(CNN) -- The U.S. should stop arresting responsible marijuana users, Rep. Barney Frank said Wednesday, announcing a proposal to end federal penalties for Americans carrying fewer than 100 grams, almost a quarter-pound, of the substance.

"The vast amount of human activity ought to be none of the government's business," Frank said on Capitol Hill. "I don't think it is the government's business to tell you how to spend your leisure time."

The Massachusetts Democrat and his supporters emphasized that only the use -- and not the abuse -- of marijuana would be decriminalized if the resolution resulted in legislation. Watch Frank lay out the proposal »

The Drug Enforcement Administration says people charged with simple possession are rarely incarcerated. The agency and the White House Office of National Drug Control Policy have long opposed marijuana legalization, for medical purposes or otherwise.

Marijuana is a Schedule I controlled substance, meaning it has a high potential for abuse and no accepted medical use, according to the drug control office.

"Smoked marijuana has not withstood the rigors of science -- it is not medicine and it is not safe," the DEA states on its Web site. "Legalization of marijuana, no matter how it begins, will come at the expense of our children and public safety. It will create dependency and treatment issues, and open the door to use of other drugs, impaired health, delinquent behavior, and drugged drivers."

Allen St. Pierre, spokesman for the National Organization for the Reform of Marijuana Laws, likened Frank's proposal -- co-sponsored by Rep. Ron Paul, R-Texas -- to current laws dealing with alcohol consumption. Alcohol use is permitted, and the government focuses its law enforcement efforts on those who abuse alcohol or drive under its influence, he said.

"We do not arrest and jail responsible alcohol drinkers," he said.

St. Pierre said there are tens of millions of marijuana smokers in the United States, including himself, and hundreds of thousands are arrested each year for medical or personal use. iReport.com: Is it time to legalize pot?

There have been 20 million marijuana-related arrests since 1965, he said, and 11 million since 1990, and "every 38 seconds, a marijuana smoker is arrested."

Rob Kampia, director of the Marijuana Policy Project, said marijuana arrests outnumber arrests for "all violent crimes combined," meaning police are spending inordinate amounts of time chasing nonviolent criminals.

"Ending arrests is the key to marijuana policy reform," he said.

Reps. William Lacy Clay, D-Missouri, and Barbara Lee, D-California, said that in addition to targeting nonviolent offenders, U.S. marijuana laws unfairly target African-Americans.

Clay said he did not condone drug use but opposes using tax dollars to pursue what he feels is an arcane holdover from "a phony war on drugs that is filling up our prisons, especially with people of color."

Too many drug enforcement resources are being dedicated to incarcerating nonviolent drugs users, and not enough is being done to stop the trafficking of narcotics into the United States, he said.

Being arrested is not the American marijuana smoker's only concern, said Bill Piper of the Drug Policy Alliance Network. Those found guilty of marijuana use can lose their jobs, financial aid for college, their food stamp and welfare benefits, or their low-cost housing.

The U.S. stance on marijuana, Piper said, "is one of the most destructive criminal justice policies in America today."

Calling the U.S. policy "inhumane" and "immoral," Lee said she has many constituents who are harassed or arrested for using or cultivating marijuana for medical purposes. California allows medical marijuana use, but the federal government does not, she explained.

House Resolution 5843, titled the Personal Use of Marijuana by Responsible Adults Act of 2008, would express support for "a very small number of individuals" suffering from chronic pain or illness to smoke marijuana with impunity.

According to NORML, marijuana can be used to treat a range of illnesses, including glaucoma, asthma, multiple sclerosis, HIV/AIDS and seizures.

Frank, who is chairman of the Financial Services Committee, said that about a dozen states have approved some degree of medical marijuana use and that the federal government should stop devoting resources to arresting people who are complying with their states' laws.

In a shot at Republicans, Frank said it was strange that those who support limited government want to criminalize marijuana.

Asked whether the resolution's passage would change his personal behavior, Frank quipped, "I do obey every law I vote for" but quickly said he did not use marijuana, nor does he encourage it.

"I smoke cigars. I don't think other people should do that. If young people ask me, I would advise them not to do it," he said.

If HR 5843 were passed, the House would support marijuana smokers possessing up to 100 grams -- about 3½ ounces -- of cannabis without being arrested. It would also give its blessing to the "nonprofit transfer" of up to an ounce of marijuana.

The resolution would not address laws forbidding growing, importing or exporting marijuana, or selling it for profit. The resolution also would not speak to state laws regarding marijuana use.

CHICAGO, July 29 -- An old drug for urinary-tract infections, methylene blue (Urolene Blue), may hold the key to a therapy that can slow the progress of Alzheimer's disease for as long as 19 months, researchers here reported.

After 24 months of treatment with 60 mg three times a day of methylthioninum chloride (rember), patients with moderate Alzheimer's disease achieved a treatment effect that "was twice the effect seen with donepezil (Aricept)," said Claude Wischik, Ph.D., of the University of Aberdeen in Scotland.

The drug called rember is a formulation of methylene blue made by TauRx Therapeutics, and Dr. Wischik is founder and chairman of TauRx Therapeutics. The drug attacks tau, which promotes tangles, as opposed to amyloid plaques.

After 50 weeks, pooled data from mild and moderate Alzheimer's disease patients indicated an 81% reduction in the rate of cognitive decline versus controls, which was a difference of 6.8 units on the Alzheimer's Disease Assessment Scale, that was highly significant (P<0.0001).

Moreover, there was a significantly greater effect size at 50 weeks than at 24 weeks (P=0.0091), he said at the International Conference on Alzheimer's Disease. At 24 weeks, patients with moderate disease had a 5.5 unit difference on the Alzheimer's Disease Assessment Scale compared with controls (P=0.021).

Methylene blue, used to treat urinary tract infections, was developed from a common dye that is used in products ranging from ink to jeans, Dr. Wischik said.

Although the drug is available, Dr. Wischik said he could not recommend widespread use of methylene blue to treat Alzheimer's disease, because proof of efficacy requires a phase III trial.

He added that the drug used in his trial was "much purer" than the formulation currently available.

In the trial reported here, 321 patients were randomized to 30 mg, 50 mg, 100 mg or placebo.

The drug, Dr. Wischik said, was effective when it dissolved in the stomach, but was not effective when the drug was absorbed through the intestines.

This was an issue for the 100-mg dose, which had "absolutely no activity because it didn't dissolve in the stomach."

Moreover, because the 100-mg dose dissolved in the intestines, it was more likely to cause diarrhea, which was reported by about 30% of patients and was the most common adverse event.

Patients were assessed at six week-intervals through 50 weeks and then followed for an additional 34 weeks.

The dropout rate in each arm of the trial was about 25%, which Dr. Wischik said was about the same as the dropout rate for trials of cholesterase inhibitors.

Dr. Wischik's trial gathered data over 84 weeks, which made it the largest and longest phase II trial of an Alzheimer's disease-modifying agent.

But limitations include the fact that the study was conducted and presented by Dr. Wischik, who is co-founder and chair of TauRx Therapeutics. Another, difficulty -- and one mentioned by other Alzheimer's researchers -- is that Dr. Wischik has not published any data on the drug.

During an interview, Dr. Wischik said he planned to publish three major papers -- preclinical, imaging, and clinical data -- but he would not do so until after his company had secured an okay from the FDA for a phase III trial.

Another potential problem is Dr. Wischik's assertion that amyloid hypothesis, which contends that the buildup of amyloid plaque in the brain was the main mechanism of Alzheimer's disease, was flat out wrong.

Alzheimer's disease, he said, "is all about tangles." Attacking tau, which promotes tangles, can dissolve tangles and thereby stop the disease process. Amyloid, he said, may exacerbate the disease process, but it is not the primary mechanism.

Sam Gandy, M.D., Ph.D., of Mount Sinai School of Medicine in New York, said that while the data were impressive, they were hardly enough to discount years of amyloid research.

The more likely explanation, Dr. Gandy said in an interview, was that both amyloid and tau were important factors. The ideal treatment, he said, might include a cocktail that targeted both.

Moreover, Dr. Gandy said that "it is dangerous to make statements about efficacy based on phase II data, since these trials are really designed to address toxicity and dosing, not efficacy."

Dr. Wischik's findings need to be reproduced and efficacy requires a phase III trial, Dr. Gandy said.

In an interview, Dr. Wischik said that a phase III trial with 1,000 to 1,200 patients is being planned, but details await talks with the FDA. He said "my agents have contacted the FDA, and we hope to meet by the end of the year."

At issue, he said, was whether the FDA would require toxicity trials in primates to be conducted prior to a phase III trial or concurrently with phase III. "Because this is an old drug, that has been around for years, we hope that the toxicity study could be done concurrently," he said.

DAVIS, Calif., July 29 -- For patients with knee osteoarthritis, an extract of the Indian frankincense plant gave significant pain relief and reduced levels of a marker of joint pathology, researchers here said.

Patients in a randomized, double-blind, 90-day trial showed significantly greater reductions in pain scores with the agent than with placebo, reported Siba R. Raychaudhuri, M.D., of the University of California Davis, and colleagues online in Arthritis Research and Therapy.

Synovial fluid levels of matrix metalloproteinase-3 also declined significantly in patients receiving the agent, whereas MMP-3 levels rose in the placebo group.

This was the agent's first randomized, placebo-controlled trial in osteoarthritis of the knee, the researchers said.

The agent, tradenamed 5-Loxin, was derived from Boswellia serrata, a plant that has long been prominent in the Ayurvedic system of traditional Indian medicine. It is already widely marketed in the U.S. as a nutritional supplement, with purported benefits including enhanced joint mobility and function.

The extract contains 30% 3-O-acetyl-11-keto-beta-boswellic acid, identified in laboratory and animal studies as the anti-inflammatory component, according to Dr. Raychaudhuri and colleagues.

In particular, the compound appears to inhibit 5-lipoxygenase, a key intermediate in the inflammatory cascade.

The study assigned 70 patients to placebo or to 100 mg or 250 mg of the extract, given orally in divided doses.

Patients at baseline had mean pain scores, on a visual analogue scale, of 56 to 57 points.

At the end of treatment, mean scores in the placebo group were 41.8 (SD 16.0), compared with 21.4 (SD 7.1) in the low-dose treatment group and 14.2 (SD 6.8) for those in the high-dose group. The declines in both treatment groups were significantly greater than in the placebo group (P<0.0001).

Similar results were also seen in the pain subscale of the Western Ontario and McMaster Universities Osteoarthritis Index (WOMUOI).

Improvements in pain scores with the agent were noted in one week in some patients, the researchers aid.

Functional assessments, including the WOMUOI stiffness and functional subscales and Lequesne's Functional Index, also showed significant advantages for the plant extract versus placebo.

For example, mean stiffness scores in the placebo group declined from 33.2 (SD 2.7) at baseline to 24.5 (SD 2.4) after treatment, whereas in the low-dose treatment group, mean scores fell from 31.8 (SD 3.6) at baseline to 14.1 (SD 3.7) following treatment (P<0.0001 versus placebo).

As with the pain scores, greater improvements were seen in the high-dose group: stiffness scores decreased from 27.8 (SD 3.4) at baseline to 9.24 (SD 2.1) after treatment (P<0.0001).

Mean MMP-3 levels in synovial fluid increased slightly in the placebo group, from 902.1 ng/ml (SD 275.1) at baseline to 928.5 (SD 216.0) following treatment.

In the low-dose and high-dose treatment groups, MMP-3 levels fell substantially: from 893.6 (SD 270.1) and 926.9 ng/ml (SD 270.5) at baseline, respectively, to 637.2 (SD 224.5) and 497.5 (SD 167.5) ng/ml after treatment (both P<0.0001 versus placebo).

MMP-3 is a cartilage-degrading enzyme. Its presence in synovial fluid is a marker of joint destruction.

"5-Loxin has potential efficacy in terms of reducing pain and improving the physical ability of osteoarthritis patients," Dr. Raychaudhuri and colleagues wrote.

In combination with animal experiments that found no mutagenic effects or other major toxicity concerns, the adverse event profile in the clinical trial indicates that the compound "is potentially safe in the treatment of osteoarthritis in humans," the researchers said.

Dr. Raychaudhuri and colleagues said the most common adverse effects were diarrhea, nausea, abdominal pain, mild fever, and general weakness, without significant difference between placebo and the active treatment groups.

The study was funded by Laila, developer of 5-Loxin. Several co-authors were Laila employees and others received research funding and/or had other relationships with the company. No other potential conflicts of interest were reported

CHICAGO, July 29 -- Diabetics who took both insulin and other medications for the disease had fewer plaques associated with Alzheimer's disease than other patients, researchers said here.

In a postmortem study, patients on combination treatment had significantly fewer beta-amyloid plaques (P=0.014) than diabetics who were on one treatment alone or patients who did not have diabetes, Michal Schnaider Beeri, Ph.D., of Mount Sinai School of Medicine in New York, reported at the International Conference on Alzheimer's Disease.

Overall, the combination group had about 80% fewer plaques compared with the other groups combined.

However, there were no significant between-group differences in the occurrence of neurofibrillary tangles.

"These results suggest that the combination [of insulin and other diabetes medications] … may beneficially influence Alzheimer's-related brain changes," Dr. Beeri said. "This also points to biological pathways in the brain, such as insulin signaling, that might be a focus for developing new treatment strategies."

Because diabetes has been associated with a greater risk of mild cognitive impairment and Alzheimer's disease in epidemiological studies, the researchers expected to see more plaques when they examined the brains of diabetics.

In a previous study by Dr. Beeri's group, however, that wasn't the case. In fact, they found fewer plaques. Other neuropathological studies have failed to find any association between diabetes and the number of plaques or neurofibrillary tangles.

Dr. Beeri and her colleagues hypothesized that the treatments for diabetes may influence the neuropathology of Alzheimer's.

To test the hypothesis, the researchers studied 248 brains -- 124 from diabetics and 124 from non-diabetics -- from the Mount Sinai School of Medicine Brain Bank. Most of the specimens came from the Jewish Home and Hospital in Bronx, N.Y., and the two groups were matched by age, sex, and severity of dementia.

The mean age of the patients at death was 81.2 and 57.3% were female. The mean clinical dementia rating was 2.4, indicating moderate to severe dementia.

Non-diabetics had slightly lower body mass indices but the difference was not statistically significant.

Of the diabetics, 29 were not on any medication, 49 were taking insulin only, 28 were taking medications other than insulin -- like glyburide or metformin -- and 18 were taking both insulin and another diabetes medication.

The researchers examined the extent of plaques and neurofibrillary tangles in several neocortical regions and in the hippocampus, entorhinal cortex, and amygdala using the CERAD (Consortium to Establish A Registry for Alzheimer's Disease) neuropathological battery.

The group that was on combination treatment for diabetes had significantly fewer beta-amyloid plaques in the entorhinal cortex (P=0.003), amygdala (P=0.009), and overall (P=0.014) compared with the other groups, which did not differ significantly from each other.

The differences approached statistical significance in the hippocampus (P=0.057) and the combined neocortical measure (P=0.052).

When the researchers additionally controlled for APOE e4 genotype, BMI, and fasting glucose at the time of nursing home admission, there was no change in the findings.

Dr. Beeri acknowledged some limitations of the study, including the inability to determine causation and potential confounding. Nor could the survivor effect be ruled out, she said.
Nevertheless, Dr. Beeri said, the results suggest that diabetes medications may influence biological pathways involved in beta-amyloid processing.

The study was funded by the National Institute on Aging. Dr. Schnaider Beeri made no disclosures.

CHICAGO, July 29 -- The rate of new cases of mild cognitive impairment in patients over 70 is higher than previously expected, results from the Mayo Clinic Study of Aging showed.

Initially healthy participants developed mild cognitive impairment at a rate of 5.3% a year (95% CI 4.3% to 6.5%), two to three times higher than the rate of new cases of dementia in the same population, Ronald Petersen, M.D., Ph.D., of the Mayo Clinic in Rochester, Minn., reported at the International Conference on Alzheimer's Disease here.

"If we extrapolate Alzheimer's incidence rates to mild cognitive impairment, we would expect perhaps 1% to 2% per year," said Dr. Petersen, who is also the vice chair of the Alzheimer's Association's medical and scientific advisory council, "but our findings were substantially higher than that."

The rate increased from 3.5% (95% CI 2.4% to 5%) in participants ages 70 to 79 to 7.2% (95% CI 5.5% to 9.3%) in those ages 80 to 89.

In addition, men were nearly twice as likely as women to develop mild cognitive impairment (HR 1.92, 95% CI 1.22 to 3.02).

Although mild cognitive impairment may represent a transitional phase to various forms of dementia, it is unknown how often it occurs in a population-based setting, the researchers said.

To find out, they turned to the Mayo Clinic Study on Aging, which randomly selected participants ages 70 to 89 from Olmsted County, Minn., in 2004; 1,786 participants were available for analysis.

Each participant underwent a baseline examination that included an assessment of cognitive function and a neurological exam. In addition, the researchers interviewed a close acquaintance of each participant. Follow-up was conducted in 15-month intervals.

The rates of mild cognitive impairment in men and women were 6.2% (95% CI 4.7% to 8.1%) and 4.4% (95% CI 3.1% to 6%), respectively.

Compared with women, men were more likely to have amnestic mild cognitive impairment (HR 2.00, 95% CI 1.12 to 3.57) as well as the non-amnestic subtype (HR 1.82, 95% CI 0.87 to 3.81), although the latter comparison did not reach statistical significance.

"These results underscore the urgency of developing new and better strategies to create disease-modifying therapies for Alzheimer's," Dr. Petersen said. "In addition, for public health purposes, we need to know how many people are cognitively impaired and potentially on the road to Alzheimer's."

Ralph Nixon, M.D., Ph.D., of New York University, and a member of the medical and scientific advisory council of the Alzheimer's Association, said, "This both magnifies the urgency of the problem of Alzheimer's disease and extends it to an even larger population but also gives some hope of early intervention that would target this population at an earlier stage of the disease."

According to Dr. Petersen, the findings may not be generalizable to populations outside of the predominantly white population of northern European descent of Olmsted County.

He noted, however, that the results of worldwide studies of mild cognitive impairment were not "drastically" different from those of the current study.

The findings are particularly important considering the shifting population distribution associated with aging baby boomers, Dr. Petersen said.

The study was supported by grants from the National Institute on Aging and by the Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program.

Dr. Peterson declared being a consultant for GE Healthcare and chair of the safety monitoring committee for Elan Pharmaceuticals.

His co-authors declared potential conflicts of interest with Elan Pharmaceuticals, sanofi-aventis, and Myriad.

Older patients who take statins may be at lower risk of developing dementia, according to findings from a prospective cohort study.

Statin users were 44% less likely to develop dementia and cognitive impairment than nonusers after controlling for other factors (P=0.010), reported Mary N. Haan, Dr.P.H., of the University of Michigan here, and colleagues in the July 29 issue of Neurology.

However, the findings were not enough to suggest that patients should take a statin unless necessary for other health reasons, the investigators cautioned.

Although these findings add evidence in favor of statins for cognitive outcomes, this area of research has been controversial with little agreement between studies, the researchers said.

At baseline, statin users and nonusers were similar, except that statin users were slightly younger, more educated, and more likely to have been born in the U.S. and covered by medical insurance.

Statin users were also more likely to have a history of diabetes and higher mean baseline cognitive scores on the Modified Mini-Mental State Examination.

During more than five years of follow-up, 130 participants developed dementia or cognitive impairment without dementia.

Of the 82 patients with dementia, 48% had possible or probable Alzheimer's disease, 23% had undetermined etiology, 13% had ischemic vascular dementia, and 13% had mixed Alzheimer's or vascular dementia.

Statin users had a 43% lower rate of dementia and non-dementia cognitive impairment than nonusers (hazard ratio 0.577, 95% confidence interval 0.376 to 0.886, P=0.012).

After controlling for baseline diabetes and stroke, statins remained associated with a 48% lower rate of dementia and non-dementia cognitive impairment (HR 0.518, 95% CI 0.336 to 0.797, P=0.003).

Further adjustment for education, smoking status, and apolipoprotein E (APOE-e4) genotype attenuated the association only slightly to a 44% lower risk compared with nonusers (HR 0.564, 95% CI 0.365 to 0.872, P=0.010).

The protective effect of statins on dementia held for both high functioning individuals with above-average cognitive scores on the Modified Mini-Mental State Examination (HR 0.546, 95% CI 0.327 to 0.912) and those with below average scores (HR 0.444, 95% CI 0.200 to 0.988).

The researchers cautioned that the findings may have been biased by differential loss to follow-up, indication bias, or competing risks.

However, they noted that statin use didn't appear to have an impact on survival (HR 0.92, 95% CI 0.69 to 1.20).


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