Company, and colleagues conducted a Phase II trial of a monoclonal antibody, known as LY2062430, that binds to the mid-domain of beta amyloid.

Fifty-two (52) people with mild to moderate Alzheimer’s and 16 volunteer subjects were studied. Alzheimer’s patients received 12 weekly infusions of placebo or antibody (100 mg every 4 weeks, 100 mg once per week, 400 mg every 4 weeks or 400 mg once per week). Volunteers received a single 100 mg dose of antibody. Safety assessments included brain imaging using magnetic resonance imaging (MRI) and examination of cerebrospinal fluid (CSF, a fluid normally present around the brain and spinal cord). In an optional sub-study, 24 Alzheimer’s patients and 13 volunteers underwent a type of brain imaging known as SPECT using a tracer (known as IMPY) that measures the amount of amyloid plaque present in the brain. Measures of symptom severity were obtained in all AD patients using the Alzheimer’s Disease Assessment Scale – Cognition (ADAS-cog).

The researchers found that following administration of the antibody, the amount of beta amyloid in blood increased substantially after the antibody bound to the beta amyloid protein. A small amount of the antibody enters the CSF, and in the Alzheimer’s patients beta amyloid also increased in CSF, similarly bound to the antibody. For patients treated with 400 mg of the antibody, the amount of the type of beta amyloid primarily found in plaque (known as AB1-42) that appeared in the blood correlated with the amount of amyloid plaque in the brains based on IMPY scans (r=0.65, p=0.02). According to Siemers, this finding suggests that some of the beta amyloid protein present in plaque moves to blood after treatment with the antibody.

Certain other types of beta amyloid thought to be primarily or exclusively found in amyloid plaque are also increased in blood and CSF of study participants. The antibody produced no change in cognitive scores or in the total amount of amyloid plaque based on IMPY scans. Siemers said that this was expected in a study of this duration.

According to the researchers, brain imaging using MRI and CSF safety assessments showed no evidence of inflammation, bleeding or other side effects throughout the trial. No side effects were identified that appeared to be related to antibody treatment.

“We saw an increase in amyloid beta, which is thought to be bound to LY2062430, in both the blood and cerebrospinal fluid of study participants,” Siemers said. “Additionally, after treatment we found a correlation between beta amyloid in blood and the amount of amyloid plaque in brain as determined by IMPY imaging, as well as an increase in blood and CSF in certain types of beta amyloid found in plaques. These biomarker data suggest that amyloid plaques in the brain may begin to ‘dissolve’ after 12 weeks of treatment with this antibody. We’re now planning a Phase III clinical trial of this drug to be started in 2009.”

Antidementia Drugs Contribute to Longer Life in People with Alzheimer’s

Survival (life span) in people with Alzheimer’s is recognized to be shorter than what is expected in cognitively normal seniors and is recognized to be influenced by several factors including age, disease severity, general debility, and gender. Approved antidementia drugs have been shown help with the symptoms of Alzheimer’s but their influence on life span is not known.

At ICAD 2008, Susan Rountree, MD, of the Alzheimer’s Disease and Memory Disorders Center of Baylor College of Medicine in Houston, Texas, reported on a study of the persistent use of antidementia drugs and their influence on survival.

The researchers followed 641 people diagnosed with Alzheimer’s at an academic medical clinic between 1989 and 2005. These individuals had been on drug therapy over the course of their Alzheimer’s for variable amounts of time and the majority had used one or more of the commercially available antidementia drugs (donepezil, galantamine, rivastigmine, tacrine, or memantine).

Total years on medication was divided by the total years of disease symptoms to determine a persistency score for each individual. Participants were divided into four groups (1st, 2nd, 3rd, 4th quartiles) ranging from the lowest to highest persistency scores and the researchers compared life span among the groups after adjustment for a variety of factors generally recognized to influence survival. The 1st quartile took drug less than 33 percent of the time, 2nd quartile = 34-55 percent of the time, 3rd quartile = 56-70 percent of the time, and the 4th quartile = 71-99 percent of the time.

Over the entire course of the study, 12 percent of participants never took any antidementia drugs. Fifty-three (53) percent of the participants died.

The researchers found an inverse and statistically significant relationship between the overall risk of death and the persistency of drug use. Those in the lowest persistency group (1st quartile) were 2.4 times more likely to die than those in the highest persistency group (4th quartile). Those with intermediate drug exposure had increased risk of death of 2.2 times (2nd quartile) and 1.5 times (3rd quartile) compared to the most persistent users. More persistent therapy was associated with a longer median survival time; the median survival between the lowest quartile group and the most persistent users was 3.12 years.

“In our study, people with Alzheimer’s who took antidementia drugs more persistently lived longer than those who took the medications for shorter time intervals,” Rountree said. “In an earlier study involving this group, we reported that persistency of treatment was also associated with long term cognitive and functional benefits. Persistent drug therapy appears to help Alzheimer’s patients live longer and the mechanism may be related to overall improvement of cognition and function resulting from current symptomatic therapies.”

About ICAD 2008
The 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) is the largest gathering of international leaders in Alzheimer research and care ever convened. At ICAD 2008, more than 5,000 researchers from 60 countries will share groundbreaking information and resources on the cause, diagnosis, treatment and prevention of Alzheimer’s and related disorders. As a part of the Association’s research program, ICAD serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community. ICAD 2008 will be held in Chicago at McCormick Place, Lake Side Center from July 26–31.

About the Alzheimer’s Association
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer’s research, care and support. Our mission is to eliminate Alzheimer’s disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. For more information, visit http://www.alz.org.

* Jeffrey Cummings. “18-Month data from an open-label extension of a one-year controlled trial of dimebon in patient with mild-to-moderate Alzheimer’s disease.” (Funder: Medivation)
* Diamanto Tsakanikas. – “Effects of uninterrupted intravenous immunoglobulin treatment of Alzheimer’s disease for 9 months.” (Funder: Baxter International)
* Eric R. Siemers. – “Safety, tolerability and biomarker effects of an Abeta monoclonal antibody administered to patients with Alzheimer’s disease.” (Funder: Eli Lilly and Company)
* Susan Rountree. – “Persistent Antidementia Drug Treatment and Survival in an Alzheimer’s Disease Cohort.” (Funders: Forest Research Institute and The Cynthia and George Mitchell Foundation)

Contact:
Alzheimer’s Association
Media line: 312.335.4078
E-mail: media@alz.org
ICAD 2008 press room, July 27-31: 312.949.3253

Amazon.com Widgets

 

Diverse Approaches to Alzheimer’s Therapies Continue to Show Progress at ICAD

A lot of good and encouraging news continues to come out of this week’s Alzheimer’s Association International Conference on Alzheimer’s Disease 2008.

–18-Month Data from an Extension of a Pivotal Trial of Dimebon in Alzheimer’s

–First U.S. Double-Blind Phase II Clinical Trial of IVIg (Immunotherapy) in Alzheimer’s

–Phase II Immunotherapy Trial with LY2062430 in Mild to Moderate Alzheimer’s

–Antidementia Drugs Contribute to Longer Life in People with Alzheimer’s

Diverse Approaches to Alzheimer’s Therapies Continue to Show Progress at ICAD

Results from clinical trials of three potential Alzheimer’s therapies raise hope for new and better treatments of the disease, according to data reported today at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) in Chicago.

A related study showed that taking antidementia drugs appears to have a positive impact on extending lifespan in those with Alzheimer’s.

These reports included:

* Eighteen-month data from an open-label extension of a pivotal trial of Dimebon (Medivation) in mild to moderate Alzheimer’s.
* Nine-month data from an interim analysis of the first U.S. Phase II trial of intravenous immunoglobulin, or IVIg (Baxter), in Alzheimer’s.
* Results of a Phase II study of a monoclonal antibody (LY2062430, Lilly) in mild to moderate Alzheimer’s.
* Research suggesting that persistent antidementia drug use increases survival in people with Alzheimer’s.

“Therapies targeting amyloid in Alzheimer’s disease must continue to be thoroughly tested,” said William Thies, PhD, Alzheimer’s Association vice president for Medical and Scientific Relations. “At the same time, we know that Alzheimer’s is a complex disease and that better treatments and preventions will likely also be complex, so we must investigate every promising drug target looking eventually towards the possibility of a multi-strategy approach.”

18-Month Data from an Extension of a Pivotal Trial of Dimebon in Alzheimer’s

In a study recently reported, Dimebon (Medivation) improved cognition and memory, activities of daily living, and behavior in a one-year placebo-controlled trial of patients with mild to moderate Alzheimer’s. At ICAD 2008, Jeffrey L. Cummings, M.D., the Augustus S. Rose Professor of Neurology, and Professor of Psychiatry and Biobehavioral Sciences, at UCLA, and colleagues reported on an open-label extension of the trial to 18 months.

One hundred eighty-three (183) people with mild-to-moderate Alzheimer’s were initially randomized into a six-month placebo-controlled study of Dimebon. Patients completing six months of treatment were offered the opportunity to re-consent for an additional six months of controlled treatment in their originally randomized group, followed by an open-label extension (OLE). Data presented at ICAD 2008 include only the 104 OLE participants (54 Dimebon, 50 placebo). All were given Dimebon for the OLE, not placebo, at a dose of 20 mg three times per day. Ninety-two (92) (88.5%) patients enrolling into OLE completed six months of treatment.

Patients originally receiving Dimebon for 12 months who continued on Dimebon for an additional six months in the OLE phase had preservation of function close to their starting baselines on the key signs and symptoms of Alzheimer’s disease 18 months after starting the study. Patients originally on placebo for 12 months who were then crossed over to Dimebon on the OLE phase also stabilized across all key measures tested. Since these patients had declined over the previous 12 months while on placebo, they stabilized at a lower level of function than those treated with Dimebon for the full 18 months.

Dimebon was well-tolerated through 18 months. Adverse events that occurred more often with dimebon compared to placebo were dry mouth, sweating and depressed mood/sadness.

“People initially treated with placebo and then crossed over to Dimebon did not show the same level of benefit as those people who took Dimebon for the full 18 months,” Cummings said. “This emphasizes the benefit of earlier treatment, and suggests the possibility that Dimebon may slow of the progression of Alzheimer’s. However, open-label extensions are not that same as placebo-controlled trials, and extrapolation of the treatment results should be done with caution. Patients are being screened now for the Phase III clinical trials.”

“Dimebon appears to work through a mechanism of action that is distinct from currently marketed Alzheimer’s drugs. Dimebon improves impaired mitochondrial function. Mitochondria are the central energy source of all cells and impaired mitochondrial function may play a significant role in the loss of brain cell function in Alzheimer’s,” Cummings added.

First U.S. Double-Blind Phase II Clinical Trial of IVIg (Immunotherapy) in Alzheimer’s

IVIg is under investigation by Baxter International as a potential anti-amyloid immunotherapy for Alzheimer’s. It contains a broad spectrum of antibodies, and is currently indicated as a therapy for people with primary immunodeficiency disorders. IVIg contains antibodies that bind to the beta amyloid aggregates that are thought to be central to Alzheimer’s. In two previous open-label studies, patients with mild to moderate Alzheimer’s showed cognitive improvement when treated with IVIg for six months.

Diamanto Tsakanikas, PhD, Norman Relkin, MD, PhD, and colleagues at Well Cornell Medical College carried out a six-month Phase II double-blind, placebo-controlled study of IVIg for Alzheimer’s followed by a 12-month, rater-blinded extension study. At ICAD 2008, they reported an interim analysis of uninterrupted IVIg treatment for 9 months.

Twenty-four people with mild to moderate Alzheimer’s (MMSE 14-26) participated in the trial. For the first six months, eight participants received placebo and 16 received IVIg at four doses ranging from 0.2 grams IVIg per kilogram of body weight every two weeks to 0.8 grams IVIg per kilogram of body weight given once per month (four people each at the four different doses). After six months, all subjects were given IVIg with the raters blinded to dose. The primary outcome measures were two standard measures of cognition and the clinician’s observation of change (a seven point scale from “markedly improved”=+3 to “marked worsening”=-3), respectively the ADAS-cog and the ADCS-CGIC, which were administered at baseline and three-month intervals thereafter.

In the total group, the researchers found statistically significant differences favoring IVIg treatment on the CGIC at three, six and nine months. At nine months, the IVIg group averaged 1.5 points higher on the CGIC. On the ADAS-cog, scores favoring IVIg reached statistical significance at nine months. The average change in ADAS-Cog score at nine months favored IVIg treatment by 5.4 ADAS points. Uninterrupted IVIg treatment also produced sustained benefits relative to initial placebo treatment in activities of daily living.

When the results for each dose were analyzed individually, subjects receiving 0.4 grams of IVIg per kilogram of body weight given every two weeks improved over baseline on ADAS-Cog, ADCS-CGIC, and a measure of daily functioning. The researchers identified this as the best dose. None of the subjects given placebo showed comparable improvements.

Treatment-related adverse events that occurred at a greater frequency with IVIg treatment as compared to placebo were rash and a transient drop in blood count. In contrast, there were more behavioral disturbances in placebo-treated patients than those who received IVIg.

“While there were relatively small numbers of participants in this study, we were nonetheless able to demonstrate that people with Alzheimer’s who get uninterrupted treatment with IVIg for nine months have statistically significant and clinically relevant improvements on both cognitive and global clinical measures,” Tsakanikas said. “A large-scale, 18-month, multicenter Phase III clinical trial of IVIg in Alzheimer’s is now getting underway, sponsored by Baxter and the National Institutes of Health, that will test whether IVIg immunotherapy provides long-term benefits and has a disease-modifying effect.”

Phase II Immunotherapy Trial with LY2062430 in Mild to Moderate Alzheimer’s

Previous research has shown that antibodies that bind to beta amyloid can be given intravenously. By binding to beta amyloid and increasing the rate of its removal from the body, these antibody infusions may slow the progression of Alzheimer’s.

Eric Siemers, MD, Medical Director of the Alzheimer’s Disease Research Team at Eli Lilly and Company, and colleagues conducted a Phase II trial of a monoclonal antibody, known as LY2062430, that binds to the mid-domain of beta amyloid.

Fifty-two (52) people with mild to moderate Alzheimer’s and 16 volunteer subjects were studied. Alzheimer’s patients received 12 weekly infusions of placebo or antibody (100 mg every 4 weeks, 100 mg once per week, 400 mg every 4 weeks or 400 mg once per week). Volunteers received a single 100 mg dose of antibody. Safety assessments included brain imaging using magnetic resonance imaging (MRI) and examination of cerebrospinal fluid (CSF, a fluid normally present around the brain and spinal cord). In an optional sub-study, 24 Alzheimer’s patients and 13 volunteers underwent a type of brain imaging known as SPECT using a tracer (known as IMPY) that measures the amount of amyloid plaque present in the brain. Measures of symptom severity were obtained in all AD patients using the Alzheimer’s Disease Assessment Scale – Cognition (ADAS-cog).

The researchers found that following administration of the antibody, the amount of beta amyloid in blood increased substantially after the antibody bound to the beta amyloid protein. A small amount of the antibody enters the CSF, and in the Alzheimer’s patients beta amyloid also increased in CSF, similarly bound to the antibody. For patients treated with 400 mg of the antibody, the amount of the type of beta amyloid primarily found in plaque (known as AB1-42) that appeared in the blood correlated with the amount of amyloid plaque in the brains based on IMPY scans (r=0.65, p=0.02). According to Siemers, this finding suggests that some of the beta amyloid protein present in plaque moves to blood after treatment with the antibody.

Certain other types of beta amyloid thought to be primarily or exclusively found in amyloid plaque are also increased in blood and CSF of study participants. The antibody produced no change in cognitive scores or in the total amount of amyloid plaque based on IMPY scans. Siemers said that this was expected in a study of this duration.

According to the researchers, brain imaging using MRI and CSF safety assessments showed no evidence of inflammation, bleeding or other side effects throughout the trial. No side effects were identified that appeared to be related to antibody treatment.

“We saw an increase in amyloid beta, which is thought to be bound to LY2062430, in both the blood and cerebrospinal fluid of study participants,” Siemers said. “Additionally, after treatment we found a correlation between beta amyloid in blood and the amount of amyloid plaque in brain as determined by IMPY imaging, as well as an increase in blood and CSF in certain types of beta amyloid found in plaques. These biomarker data suggest that amyloid plaques in the brain may begin to ‘dissolve’ after 12 weeks of treatment with this antibody. We’re now planning a Phase III clinical trial of this drug to be started in 2009.”

Antidementia Drugs Contribute to Longer Life in People with Alzheimer’s

Survival (life span) in people with Alzheimer’s is recognized to be shorter than what is expected in cognitively normal seniors and is recognized to be influenced by several factors including age, disease severity, general debility, and gender. Approved antidementia drugs have been shown help with the symptoms of Alzheimer’s but their influence on life span is not known.

At ICAD 2008, Susan Rountree, MD, of the Alzheimer’s Disease and Memory Disorders Center of Baylor College of Medicine in Houston, Texas, reported on a study of the persistent use of antidementia drugs and their influence on survival.

The researchers followed 641 people diagnosed with Alzheimer’s at an academic medical clinic between 1989 and 2005. These individuals had been on drug therapy over the course of their Alzheimer’s for variable amounts of time and the majority had used one or more of the commercially available antidementia drugs (donepezil, galantamine, rivastigmine, tacrine, or memantine).

Total years on medication was divided by the total years of disease symptoms to determine a persistency score for each individual. Participants were divided into four groups (1st, 2nd, 3rd, 4th quartiles) ranging from the lowest to highest persistency scores and the researchers compared life span among the groups after adjustment for a variety of factors generally recognized to influence survival. The 1st quartile took drug less than 33 percent of the time, 2nd quartile = 34-55 percent of the time, 3rd quartile = 56-70 percent of the time, and the 4th quartile = 71-99 percent of the time.

Over the entire course of the study, 12 percent of participants never took any antidementia drugs. Fifty-three (53) percent of the participants died.

The researchers found an inverse and statistically significant relationship between the overall risk of death and the persistency of drug use. Those in the lowest persistency group (1st quartile) were 2.4 times more likely to die than those in the highest persistency group (4th quartile). Those with intermediate drug exposure had increased risk of death of 2.2 times (2nd quartile) and 1.5 times (3rd quartile) compared to the most persistent users. More persistent therapy was associated with a longer median survival time; the median survival between the lowest quartile group and the most persistent users was 3.12 years.

“In our study, people with Alzheimer’s who took antidementia drugs more persistently lived longer than those who took the medications for shorter time intervals,” Rountree said. “In an earlier study involving this group, we reported that persistency of treatment was also associated with long term cognitive and functional benefits. Persistent drug therapy appears to help Alzheimer’s patients live longer and the mechanism may be related to overall improvement of cognition and function resulting from current symptomatic therapies.”

About ICAD 2008
The 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) is the largest gathering of international leaders in Alzheimer research and care ever convened. At ICAD 2008, more than 5,000 researchers from 60 countries will share groundbreaking information and resources on the cause, diagnosis, treatment and prevention of Alzheimer’s and related disorders. As a part of the Association’s research program, ICAD serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community. ICAD 2008 will be held in Chicago at McCormick Place, Lake Side Center from July 26–31.

About the Alzheimer’s Association
The Alzheimer’s Association is the leading voluntary health organization in Alzheimer’s research, care and support. Our mission is to eliminate Alzheimer’s disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. For more information, visit http://www.alz.org.

* Jeffrey Cummings. “18-Month data from an open-label extension of a one-year controlled trial of dimebon in patient with mild-to-moderate Alzheimer’s disease.” (Funder: Medivation)
* Diamanto Tsakanikas. – “Effects of uninterrupted intravenous immunoglobulin treatment of Alzheimer’s disease for 9 months.” (Funder: Baxter International)
* Eric R. Siemers. – “Safety, tolerability and biomarker effects of an Abeta monoclonal antibody administered to patients with Alzheimer’s disease.” (Funder: Eli Lilly and Company)
* Susan Rountree. – “Persistent Antidementia Drug Treatment and Survival in an Alzheimer’s Disease Cohort.” (Funders: Forest Research Institute and The Cynthia and George Mitchell Foundation)

Contact:
Alzheimer’s Association
Media line: 312.335.4078
E-mail: media@alz.org
ICAD 2008 press room, July 27-31: 312.949.3253

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Detection and Diagnosis of Alzheimer’s Disease

Dr. Dean Reports: “As the numbers grow so does the likelihood you will face Alzheimer’s in your life. Discover what researchers are learning about this mind robbing condition.”

 

I broke down on live TV over my dad’s Alzheimer’s

The article on the following page is important and uplifting. I remember during those first few months of caring for my mother how sad and frustrated I was feeling. Then, I met a young couple in the gym that had gone through the entire experience from beginning to end with their mother who suffered and died from Alzheimer’s disease.

I remember as I related my own experience to them how they shook their heads up and down indicating they knew exactly what I was experiencing. They recounted their similar experiences and always with a smile on their face. I remember feeling immediately “I was not alone”. The feelings of frustration, fear and sadness dissipated and I now find myself thinking, “I can do it”.

‘Alzheimer’s is such a cruel disease because that vibrant person is taken away from you. They are still there in body but it’s like the shell. The person you remember has gone.’


I broke down on live TV over my dad’s Alzheimer’s.

Driving across Dartmoor with her parents one sunny afternoon in 1995, Ruth Langsford’s father Dennis observed a beautiful barn conversion and said he had admired it earlier in the day.

When Ruth irritably pointed out that she had taken a different road on the outward journey, he insisted she was wrong. ‘He got quite cross and we had a discussion that almost turned into a row, while Mum kept quiet in the back of the car. He was adamant that he was right,’ Ruth recalls.

‘Then we saw a man leaning over a five-bar gate and Dad said, “I remember that man. He waved at us.” At that moment I thought, oh my God, he’s gone mad. What’s the matter with him?

‘When I got home I even got a map out to show him the way we had gone. But he still wouldn’t have it. That evening I said to my Mum I thought something wasn’t right.’

While the incident may have been minor, it disturbed Ruth, a presenter on ITV1’s This Morning and long-term partner of Eamonn Holmes of Sky Breakfast News. She believes now it was the first real indicator that her father was in the early stages of Alzheimer’s.

The condition, thought to affect half the 700,000 dementia patients in the UK, begins with short-term memory loss, clumsiness and problems with communication, and gradually robs sufferers of their faculties, leaving them unable to remember close family or perform even the simplest tasks unaided.

Today, Dennis, 81, is in the advanced stages of the illness, and is in full-time residential care in Cornwall.

And as she speaks about her father’s illness, Ruth, 48, known for her warmth and humour on the This Morning sofa – regularly co-hosting the Friday edition with Phillip Schofield – often loses her composure.

‘I think he still knows my Mum – his eyes always light up when she walks in the room, but sometimes I’m not sure if he knows me anymore,’ says Ruth, her eyes filling with tears.

‘It is very hard. I adore my Dad. The only way I can describe it is that you are grieving for a loved one while they are still alive. It is the saddest kind of bereavement.’

She adds: ‘He was the most clever, funny, vibrant man. He played rugby, scrambled motorbikes and flew gliders. He was handsome, the best storyteller ever and the life and soul of the party.

‘He was a fantastic father and, in my opinion, a New Man ahead of his time. He taught my sister Julia and me to fish and sail. We had such good times and love him to bits.

‘Alzheimer’s is such a cruel disease because that vibrant person is taken away from you. They are still there in body but it’s like the shell. The person you remember has gone.’

Her mother Joan admitted that the incident in the car was not the first worrying episode.

When his camera had gone missing, it turned out he had left it in the garden shed. Slippers turned up in the fridge.

She had voiced her concerns to her GP, tentatively suggesting Alzheimer’s, only to be told that it was probably forgetfulness and old age.

Despite the alarm bells, Ruth reveals it took several years for her family to get the truth that he was suffering from dementia, and by the time he was formally diagnosed 11 years ago, the disease of the brain was so advanced that doctors could do little to halt its progression with drugs.

‘My father was a former Army man – meticulous and tidy,’ says Ruth.

‘I knew it wasn’t right. When I was a child, if I borrowed the Sellotape, it had to go back in the drawer in exactly the right place.’

Her father’s vagueness was also a tricky subject to broach as he was ‘a fiercely proud, independent man who disliked any fuss’.

In the military for 30 years, rising through the ranks to warrant officer, Dennis moved his family to various Army bases abroad.

Ruth was born in Singapore and her sister Julia, now 50, and a landscape gardener, was born in Germany. Her parents have been married 54 years.

‘They met at a dance when Mum was in the Wrens. My dad was a young soldier and she was a gorgeous redhead.

‘Apparently, when he saw her on the other side of the room he said to one of his friends, “I’m going to marry that girl.”‘ After he left the Army in 1972 the couple moved to Cornwall where Dennis was born. They set up home in the village of Millbrook on the beautiful Rame Peninsula, where he worked in the education department for Devon County Council.

‘I don’t think he was ever as happy as he was in the Army. He eventually retired when he was 65. That’s another thing that is so sad. My parents had so many plans for their retirement. Dad had lots of hobbies and interests – he loved photography, pottery and music.’

Until this point, Dennis had been fit and healthy. He had a small heart attack in 1996 but had recovered after a pace-maker was fitted.

As his Alzheimer’s progressed, Joan’s fears intensified.

‘Often Mum would discuss the latest bizarre thing he’d done, but because we weren’t living with it, we’d say, “I’m sure it’s nothing.” It was only when I spent time with him that I saw what she meant.’

The turning point was in 1997 when the couple visited London and Ruth took them to Wimbledon Village for afternoon tea. Once again, Dennis swore blind he had been to the café recently.

‘But he was clearly talking about when we were children. I felt sick inside. And for the first time I didn’t argue with him. Mum and I just said: “Really?” I knew something was seriously wrong.’

When she returned home, Joan, 77, went to the GP alone at Ruth’s insistence. The doctor suggested a Mini Mental State Examination (MMSE), a series of simple questions to test mental ability relating to dementia.

The test – carried out at home by an old-age psychiatrist – confirmed the family’s fears, but they agreed not to tell him.

‘I still question whether that was the right thing to do, but every family has to deal with it their own way,’ Ruth says. ‘But Dad did get to the stage where he was aware things weren’t quite right.’

Some days, Ruth feels angry that the disease has robbed her five-year-old son, Jack, of a loving grandfather. ‘I take Jack to the park and see grandparents playing with their grandchildren – it breaks my heart.’

Eamonn, 48, whom she has been with for 12 years, has been a great support. She says: ‘He loves my Dad. The two of them would always tease me. Eamonn’s a great family man. He lost his own father when he was only in his 60s and was devastated.

‘I wish we had been given more information. He’s never been put on medication and there are drugs available that can slow Alzheimer’s progress. Now I wonder why we didn’t ask, but it’s too late.’

Despite the diagnosis, the implications of day-to-day caring for a sufferer didn’t sink in. Ruth regularly visited Cornwall from her home in Surrey, but realises her mum protected her from her physical struggle.

Dennis would often close all the curtains in the middle of the day, or Joan would wake to find him fully dressed at four in the morning.

‘In a way it’s like being a new mother with a baby,’ says Ruth.

‘Fortunately, he’s never been physically aggressive, as some dementia sufferers can be. But he was verbally aggressive a few times and that really upset her. Much as he was quite fiery, he was never cruel before.

‘Suddenly he would say quite nasty things to her that really upset her. But that wasn’t Dad. He adored Mum.’

A health worker visited Joan regularly, and in recent years Dennis was in a respite home for a week at a time to give her a break.

The final straw was when Ruth bumped into a friend of her mother. ‘She said innocently, “We’ve been worried about your Mum, she looks so tired.”

‘I felt like the worst daughter in the world. She was trying to protect us and be strong for the man she loved and adored.

‘My sister and I are really close but we felt guilty that we didn’t have the full picture. We discovered Dad had fallen over a few times. We were worried about her getting ill.’

Eighteen months ago Dennis moved full-time into a local care home, where he seems content, and Joan visits regularly.

‘I was distraught but we had to admit defeat. It’s hardest for my mum. For her life partner, her lover and friend to be getting to the stage now where he doesn’t recognise us, is just devastating,’ says Ruth.

Ruth had never spoken publicly about her father’s illness until last year, during a studio discussion on This Morning, when she broke down on air talking to a caller about Alzheimer’s.

‘Thankfully, I was co-presenting with Eamonn.

He squeezed my back to comfort me and he made a joke to break the ice.’

Ruth was deluged by emails and letters from viewers with similar stories. The Alzheimer’s Society approached her initially to offer support, then to ask her to be an ambassador for the charity.

‘Now we think the disease started five years before we were told Dad had Alzheimer’s. Early diagnosis is key – for treatment and to prepare you and your family emotionally.’

By 2025 there will be one million dementia sufferers in the UK according to last year’s Dementia UK report prepared by the LSE and King’s College, London.

One in three people over 65 will die with dementia, yet up to two thirds will never receive a formal diagnosis. Early diagnosis is crucial, but those with dementia and their families often say that finding out about the problem was the start of getting back in control.

‘I do feel guilty that I didn’t pursue a diagnosis earlier on,’ says Ruth. ‘The truth is that I didn’t want him to be ill. The thought of it frightened me and I was running away from it. I didn’t want my dad to get old and doddery.

‘I miss talking to him, I miss going to him for advice. I miss Christmas shopping together and going to the pub together or sneaking off down the garden for a crafty fag. He was my mate as well as my dad.’

Ruth is keen to promote a new Alzheimer’s Society initiative, Worried About Your Memory? (WAYM?), encouraging individuals and families to seek help when they notice those vital early signs of forgetfulness.

‘GPs are busy and if episodes are sporadic, then it’s understandable not to take it too seriously,’ says Ruth.

‘We all forget things but if you are genuinely worried about your memory, don’t think, “It’s just me being dotty”. Go and see your doctor.’

This weekend, Ruth, who will be appearing on This Morning from July 21 until the end of August, will have made the 500-mile round trip with her sister Julia to Cornwall to visit Dennis on Father’s Day, with a kiss, a card and his favourite Mars bars and Maltesers.

‘He seems in a good place. My theory is that he is back in the Army, which he loved.

‘He says the same thing over and over again: “They’re a lovely bunch of lads in here.” And that is all he says. Over and over again. He’s as happy as Larry.’

• For information on the Worried About Your Memory? campaign, visit http://www.alzheimers.org.uk or call the Alzheimer’s Society Dementia Helpline, 0845 300 0336.

10 things to know about Alzheimer’s

• German psychiatrist Alois Alzheimer identified the first case in 1906. It was officially recognised by the medical profession in 1910.

• Alzheimer’s is the most frequent type of dementia in the elderly, affecting almost half the 700,000 patients with dementia in the UK.

• About two per cent of those aged 65 show signs of the disease. Every five years after the age of 65, the probability of developing the disease doubles. Some ten per cent of Alzheimer’s cases are inherited.

• It is diagnosed by using brain scans, patient history and observing behaviour.

• A shrinking vocabulary, problems talking and short-term memory loss are normally the first signs. Difficulty writing and dressing are also common.

• In the late stages, language is lost and patients cannot perform even simple tasks. Finally deterioration of muscle leads to sufferers becoming bedridden.

• Average life expectancy is about seven years after diagnosis, and less than seven per cent of patients live more than 14 years.

• There is no cure, but a type of drug called cholinesterase inhibitors can slow down progression in those with moderate Alzheimer’s.

• Anti-depressants are prescribed to help treat the depression that can be associated with the disease.

• Sufferers have included US President Ronald Reagan, British Prime Minister Harold Wilson and writer Iris Murdoch.

 
 
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