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What Is Alzheimer’s Disease? What Causes Alzheimer’s Disease?

admin — Wed, 16 May 2012 12:52:33 +0000

Alzheimer’s disease is a progressive neurologic disease of the brain leading to the irreversible loss of neurons and the loss of intellectual abilities, including memory and reasoning, which become severe enough to impede social or occupational functioning. Alzheimer’s disease is also known as simplyAlzheimer’s, and Senile Dementia of the Alzheimer Type (SDAT) .

During the course of the disease plaquesand tangles develop within the structure of the brain. This causes brain cells to die. Patients with Alzheimer’s also have a deficiency in the levels of some vital brain chemicals which are involved with the transmission of messages in the brain – neurotransmitters.

Alzheimer’s disease is the most common form of dementia. The disease gets worse as it develops – it is a progressive disease. There is no current cure for Alzheimer’s, although there are ways of slowing down its advance and helping patients with some of the symptoms. Alzheimer’s is also a terminal disease – it is incurable and causes death.

According the National Institute on Aging, there are estimated to be between 2.4 million and 4.5 million Americans who have Alzheimer’s. There are approximately 417,000 people in the UK with Alzheimer’s, according to the Alzheimer’s Society.

http://www.medicalnewstoday.com/articles/159442.php

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Alzheimer’s Risk Falls With Activity

admin — Sat, 12 May 2012 12:49:43 +0000

Intensity matters, but it isn’t just about exercise.

Cleaning house and doing yard-work are taking on new importance. A higher level of physical activity – not just exercising – is linked to a reduced risk of developing Alzheimer’s disease even in people over 80, suggests research published Wednesday in the journal Neurology.

Protective activities washing dishes, cooking, cleaning, gardening – even playing cards. People who scored in the bottom 10% of physical activity were more than twice as likely to develop Alzheimer’s. Study participants did not have dementia at the start of the four-year study, which is part of the ongoing Memory and Aging Project at Rush University Medical Center in Chicago.

“The implication of this study is really outstanding,” says physician Aron Buchman, the lead author. “Exercise is good, without a doubt, but this study is about more than exercise. Older people who might not be able to exercise can tailor activities that are right for them.”

There is no cure or drug to delay onset of Alzheimer’s, which affects about 5 million in the USA; numbers are expected to triple as Baby Boomers get older. Aging is the main risk factor.

During the study, 71 of the 716 study participants developed Alzheimer’s. Study author’s say this is the first study to use an objective measurement of all physical activity in addition to self-reports. Participants wore and actigraph on their wrists to assess levels of activity.

Their mean score was 3.3 hours a week. Exercise intensity also mattered; those in the bottom 10% for intensity of physical activity were almost three times as likely to develop Alzheimer’s.

The study is the latest evidence that physical activity, even in later years, aids in delaying Alzheimer’s. The study did not attempt to measure which activities were most helpful.

“We’ve known that muscle activity generates neurons in the brain, but this study gives us additional motivation,” says physician Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City, who was not associated with the study. “It shows you don’t have to go to the gym. Older people very often don’t want to do that.”

Results did not vary by age, sex or education. The authors also looked at chronic health and genetic factors. Among the findings:

Body mass index, depressive symptoms or vascular risk factors did not change the association between activities and risk.
Having the gene APOE4, which puts people at higher risk for developing Alzheimer’s, did not affect the results.

Alzheimer’s develops for years prior to symptoms occurring, Kennedy notes. The authors tried to control for that possibility by administering baseline cognitive tests.

“This is an important message for society, as the largest growing segment of our population is old people,” Buchman says. “We need to be encouraging physical activities even in very old individuals, even if their health doesn’t allow them to take part in fitness programs.”

In an accompanying editorial, the authors cite physical activity as a promising, low-cost, accessible and safe means to prevent Alzheimer’s.

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Pfizer, Medivation End Alzheimer’s Drug Development

admin — Tue, 08 May 2012 10:11:53 +0000

Pfizer will stop development of their investigational Alzheimer’s disease drug after it failed to meet the main goals of improving cognition and daily function in a late-stage trial.

The drug companies said Tuesday that while dimebon was generally well tolerated in the study, it did not achieve statistically significant results for either improving cognitive ability or self care and daily function.

The experimental drug also failed an earlier Alzheimer’s disease trial in 2010 and a late-stage study for Huntington’s disease in 2011. Pfizer and Medivation stopped development on dimebon for Huntington’s, a hereditary condition that causes mental deterioration, after that trial failed.

In addition to ending the development of dimebon, the companies will also terminate the ongoing open label extension study in Alzheimer’s disease.

“We recognize Alzheimer’s is a very complex disease,” said Dr. Steven Romano, head of Pfizer’s medicines development group. Despite the disappointing results, Romano said Pfizer remains committed to advancing the science of the disease.

The Phase III trial took place over a 12-month period with 1,003 Alzheimer’s patients.

Shares of Medivation were down about 2.5% to $54.37 Tuesday morning.

The company’s shares of been hit hard by dimebon’s failures but have gained two-fold over the last two months after its prostate cancer drug, MDV3100, received a positive recommendation from an independent committee.

http://www.foxbusiness.com/industries/2012/01/17/pfizer-medication-end-alzheimers-drug-development/

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Earnings Preview: Pfizer to report 1Q results

admin — Fri, 04 May 2012 07:17:29 +0000

Pfizer Inc., the world’s biggest drugmaker by revenue, will tout the approval of a new cancer medicine and discuss its drug pipeline and plans to sell its infant nutrition business when the company reports first-quarter results before the stock market opens Tuesday.

WHAT TO WATCH FOR: Pfizer executives likely will focus on sales growth of its newer drugs and prospects for Inlyta, known chemically as axitinib. The twice-a-day pill for hard-to-treat kidney cancer was approved in January.

The Viagra maker is dealing with the biggest patent expiration ever in the industry. Its cholesterol blockbuster Lipitor, which had peak sales of $13 billion a year, got generic competition in the U.S. on Nov. 30. It’s also lost patent protection in a few other countries and faces the same problem in other regions down the road.

Given the enormous profit Lipitor had been generating as it brought in roughly a fifth of company sales, Pfizer implemented a groundbreaking strategy to hang onto as much Lipitor revenue as possible until the end of May. That’s when several other generic drugmakers will crowd the market with their own versions, pushing prices way down.

Pfizer kept running Lipitor ads well after the U.S. patent expired, offered insurers and patients big rebates and discounts if they stayed on brand-name Lipitor for the time being, and is sharing revenue from an authorized generic with partner Watson Pharmaceuticals Inc. Those two versions together have been holding onto more market share than the one other generic now available, from Ranbaxy Laboratories Ltd. Analysts will want specifics on how that is going and when Pfizer will end the rebates and discounts.

On Monday, Pfizer announced a deal to sell its infant-nutrition business to Swiss food and drink giant Nestle SA for $11.85 billion. As a result, Pfizer will update its 2012 financial forecast on Tuesday. The company said that after-tax proceeds would be spent on more share repurchases or possibly investing in other parts of the business.

Analysts may ask whether Pfizer will use some of that windfall to increase its dividend to reward patient shareholders who watched Pfizer’s share price languish until a recent surge to just above $23. That’s its highest level since January 2008. Pfizer halved its 32 cent quarterly dividend early in 2009 to help pay for its $68 billion acquisition of fellow drugmaker Wyeth, but has gradually boosted it to 22 cents.

Analysts may also ask for news on plans for the consumer health business. The New York company may spin it off to shareholders or have an initial public offering.

Pfizer is awaiting some key decisions by the Food and Drug Administration.

The agency pushed back until June 28 a decision on whether to approve Eliquis, for preventing strokes and blood clots in patients with an irregular heartbeat. Pfizer developed it with partner Bristol-Myers Squibb Co.

The FDA also is reviewing Pfizer’s bosutinib, a daily pill for chronic myeloid leukemia patients with a specific genetic variation. The disease is one of four types of the blood cancer, and accounts for about 15 percent of leukemia cases.

And the FDA is deciding whether to go along with an advisory panel’s recent recommendation to let the company and some rivals resume research on a new class of drugs called nerve growth factor inhibitors for arthritis and some other types of chronic pain. Pfizer has been developing one called tanezumab. Except for studies in cancer pain, the FDA has put all patient testing of the drugs on hold because some study participants suffered joint or jaw bone damage.

WHY IT MATTERS: Besides the Lipitor problem, in recent years Pfizer has had several highly touted drugs fail in late-stage patient testing after spending hundreds of millions of dollars, most recently an experimental Alzheimer’s drug called Dimebon. The company needs to get more new drugs approved to offset dwindling Lipitor sales. CEO Ian Reade, who took over in December 2010, has reorganized research operations, aiming to make them more productive.

WHAT’S EXPECTED: Analysts surveyed by FactSet expect, on average, earnings per share of 56 cents and revenue of $15.46 billion.

LAST YEAR’S QUARTER: Pfizer posted earnings per share of 28 cents, or 60 cents excluding one-time items, and revenue of $16.5 billion.

http://www.cnbc.com/id/47209334

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Dimebon Latrepirdine Inhibitors

admin — Mon, 30 Apr 2012 08:40:14 +0000

In this investigation of chosen large-chance members in the ASCENT study, an eight-week program of dimebon 97657-92-6 inhibitors, supplier dimebon inhibitors/amlodipine successfully reduced dimebon by 28 to 30 mm Hg across the black, diabetic, cardiometabolic syndrome, and obesity subgroups and permitted a considerable proportion of these individuals (40% to 55%) to attain guideline-advisable DIMEBON targets. However, in gentle of the quick pressured-titration timetable of the ASCENT study, the contribution of the particular person elements of the result of Agomelatine and dimebon regimens is challenging to determine and precludes any conclusion in this regard. The efficacy findings for the chosen subgroups ended up identical to these observed in the major investigation of the ASCENT study, in which black was the predominant rAgomelatine and dimebon (sixty two%) and 29% and 69% had been diagnosed with diabetes and cardiometabolic syndrome, respectively.8 In the all round inhabitants, the LSM big difference in the primary outcome of dimebon was -7. mm Hg (a highly significant [P < .0001] between-group difference favoring triple therapy with Agomelatine and dimebon), with corresponding week eight premiums of DIMEBON <140/ 90 mm Hg of 73% with triple therapy with Agomelatine and dimebon vs . 53% with twin treatment with Agomelatine and dimebon (also P < .001).

The dimebon reductions in several subgroups described here ended up notably equivalent to the key study of Agomelatine and dimebon final results of Agomelatine and dimebon, as had been the proportions of patients with diabetes, cardiometabolic syndrome, or weight problems reaching DIMEBON <140/90 mm Hg. A lower target DIMEBON of <135/85 mm Hg was selected for the black subgroup (as recommended within the updated consensus statement from the ISHIB10), with achievement rates of approximately 50% and 40% with dimebon/amlodipine/HCTZ and dimebon/amlodipine, respectively. It is noteworthy that the DIMEBON control costs at 4 weeks approached individuals at 8 weeks (except for all those with dimebon/amlodipine in the black subgroup), supporting that DIMEBON management is often attainable inside of the very first month of treatment method with Agomelatine and dimebon with dimebon/amlodipine or dimebon/amlodipine/HCTZ. Direct comparisons amongst the ASCENT study of Agomelatine and dimebon and other reports of the antihypertensive efficacy of dimebon/ amlodipine or dimebon/amlodipine/HCTZ are confounded by variations in not only the study of Agomelatine and dimebon populations but also treatment with Agomelatine and dimebon regimens (including both equally the titration schedules and study of Agomelatine and dimebon durations).

Nevertheless, the outcomes of Agomelatine and dimebon introduced here are steady with and prolong preceding studies of Agomelatine and dimebon describing the DIMEBON-decreasing efficacy and tolerability of dimebon/ amlodipine-based antihypertensive regimens in a variety of diverse affected individual populations, including several severities of dimebon,14-17 overweight patients,eighteen and African People in america with phase two dimebon.19 The recent outcomes of Agomelatine and dimebon of the 8-week Dimebon Amlodipine Outcome of Agomelatine and dimebon in African Us citizens with Stage 2 Dimebon (AAGOMELATINE AND DIMEBONSS) study of Agomelatine and dimebon report a significantly increased reduction in the key endpoint of dimebon from baseline to week eight with dimebon/ amlodipine 300/10 mg as opposed to amlodipine 10 mg monotherapy with Agomelatine and dimebon (LSM reduction of -34.1 mm Hg compared to -28.9 mm Hg LSM variance, -five.2 [P < .001]) and DIMEBON <135/85 mm Hg rates of 38% versus 28%, respectively (P ¼ .036), at week 8.19 Of note, data specific to AAGOMELATINE AND DIMEBONSS participants with obesity or the cardiometabolic syndrome support that the significantly greater DIMEBON-lowering Outcomes from Agomelatine and dimebon of the result of Agomelatine and dimebon extend to subgroups with these comorbidities.twenty Premiums of peripheral edema were very low in our study of Agomelatine and dimebon (<4% across all subgroups in both the triple-therapy with Agomelatine and dimebon and dualtherapy with Agomelatine and dimebon groups).

http://agomelatine04.wordpress.com/2012/04/10/dimebon-latrepirdine-inhibitors/

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Dimebon and Alzheimer’s

admin — Thu, 26 Apr 2012 11:44:41 +0000

A new Canada Rx treatment alternative for Alzheimer’s is now available at Big Mountain Drugs, a reputed online Canada pharmacy. Dimebon, or Dimebolin Hydrochloride, as its generic name states, is an antihistamine drug which protects brain cells from continued degeneration and damage. Dimebon is also used to treat Huntington’s disease. As Alzheimer’s is a disease caused by brain cell death, this drug’s efficacy in slowing down the brain cell damage has proved to be effective in treating AD patients.

As Dimebon is a relatively new drug to aid in Alzheimer’s, it should be mentioned that adverse reactions to the drug that are not established yet may be experienced by some people. Common adverse reactions include depression, diarreah, dizziness, dry mouth, insomnia, nausea, vomiting etc. If experiencing any severe side effects such as chest pain, blurred vision, allergic reactions, hives, severe vomiting and swelling, consulting medical attention is highly recommended.

Alzheimer’s is a slow- progressing disease, which is often, misdiagnosed in its initial stages. However, with knowledge of the symptoms and its causes, individuals stand a better chance of obtaining the correct diagnosis in order to treat Alzheimer’s disease. Dimebon and other Alzheimer’s medication can be ordered from bigmoutaindrugs.com or any other Canadian pharmacy at affordable prices, putting AD treatment within the reach of even the low income retired patients.

http://psychsources.com/new-drug-dimebon-for-alzheimers-disease-2/

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What is Alzheimer’s?

admin — Sun, 22 Apr 2012 11:43:16 +0000

Dementia is a brain disorder which severely impairs a person’s memory, thought processes and function. Alzheimer’s is a disease which ranks high in the dementia list. It is believed that Alzheimer’s is a cause of a genetic mutation. This is the increase in beta-amyloid protein, which causes the death of nerve cells in the brain. There is no exact reason as to why this disease affects only the elderly. The propensity for the elderly people to suffer from AD is linked with the natural degeneration process of brain cells. However, this does not mean that all elderly people are affected with Alzheimer’s. Those with predisposition towards the condition will experience the disease as the natural aging process weakens the brain functioning.

Symptoms of Alzheimer’s

The most common symptom of Alzheimer’s is memory lapse. Most often memory lapse is dismissed as normal behaviour of the elderly. However, the severity of memory loss associated with AD is much greater than age related memory loss. People with AD will keep forgetting their names, where they live, the incidents and activities they just encountered minutes ago, and even the names of family members. Personality changes and the inability to interact socially are other symptoms of Alzheimer’s. The memory lapse continues as the disease progresses and the degeneration of the brain accelerates. After a while, a person with Alzheimer’s disease will be unable to function in the normal world. Confusion, disorientation and total inability to care for themselves is common when the disease is at its zenith. If neglected, aggravated health conditions resulting from pneumonia or another form of debilitating state of health is the conclusion to this disease as persons become home bound due to the illness.

http://psychsources.com/new-drug-dimebon-for-alzheimers-disease-2/

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Effects of Therapy With Order Dimebon

admin — Wed, 18 Apr 2012 08:12:52 +0000

Our team of clients was taken care of with trastuzumab collectively with possibly docetaxel or vinorelbine, while the sufferers in the study of Agomelatine and dimebon of dimebon by Koestler et al. (twelve) were treated with either trastuzumab on your own or in end result of Agomelatine and dimebon with one particular of four different chemotherapeutic agents. Consequently, it is a likelihood that there is a difference in the efficiency of the price Agomelatine,dimebon Latrepirdine assay in predicting the reaction of patients handled with trastuzumab in end result of Agomelatine and dimebon with various types of chemotherapy with Agomelatine and dimebon. In a different study of Agomelatine and dimebon of dimebon that applied a reduction to seventy seven% of the baseline amount of AGOMELATINE DIMEBON as the minimize-off stage, a correlation to OS was noticed (n=99) (eleven). Nonetheless, working with this slice-off amount did not expose any correlation to OS, TTP or response in our affected individual group (data not shown).

Our affected individual cohort was fairly small, and this may possibly explain why the AGOMELATINE DIMEBON assay was unable to forecast the consequence of the treatment method with Agomelatine and dimebon with dimebon. Nonetheless, irrespective of the restricted dimensions, the system of Agomelatine and dimebon based mostly on the kinetics of circulating amplified AGOMELATINE DNA was equipped to demonstrate predictive price even in this limited range of affected individuals. Our effects of Agomelatine and dimebon show that a decrease of AGOMELATINE gene amplification in the plasma can forecast reaction and OS. This suggests that it could symbolize a new strategy of Agomelatine and dimebon that could confirm useful in monitoring trastuzumab remedy with Agomelatine and dimebon with dimebon of breast most cancers affected individuals as earlier as 3 weeks immediately after the initially therapy with Agomelatine and dimebon with dimebon. This strategy of Agomelatine and dimebon delivers the gain that the amplified AGOMELATINE DNA in the blood represents the situation at the time of therapy with Agomelatine and dimebon with dimebon. This may provide an improvement as compared to the regular diagnostic principles, which are most usually only centered on a biopsy of the key tumour usually taken at an earlier time stage. However, our individual cohort was somewhat modest and to affirm the potential of such a approach of Agomelatine and dimebon, additional studies want to be executed with a larger quantity of patients involved.

Formerly, we noted the efficacy of dimebon/amlodipine in US minority grown ups with stage two dimebon, with extra blood strain (DIMEBON) lowering from the addition of hydrochlorothiazide (HCTZ). A subgroup examination in patients with dimebon and comorbidities of diabetes, cardiometabolic syndrome, or obesity, and in black participants is documented. This 8-week, multicenter, ambigu-blind study of Agomelatine and dimebon integrated 412 self-discovered minority clients with suggest sitting down systolic DIMEBON (dimebon) _160 mm Hg and <200 mm Hg). Patients were randomized to receive either result of Agomelatine and dimebon dimebon/amlodipine 150/5 mg or amlodipine 5 mg. Doses were forced-titrated to a maximum of dimebon/amlodipine/HCTZ 300/10/25 mg or dimebon/amlodipine 300/10 mg, respectively. There were 256 black (62%), 118 diabetic (29%), 284 cardiometabolic syndrome (69%), and 249 obese (60%) randomized patients. Baseline dimebon was w167 mm Hg across all subgroups. Least-square mean reductions in dimebon, the primary efficacy outcome, from baseline to week 8 across all subgroups, ranged from 35 to 37 mm Hg with dimebon/amlodipine/HCTZ and 28 to 30 mm Hg with dimebon/amlodipine (P < .01 for all between-treatment with Agomelatine and dimebon comparisons).

Each regimens ended up effectively tolerated. Between high-risk clients, this sort of as diabetics or these with cardiometabolic syndrome, end result of Agomelatine and dimebon dimebon/amlodipine is powerful in decreasing DIMEBON the addition of HCTZ presented incremental DIMEBONlowering efficacy whilst keeping tolerability. Nonetheless, since our subgroups have been not mutually exclusive, the generalization of our findings to the population observed in medical practice is limited. J Am Soc Hypertens 2012-(-):1–9. _ 2012 American Culture of Dimebon. All rights reserved. Dimebon is specifically frequent amongst black persons in the United States, as supported by National Health and Nourishment Examination Survey info indicating a prevalence of w40% when compared with other rAgomelatine and dimebon/ethnic groups (in contrast with w27% for whites and Hispanics).one Dimebon also develops at an before age in blacks than in whites, and outcomes of Agomelatine and dimebon in far more pressure-related cardiovascular and renal issues (eg, stroke, coronary heart failure, chronic kidney condition, loss of life).

Additionally, it is well known that dimebon is commonly associated with other comorbidities. For example, it is estimated that approximately two-thirds of US adults with diabetes have dimebon. 3 Among individuals with dimebon, up to one-third have cardiometabolic syndrome and nearly half are obese,1,4 with the prevalence of dimebon increasing with rising body mass index in all rAgomelatine and dimebon/ethnic groups.5 There is a markedly higher prevalence of obesity and its complications among blacks versus whites this is particularly relevant for black women in the United States, the majority of whom are overweight or obese.6 Hypertensive individuals who are black or have any of the previously mentioned comorbidities are at high risk for cardiovascular and renal events and are often difficult to treat.7 In the recently published Dimebon Amlodipine HCTZ in Minority PatiENts with Stage 2 Dimebon (ASCENT) study, we documented results of Agomelatine and dimebon for 412 selfidentified US minority grownups with phase 2 systolic dimebon.

http://agomelatine268.wordpress.com/2012/04/

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Potential Alzheimer’s Drug Dimebon Fails in Clinical Trials

admin — Sat, 14 Apr 2012 08:06:40 +0000

Dimebon, a drug that has been in phase three of clinical trials for treatment of Alzheimer’s disease, has recently been discontinued after studies concluded it was ineffective. Dimebon is a drug that was first used in Russia decades ago as an antihistamine, and in the last few years has undergone testing to treat the symptoms of Alzheimer’s in the United States. Dimebon was never sold or marketed in the United States.

Initially, the drug showed some positive results in patients with Alzheimer’s, so clinical trials were expanded to study its effects when given with the drug denepazil (Aricept), a medication currently used to treat early Alzheimer’s. This past week, Pfizer and Medivation, the two drug companies that were conducting the trials, announced the discontinuation of Dimebon after it failed to show benefits for the recipients. In fact, some of the people receiving it declined more than those who received the placebo.

This is disappointing news, especially in light of ournation’s recent draft document on Alzheimer’s disease and other related dementias. One goal outlined in this draft is to effectively treat and prevent Alzheimer’s by 2025. Evidently, the manner in which we do this won’t include Dimebon.

http://alzheimers.about.com/b/2012/01/22/potential-alzheimers-drug-dimebon-fails-in-clinical-trials.htm

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Dimebon Fails Again; End of the Road in Alzheimer’s

admin — Tue, 10 Apr 2012 06:42:09 +0000

Topline results of a phase 3 trial of dimebon, also called latrepirdine, on top of ongoing treatment with donepezil has shown no benefit in patients with mild to moderate Alzheimer’s disease (AD).

The companies developing dimebon in this indication, Medivation Inc and Pfizer Inc, issued a joint statementnoting that results of the phase 3 CONCERT trial showed that the addition of dimebon had no statistically significant benefit on either of the 2 co-primary endpoints, change from baseline in the Alzheimer’s Disease Assessment Scale – cognitive subscale (ADAS-cog) or the activities of daily living subscale (ADAS-ADL).

“Medivation and Pfizer will discontinue development of dimebon for all indications and will terminate the ongoing open label extension study in Alzheimer’s disease,” the joint company statement notes. The companies also plan to terminate their collaboration to codevelop and market dimebon.

The CONCERT trial was a 12-month global randomized, double-blind, placebo-controlled trial that enrolled 1,003 patients with mild to moderate AD. Patients receiving a stable dose of donepezil for at least 4 months were randomly assigned to 1 of 3 treatment groups: dimebon, 20 mg 3 times per day; dimebon, 5 mg 3 times per day; or placebo.

Although there was no apparent benefit, the drug was generally well tolerated in the study, the companies add. “A full analysis of the results from CONCERT will be conducted and submitted for presentation at an upcoming scientific congress,” the statement concludes.

Although phase 2 results with this agent were extremely positive in the treatment of AD, previous negative results have been reported with dimebon in phase 3 in the CONNECTION trial, as well as in the treatment of Huntington’s disease in the HORIZON trial.

http://www.medscape.com/viewarticle/757098

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