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Concerned Zimbabwe’s Citizens Start an Anti-Drug Campaign

While that may help, when young people have finished playing, they still find themselves unemployed and in the same conditions

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Drugs, Africa
A street vendor sells illegal and false drugs in a street of Adjame in Abidjan, Ivory Coast. VOA

A group of concerned Zimbabweans has started an anti-alcohol and drug campaign, targeting communities in which unemployed young people resort to drinking and using narcotics to alleviate the stress of not having work. Those involved in the campaign say the solution lies largely with improving the country’s moribund economy.

Fewer than three in 10 young Zimbabweans have steady jobs. Many are idle and see no economic opportunity. For some, that leads to problems with alcohol and drugs.

Church leaders, community leaders, and government officials have started warning youths of the impact of drug and alcohol abuse in Zimbabwe and its effect on their physical wellbeing and mental health.

With drug use growing in Zimbabwe, President Emmerson Mnangagwa’s government has called for an all-stakeholders meeting on February 1 to come up with possible solutions.

Zimbabwe’s deputy director of Mental Health Services, Dr. Chido Rwafa, says the government cannot deal with the problem of substance abuse alone.

HIV, Drugs
More than half of the people surveyed who inject drugs said they avoided health-care services, citing discrimination or fear of law enforcement authorities.VOA

“Alcohol and substance use is a rising problem in all of Africa, and also in Zimbabwe, and it has become one of our top three diagnoses that we are seeing in our mental health unit, so it is becoming a problem. We need a coordinated approach to this problem. It is a multi-sectorial problem. We need a combined effort between government, between non-governmental organizations, with the community itself,” Rwafa said.

Youths are susceptible to peer pressure and can easily gain access to drugs, says Dr. Rwafa. Once hooked on drugs, they also become more likely to engage in criminal activities.

This 20-year-old asked us not to film him when he was smoking cannabis. He says drug use would fall if more people could find employment.

“The best way is just to improve our country economically such that all those people loitering in the streets will find jobs and will be focused. We are going nowhere. Even if you are to look (in the streets), there are some other people damaged (by drugs). Fifty percent of youths in the streets, they can not even work. Their life has been destructed by drugs etc. It is not that they want drug abuse,” Mandizha said.

drug
Young people with the Ngoma Yorira Theatre Association get ready for a performance at “Theatre in the Park” in Harare, Zimbabwe, as they campaign against drug abuse, Feb, 2, 2018. VOA

Roman Catholic Priest Cloudy Maganga is trying to reduce substance abuse by youths by keeping them busy and offering counseling.

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“Within our hall, upstairs we are creating what we call a study center for the young people. We will have computers… We have also started what we call the sports for the young people. We have created a volleyball pitch, we have created also a netball pitch for the young people so that when they are free, during their free time, they can be engaged in sports, everyone here. So at least with that we are removing them from being just idle,” Maganga said.

While that may help, when young people have finished playing, they still find themselves unemployed and in the same conditions youths like Takudzwa Mandizha say make them turn to drugs. (VOA)

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Scientists Explore Novel Ways to Attack Alzheimer’s in Wake of String of Disappointing Drug Failures

Contrary to popular perception, "there are a lot of changes that happen in the aging brain that lead to dementia in addition to plaques and tangles"

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Drugs, Alzheimer, Dementia, Hospitalisation, Risk
Dr. William Burke goes over a PET brain scan, Aug. 14, 2018 at Banner Alzheimers Institute in Phoenix, Arizona. VOA

When researchers at the University of Kentucky compare brains donated from people who died with dementia, very rarely do they find one that bears only Alzheimer’s trademark plaques and tangles — no other damage.

If they do, “we call it a unicorn,” said Donna Wilcock, an Alzheimer’s specialist at the university’s aging center. Contrary to popular perception, “there are a lot of changes that happen in the aging brain that lead to dementia in addition to plaques and tangles.”

That hard-won lesson helps explain how scientists are rethinking Alzheimer’s.

For years researchers have been guided by one leading theory — that getting rid of a buildup of a sticky protein called amyloid would ease the mind-robbing disease. Yet drug after drug has failed. They might clear out the gunk, but they’re not stopping Alzheimer’s inevitable worsening. Today’s treatments only temporarily ease symptoms.

Scientists, Alzheimers, Drug
When researchers at the University of Kentucky compare brains donated from people who died with dementia, very rarely do they find one. Pixabay

The new mantra: diversify.

With more money — the government had a record $2.4 billion to spend on Alzheimer’s research this year — the focus has shifted to exploring multiple novel ways of attacking a disease now considered too complex for a one-size-fits-all solution. On the list, researchers are targeting the brain’s specialized immune system, fighting inflammation, even asking if simmering infections play a role.

Most of these fresh starts are in the earliest research stages. It’s far from clear that any will pan out, but “the field is now much more open-minded than it ever was to alternative ideas,” Wilcock said.

Breaking the plaque and tangle link

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No one knows what causes Alzheimer’s but amyloid deposits were an obvious first suspect, easy to spot when examining brain tissue. But it turns out that gunk starts silently building up 20 years before any memory loss, and by itself it’s not enough to cause degeneration.

Sometime after plaques appear, another protein named tau starts forming tangles inside neurons, heralding cell death and memory loss.

But again, not always: Autopsies show sometimes people die with large amounts of both plaques and tangles, yet escape dementia.

So something else — maybe several other things — also must play a role. One possible culprit: The brain’s unique immune cells, called microglia.

Scientists, Alzheimers, Drug
If they do, “we call it a unicorn,” said Donna Wilcock, an Alzheimer’s specialist at the university’s aging center. Pixabay

No surprise if you’ve never heard of microglia. Neurons are the brain’s rock stars, the nerve cells that work together to transmit information like memories. Microglia are part of a different family of cells long regarded as the neurons’ support staff. But “it’s becoming clear they’re much more active and play a much more significant role,” said Dr. Richard Hodes, director of the National Institute on Aging.

One microglial job is to gobble up toxic proteins and cellular debris. Recently, a mutation in a gene called TREM2 was found to weaken microglia and increase the risk of Alzheimer’s. Dr. David Holtzman at Washington University in St. Louis took a closer look — and says microglia may be key to how the amyloid-tau duo turns toxic.

In donated human brains, his team found more tau tangles clustered around amyloid plaques when people harbored microglia-weakening TREM2 mutations. The researchers altered the TREM2 gene in mice and seeded their brains with a little human tau. Sure enough, more tangles formed next to plaques in mice with weak microglia than in those with functional immune cells, they recently reported in Nature Neuroscience.

Why? Normal microglia seem to restrict amyloid plaques, which limits damage to surrounding tissue — damage that can make it easier for tau to take hold, he explained.

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While it was known that amyloid buildup drives tau tangles, “we never had a good clue as to how it is doing that,” Holtzman said. The new findings “would argue that these cells are sort of a missing link.”

Separately, biotech company Alector Inc. has begun first-step patient testing of a drug designed to boost TREM2 and better activate microglia.

 The germ conundrum

Could gum disease or herpes be to blame? The idea that infections earlier in life could set the stage for Alzheimer’s decades later has simmered on the edge of mainstream medicine, but it’s getting new attention. It sounds weird, but both the germ that causes gum disease and different strains of herpes viruses have been found in Alzheimer’s-affected brain tissue.

Researchers in New York are testing the herpes drug valacyclovir in 130 people with mild Alzheimer’s who have evidence of infection with certain herpes strains.

And Cortexyme Inc. is enrolling more than 500 early-stage patients around the country to test a drug that targets potentially neuron-damaging substances produced by gingivitis bacteria.

Whether the germ theory is a worthwhile pursuit was hotly debated at an international Alzheimer’s Association meeting in July. One skeptic, Dr. Todd Golde of the University of Florida, cautioned that germs’ mere presence doesn’t mean they caused dementia — they could be a consequence of it.

Still, a 2018 study from Taiwan offered a hint that treating herpes infection might lower later dementia risk. And a U.S. study found certain herpes viruses affected the behavior of Alzheimer’s-related genes.

“Maybe these are just opportunistic pathogens that have space to spring up in the brains of people affected with Alzheimer’s disease,” said Benjamin Readhead of Arizona State University, who co-authored that U.S. paper. But, “it looks at least plausible that some of these pathogens are capable of acting as accelerants of disease.”

 A common denominator

One key commonality among emerging Alzheimer’s theories is how aggressively the brain’s immune system defends itself — and thus how inflamed it becomes.

Inflammation is a normal part of the body’s response to illness and injury, one method of fighting infection or healing wounds. But when inflammation is too strong, or doesn’t go away, it’s like friendly fire that harms cells. Remember how some people have lots of plaques and tangles but no dementia? A few years ago Massachusetts General researchers found strikingly little inflammation surrounded all the gunky buildup in the resilient brains — but the Alzheimer’s-affected brains harbored a lot.

Research since has found similar inflammatory effects with other forms of dementia — like vascular dementia, where tiny blood vessels that feed the brain are lost or blocked, and dementias caused by Lewy bodies or other toxic proteins. A growing list of genes linked to inflammatory processes also may play a role.

A handful of drugs are being explored in the quest to tamp down inflammation’s damaging side without quashing its good effects. Take those microglia, which Holtzman said “may be a two-edged sword.”

Early on, before there’s too much plaque, revving them up may be good. But later on, a hyperactive swarm around growing plaques spews out inflammatory molecules.

In addition to their immune system job, microglia also secrete molecules that help nourish neurons, noted Kentucky’s Wilcock. The goal is to restore the natural balance of a healthy brain’s environment, she said, so microglia “can perform their essential functions without damaging surrounding tissue.”

Amyloid’s still in the picture

All those drug flops weren’t a waste of time.

“Every time there’s a failure it’s absolutely clear that we learn a lot,” Emory University neurologist Dr. Allan Levey recently told the government’s Alzheimer’s advisory council.

One lesson: Timing may matter. Most of the failed anti-amyloid drugs were tested in people who already had at least mild symptoms. Some studies seeking to prevent memory loss in the first place still are underway. Several anti-tau drugs also are being tested.

Another lesson: Most people have a mix of different dementias, which means they’ll need a variety of treatments.

“Now we have an opportunity, a real opportunity, to expand and try all these avenues,” said Alzheimer’s Association chief science officer Maria Carrillo. “The triggers as we understand them are broad.” (VOA)