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Report offers evidence-based recommendations aimed at reducing Illinois gun violence

Johns Hopkins report identifies weaknesses or gaps in current Illinois law and offers recommendations to reduce gun violence

JOHNS HOPKINS UNIVERSITY BLOOMBERG SCHOOL OF PUBLIC HEALTH

Illinois could reduce the number of people killed each year by gun violence by implementing ten policies supported by available research, according to a new report authored by researchers at the Johns Hopkins Center for Gun Policy and Research. The center is based at the Johns Hopkins Bloomberg School of Public Health.

The recommended policies include strengthening the state's gun purchaser licensing system by requiring an in-person application to law enforcement, fingerprinting and safety training. New data in this report suggest that purchaser licensing is more effective in reducing firearm homicides when these systems require in-person applications with law enforcement agencies.

The report also recommends expanding current firearm prohibitions for domestic abusers and individuals convicted of multiple alcohol-related offenses, and providing more funding for local initiatives proven to reduce gun violence.

The report, Policies to Reduce Gun Violence in Illinois: Research, Policy Analysis, and Recommendations, was commissioned by the Joyce Foundation. It is available for download from the Johns Hopkins Center for Gun Policy and Research here.

"Compared to many other states, Illinois has relatively strong firearm laws overall, yet many opportunities exist for the state to strengthen their approach to reducing the diversion of guns for criminal use and gun violence," says the report's lead author, Cassandra Crifasi, PhD, MPH, deputy director of the Johns Hopkins Center for Gun Policy and Research. "Importantly, the policies and strategies outlined in this report are applicable to other states considering evidence-based approaches to reduce firearm homicide and suicide and don't infringe upon the rights of law-abiding gun owners."

Currently, Illinois is one of nine states that requires individuals to obtain a license or permit from law enforcement--called a Firearm Owner's Identification (FOID) in Illinois--to acquire a handgun. Previous research from the report authors found that handgun purchaser licensing is effective at reducing gun homicides, suicides and shootings of law enforcement officers.

Illinois is one of two states with permitting requirements that allows individuals to apply for their license online or by mail. Illinois also does not require applicants to undergo any training prior to application. The state also does not mandate, as some states do, that individuals seeking to buy a firearm from a private seller who is not a licensed gun dealer pass a background check; private sellers are only required to check if the prospective purchaser's FOID is valid. Illinois FOIDs are valid for 10 years, but if private sellers fail to verify that a prospective purchaser's FOID is valid, current law provides no criminal penalties.

The individual who shot and killed five people last Friday in Aurora, Illinois was reportedly prohibited from owning a firearm. According to media accounts, he was approved for a FOID card after passing a background check and was able to purchase a firearm despite having a felony conviction; Illinois' FOID application does not require fingerprinting. When he later applied for a concealed carry permit, which requires fingerprinting, state officials discovered the prohibiting condition.

"Illinois arguably has the weakest of all handgun purchaser licensing laws," says report co-author Daniel Webster, ScD, MPH, director of the Johns Hopkins Center for Gun Policy and Research. "Strengthening this existing law to require an in-person application with fingerprinting, requiring the police to conduct a background check while verifying the FOID card and requiring more frequent renewal of licensing would be a wise investment in public safety."

Illinois law does not require law enforcement to remove firearms when gun owners are identified as prohibited after a FOID card has been issued. The report recommends that if individuals are later identified as prohibited and fail to surrender their FOID and/or firearms upon notice of revocation, law enforcement should dispossess these prohibited individuals of their firearms.

In addition to strengthening the state's purchaser licensing law and identifying promising new legislation, the authors underscored the importance of robust enforcement of new state laws that regulate retail gun sellers and create a process for removing firearms from people planning to harm themselves or others through court-ordered extreme risk protection orders.

Other evidence-based recommendations include modifying existing domestic violence-related firearm prohibitions to last the length of the order or two years; extending firearm prohibition to individuals convicted of multiple alcohol-related offenses; providing law enforcement discretion to deny concealed carry licenses to those identified as legal but dangerous; banning the sale and possession of new assault weapons and requiring current assault weapon owners to register them; banning the possession of large-capacity magazines (more than 10 rounds); and providing funding to support community programs such as focused deterrence, outreach and conflict mediation involving high-risk individuals.

"Addressing gun violence requires a comprehensive evidence-based approach encompassing enforcement of existing laws, strengthening of current laws identified as weak, adoption of new evidence-based laws and funding for violence prevention programs," says Crifasi. "By considering the policy recommendations put forth in this report, Illinois has an opportunity to decrease their rates of firearm homicide and suicide, and serve as a model for other states seeking to reduce the toll of gun violence in their communities."­­

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"Policies to Reduce Gun Violence in Illinois: Research, Policy Analysis, and Recommendations" was written by Cassandra K. Crifasi, Alexander McCourt and Daniel W. Webster. All researchers are with the Johns Hopkins Center for Gun Policy and Research. The report was published by the Johns Hopkins Center for Gun Policy and Research.

This research was supported by the Joyce Foundation.

Eureka Alert

“Consequences of Irresponsible Pritzker Budget Proposal Will Cost Illinois and Future Generations $150B More” (Illinois Retired Teachers Association)

RETIREES IMPLORE PRITZKER TO STOP RAID OF $500M FOR 2019 PENSION FUND.

(February 20, 2019 - Springfield, Ill.) - Members of the Illinois Retired Teachers Association (IRTA) are imploring Governor J.B. Pritzker to cease the decades-long practice of not fully funding the pension systems. IRTA members appreciate the difficult fiscal condition that the Governor inherited but taking pension holidays is not the solution.

“The Illinois Retired Teachers Association has serious concerns about the Governor’s proposed pension holiday,” IRTA President Roger Hampton said. “We are supportive of the proposals to infuse additional revenues into the pension funds for solvency, but not to underfund systems by hundreds of millions of dollars or by raiding one fund to give more to another. Delaying pension payments just kicks the can down the road again and costs future generations of Illinois taxpayers (if any left) billions of dollars.”

During his budget address Wednesday, Governor Pritzker proposed allocating $4.237 billion into the Illinois Teachers’ Retirement System (TRS), a figure $576,000,000 too short of what is legally and ethically required to pay for the pension benefits of retired teachers and current teachers. It will result in reduced pension payments to TRS for years to come but will generate a nearly $150 billion in increased costs to Illinois taxpayers, including the 417,292 members of TRS.

“TRS is currently very poorly funded by actuarial standards at 40% of the assets needed for current benefits,” IRTA Executive Director Jim Bachman said. “If Illinois had not taken pension holidays, like the ones being proposed, the cost of TRS would be $1.2 billion. The State is paying 400% more because of statutory underfunding and a history of pension holidays. The Illinois Retired Teachers do not believe that the solution to the poorly funded pension systems is to make them more poorly funded and to continue the tradition that got Illinois in this problem in the first place.”

“The State of Illinois must keep its promises to the people, like retired teachers that have always kept up their end of the bargain,” Hampton concluded. “The State of Illinois must fund its pensions and retiree healthcare promises at levels that are both legally and ethically justified.”

It should be noted that this pension holiday is focused only on teachers outside of the City of Chicago. Pritzker did propose increasing the payments to the Chicago Teachers’ Pension Fund.

"Let’s call it the teacher pension death watch” by Fred Klonsky

“I’ve been writing about retired teacher Jeri Shanahan for years. She is part of a shrinking group of retired Illinois teachers who got caught in the cracks years ago when the law changed regarding Medicare.

“When I first met Jeri, the number of teachers who were forced to pay exorbitant fees for health coverage was about 600. Half are now dead. You can go to the above link and read more about the issue if you want.

“Shanahan is still around, and she gives me a call every couple of months. I listen and Jeri talks about the lack of fairness in the system. What gets unsaid by both of us is that Illinois’ politicians do have an unspoken plan for her and the rest of the 300 or so that are still around.

“They will wait for the rest of those caught in Jeri Shanahan’s situation to die. Problem solved.

“I put Jeri in touch with my State Representative Will Guzzardi last year. When I talked to him afterward, he said he couldn’t get to it until after the veto session. I thought there might be a certain urgency but I haven’t heard anything since. Neither has Jeri.

“But Guzzardi is not alone. Both state teacher unions won’t touch it. Neither will the Illinois Retired Teachers Association. As one IEA lobbyist told me, they have bigger fish to fry.

“It’s just 300 old people, most over 80 years old.  How long will this be an issue? Let’s call it the teacher pension death watch.

“The reality is that the retiree death watch is also the plan for the larger pension debt. The current Illinois public pension liability is now somewhere over 130 billion.

“Chicago Tribune’s columnist, Kristen McQueary, writes today again calling for Governor Pritzker to back a constitutional amendment that would take out the pension protection clause from the state’s constitution.

“The current language prohibits any reduction in current benefits for public employees. The Illinois Supreme Court has already ruled that this language is clear and unmistakable and was intended to do exactly what is says when it was written 50 years ago by the constitution’s creators.

“The Court blocked any legislative cuts to benefits. Which is why Kristen McQueary has no clue. Even if the pension protection clause was erased, it would not unprotect current public employees (not only current retirees) from receiving contractual benefits. The liability will only grow up to a point.

“But at a certain point, public employees covered under Tier 1 will begin to decline. Could they change the contract for a public employee hired today? Sure. But the legislature can and already has done that without a constitutional change. They created Tier 2 and Tier 3. They reduced the benefits of employees hired after January 1, 2011.

“However, they can’t undo the constitutional and contractual arrangement retroactively. So, while McQueary accuses the Governor of proposing pension solutions that are smoke, it is McQueary bogarting the joint.

“There is nobody in Springfield that is proposing a plan that will pay the 130 billion dollar pension liability. I predict nobody ever will.

“At a certain point over the next 30 years, nearly all of those of us in Tier 1 will be dead. And as with Jeri Shanahan and her 300 or less fellow retirees, that problem will be solved” (The Trib’s Kristen McCreary and the Retired Teacher Death Watch by Fred Klonsky). 

I also posted about Jeri Shanahan in the following articles:

Why are approximately 600 TRS retirees paying more for health insurance than anyone else? (June 18, 2013)

Amid all the Medicare Advantage confusion, have we forgotten there are more than 600 TRS retirees who pay more for health insurance than anyone else? (Oct. 30, 2013)

Why are 602 teacher retirees who live in Illinois still paying more for their health insurance? (July 11, 2014)

“President Trump’s attempt to spend money for building a wall without congressional appropriation of funds for this purpose directly violates the Constitution”-Erwin Chemerinsky

Express and Inherent Presidential Powers: There are four approaches based upon the court case Youngstown Sheet & Tube Co. v. Sawyer, 343 U.S. 579, 634 (1952):

1) There is no inherent presidential power; the president may act only if there is express constitutional or statutory authority.

2) The president has inherent authority unless the president interferes with the functioning of another branch of government or usurps the powers of another branch.

3) The president may exercise powers not mentioned in the Constitution so long as the president does not violate a statute or the Constitution.

4) The president has inherent powers that may not be restricted by Congress and may act unless the Constitution is violated (Chemerinsky 331).

“The federal courts and ultimately the Supreme Court should quickly and emphatically hold that President Trump’s attempt to fund the border wall by declaring a national emergency is illegal and unconstitutional. In 1974, when President Richard Nixon made an unprecedented claim of executive power to resist complying with a subpoena from the Watergate special prosecutor, the Supreme Court unanimously rejected this assertion and enforced constitutional checks and balances. We should hope and expect that even the conservative Roberts Court, with two justices appointed by President Trump, will likewise follow the Constitution and reject Trump’s dangerous claim of emergency powers.

“The Constitution has no clause that gives the president emergency powers. This was a deliberate and wise choice. The framers of the Constitution wanted to make sure that its requirements, including checks and balances, are enforced even in times of crisis. Indeed, when prior presidents have tried to claim inherent power to deal with emergencies, the Supreme Court has rejected such claims.   

“During the Korean War, President Harry Truman seized the steel mills to assure continued steel production in the face of a labor dispute. The Supreme Court, in Youngstown Sheet & Tube v. Sawyer (1952), decisively ruled against President Truman and rejected his claimed authority to take actions to deal with a national emergency. The Court stressed that Truman’s actions violated the separation of powers and usurped the powers of Congress.

“Likewise, President Trump’s attempt to spend money for building a wall without congressional appropriation of funds for this purpose directly violates the Constitution. The Constitution reads, ‘No Money shall be drawn from the Treasury, but in Consequence of Appropriations made by Law.’ Under the Constitution, Congress has the power of the purse and it is impermissible for the president to spend money without specific statutory authorization. 

“No such authorization exists for building the border wall. Trump repeatedly has urged Congress to provide such funds. Even when Republicans controlled both houses of Congress, from 2017 to 2019, Trump could not get this authorization. More recently, the government shut down for a month because Congress would not appropriate the funds Trump wanted to build the wall. For Trump to fund the wall unilaterally without congressional approval, even by claiming a national emergency, is clearly unconstitutional.  

“Trump likely will claim the authority to fund building the wall under the National Emergencies Act of 1976. One provision says that if there is a national emergency, funds in the Defense Department budget that are not ‘obligated’ can be used for construction projects to support the armed forces. It reads: ‘Secretary of Defense, without regard to any other provision of law, may undertake military construction projects, and may authorize Secretaries of the military departments to undertake military construction projects that are necessary to support such use of the armed forces.’ The statute is about construction projects to support the armed forces. Trump’s wall is not about that at all.

“Members of Congress have standing to sue President Trump for violating the separation of powers and nullifying the spending power possessed by Congress. In 2016, U.S. District Court Judge Rosemary Collyer held that members of the Republican-controlled Congress had legal standing to sue the president to challenge the spending of federal funds without specific federal authorization. She held that the Obama administration was violating the Constitution by paying, without a congressional appropriation, the promised reimbursements to health insurers who provide coverage at reduced costs to low-income Americans. ‘Paying [those] reimbursements without an appropriation thus violates the Constitution,’ she wrote. ‘Congress is the only source for such an appropriation, and no public money can be spent without one.’

“At the time, Republican House Speaker Paul Ryan called the ruling ‘a historic win for the Constitution and the American people. The court ruled that the administration overreached by spending taxpayer money without approval from the people's representatives.’

“Members of Congress should now sue President Trump—and should prevail in court. No court should accept President Trump’s claim of a ‘national emergency.’ Trump has been calling for the wall for years. The claim of ‘national emergency’ is a pretext to allow the president to do whatever he wants.

“If my prediction is wrong and Trump wins in court, Democratic presidential candidates should prepare their own wish lists of what can be done without congressional approval. A Democratic president could follow the Trump example and declare a national emergency to deal with the problem of climate change—a genuine emergency.

“But whether we have a Democratic or Republican president, and no matter how noble the cause, we should be frightened of presidents acting unilaterally to deal with a national emergency. That would completely undermine the checks and balances and the separation of powers that are at the core of our constitutional system of government. Until and unless Congress authorizes funds for the border wall, it is unconstitutional and illegal for President Trump to use any other funds for this purpose” (Trump’s ‘Emergency’ Action: Unlawful and Unconstitutional).

Works Cited:

Chemerinsky, Erwin. Constitutional Law: Principles and Policies, 2^nd ed. New York: Aspen Publishers, 2002.

Chemerinsky, Erwin. “Trump’s ‘Emergency’ Action: Unlawful and Unconstitutional.” The American Prospect, 15 February 2019 https://prospect.org/article/trumps-emergency-action-unlawful-and-unconstitutional

"Why do some British people not like Donald Trump?" by Nate White

"A few things spring to mind. Trump lacks certain qualities which the British traditionally esteem. For instance, he has no class, no charm, no coolness, no credibility, no compassion, no wit, no warmth, no wisdom, no subtlety, no sensitivity, no self-awareness, no humility, no honour and no grace - all qualities, funnily enough, with which his predecessor Mr. Obama was generously blessed.

“So for us, the stark contrast does rather throw Trump’s limitations into embarrassingly sharp relief. Plus, we like a laugh. And while Trump may be laughable, he has never once said anything wry, witty or even faintly amusing - not once, ever.

“I don’t say that rhetorically, I mean it quite literally: not once, not ever. And that fact is particularly disturbing to the British sensibility - for us, to lack humour is almost inhuman. But with Trump, it’s a fact. He doesn’t even seem to understand what a joke is - his idea of a joke is a crass comment, an illiterate insult, a casual act of cruelty.

“Trump is a troll. And like all trolls, he is never funny and he never laughs; he only crows or jeers. And scarily, he doesn’t just talk in crude, witless insults - he actually thinks in them. His mind is a simple bot-like algorithm of petty prejudices and knee-jerk nastiness. There is never any under-layer of irony, complexity, nuance or depth. It’s all surface.

“Some Americans might see this as refreshingly upfront. Well, we don’t. We see it as having no inner world, no soul. And in Britain we traditionally side with David, not Goliath. All our heroes are plucky underdogs: Robin Hood, Dick Whittington, Oliver Twist.

“Trump is neither plucky, nor an underdog. He is the exact opposite of that. He’s not even a spoiled rich-boy, or a greedy fat-cat. He’s more a fat white slug. A Jabba the Hutt of privilege. And worse, he is that most unforgivable of all things to the British: a bully. That is, except when he is among bullies; then he suddenly transforms into a sniveling sidekick instead.

“There are unspoken rules to this stuff - the Queensberry rules of basic decency - and he breaks them all. He punches downwards - which a gentleman should, would, could never do - and every blow he aims is below the belt. He particularly likes to kick the vulnerable or voiceless - and he kicks them when they are down.

“So the fact that a significant minority - perhaps a third - of Americans look at what he does, listen to what he says, and then think 'Yeah, he seems like my kind of guy’ is a matter of some confusion and no little distress to British people, given that: 1) Americans are supposed to be nicer than us, and mostly are; 2) You don't need a particularly keen eye for detail to spot a few flaws in the man.

“This last point is what especially confuses and dismays British people, and many other people too; his faults seem pretty bloody hard to miss. After all, it’s impossible to read a single tweet, or hear him speak a sentence or two, without staring deep into the abyss. He turns being artless into an art form; he is a Picasso of pettiness; a Shakespeare of shit. His faults are fractal: even his flaws have flaws, and so on ad infinitum.

“God knows there have always been stupid people in the world, and plenty of nasty people too. But rarely has stupidity been so nasty, or nastiness so stupid. He makes Nixon look trustworthy and George W look smart. In fact, if Frankenstein decided to make a monster assembled entirely from human flaws - he would make a Trump. And a remorseful Doctor Frankenstein would clutch out big clumpfuls of hair and scream in anguish: ‘My God… what… have… I… created?’”

“A new culprit has emerged in the quest to understand how Alzheimer’s attacks the human brain”

“A team of scientists at the Fisher Center for Alzheimer’s Research laboratory at Rockefeller University managed to isolate a metabolite called C99 and found — quite unexpectedly — that it seems to cluster in regions of the brain that are most susceptible to Alzheimer’s.

“‘It was a total surprise because we saw the places where C99 accumulates in the brain of Alzheimer’s patients are exactly the places where neurons later are going to die,’ says Victor Bustos, senior research associate at the Fisher Center for Alzheimer’s Research. ‘C99 becomes a very good marker for neurodegeneration.

“In the world of dementia research, having a new ‘marker’ is important because these are the targets scientists go after when they test drugs in the hopes of finding a cure for Alzheimer’s. So far, that cure has been elusive, and this discovery suggest a possible reason why. Perhaps researchers have been aiming at the wrong target.

“The markers most associated with Alzheimer’s are the so-called ‘plaques’ and ‘tangles’ that accumulate in the brain of people with this disease. The plaques are clumps of beta-amyloid protein that coat neurons as the disease advances, and the tangles are tau proteins that go awry inside the neurons.

“Alzheimer’s research has focused heavily on medicines that seek to clear way amyloid plaque, but those efforts have led to a long string of disappointing results. Even when the drugs have reduced plaque, the memory of Alzheimer’s patients has not improved. Bustos says some regions of the brain are heavily affected by Alzheimer’s, while other regions aren’t. For someone suffering from the disease, beta-amyloid is present in high amounts in both regions, he says. ‘So that is kind of an argument to say beta-amyloid may not be well-enough related to Alzheimer’s disease to be the cause of Alzheimer’s,’ Bustos says.

“What he and his colleagues did was go in search of other potential culprits, using a technique that includes sophisticated super-resolution microscopy. ‘We decided to look at C99 because it is the precursor of beta-amyloid,’ Bustos says. ‘Before beta-amyloid becomes beta-amyloid, it is first called C99. You can call it an intermediate in the production of amyloid.’

“Bustos and his colleagues knew they had found something important when C99 showed up in high concentrations in areas of the brain most involved in memory, but not in other areas of the brain less susceptible to Alzheimer’s. ‘The hippocampus is one of the first areas to degenerate in Alzheimer’s disease, and we observed an early accumulation of C99 in the hippocampus,’ he says. ‘Later, after the hippocampus has degenerated, the frontal cortex starts to degenerate. We observed the same pattern. There was a secondary accumulation of C99 in the frontal cortex. Those are areas that are vulnerable to Alzheimer’s.’

“The significance of this result led the research team to post its findings online, rather than wait out the lengthy process of getting it published in a peer-review journal. ‘That way, people can know about these findings,’ Bustos says. ‘We have had an extraordinary response. In less than a week after it was public, I could see that already 3,600 people had looked at the paper, which is an extraordinary number.’

“Dr. Michelle Papka, founder and director of the Cognitive and Research Center of New Jersey, has read the paper and describes it as ‘a very interesting finding and a very worthwhile hypothesis to pursue.’ Papka was not involved in this study, but has been treating people with Alzheimer’s and engaging in dementia research for more than two decades. She describes the finding just published as a ‘pilot study, a preliminary first step.’

“If further research were to confirm that C99, not amyloid, is a primary driver of neurological damage in Alzheimer’s patients, that could open new avenues of research that might bring better results. ‘If it turns out this is correct, some of these anti-beta preventions may have been going after the wrong targets, and that may be why some have led to futile results,’ Papka says. ‘This type of research might help us determine more specifically what we need to target.’

“Based on his research, Bustos is not suggesting that amyloid is the wrong target. ‘I believe both C99 and amyloid contribute to the disease because amyloid is a toxic substance,’ he says. However, he says past efforts may have been flawed because many of the medicines used to attack beta-amyloid in clinical trials have done so in a way that actually raises the level of C99 in the brain.

“‘We believe C99 is the most toxic substance, so what we propose is that instead of reducing amyloid and increasing C99, we should aim at strategies that decrease both C99 and amyloid,’ he says. ‘What this study is telling the pharmaceutical companies is, please focus your resources on lowering C99; it’s a much better target than amyloid alone.’”

The Fisher Center lab at Rockefeller University is a leading scientific center focusing on Alzheimer’s disease. The research involving C99 was funded by the Fisher Center for Alzheimer’s Research Foundation, whose mission is to understand the causes of Alzheimer’s, improve the care of those living with it and find a cure. For more information, visit the foundation’s website at www.alzinfo.org

SCIENTISTS GET A ‘TOTAL SURPRISE’ AND A PROMISING NEW CLUE FOR HOW TO CURE ALZHEIMER’S 

Stress Linked to an Increased Risk of Dementia

“Men and women who had high blood levels of cortisol, the so-called stress hormone, performed worse on tests of memory than those with normal cortisol levels. They also had smaller brains volumes, which has been linked to an increased risk of dementia later in life.

“‘Cortisol affects many different functions, so it is important to fully investigate how high levels of the hormone may affect the brain,’ said study author Dr. Justin B. Echouffo-Tcheugui of Harvard Medical School. Cortisol, produced by the adrenal glands, helps the body respond to stress. It helps to control inflammation, blood sugar and blood pressure levels, among other body functions. Persistently high cortisol levels are a sign of chronic stress.

“For the study, researchers looked at 2,231 men and women, most in their 40s or 50s. All were part of a larger study and free of dementia. Study participants were given tests of memory and thinking skills at the start of the study, and again eight years later. Doctors also collected blood tests to measure cortisol levels, and most had MRI brain scans to assess brain size.

“Participants were divided into three groups: low, middle and high cortisol levels. Those with the highest cortisol levels, a sign of stress, had lower scores on tests of memory and thinking skills than those with normal levels of cortisol. They also had slightly smaller brain volumes. No links were found between low cortisol levels and memory or brain size.

“The researchers controlled for smoking, high blood pressure, blood vessel disease and other factors that can impact brain health. Still, the ties between cortisol levels and memory impairment and brain size persisted. The findings were published in Neurology.

“‘Our research detected memory loss and brain shrinkage in middle-aged people before symptoms started to show,’ said Dr. Echouffo-Tcheugui. As a result, ‘It’s important for people to find ways to reduce stress, such as getting enough sleep, engaging in moderate exercise, incorporating relaxation techniques into their daily lives, or asking their doctor about their cortisol levels and taking a cortisol-reducing medication if needed.’”

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by Marc Flajolet, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Justin B. Echouffo-Tcheugui, MD, PhD; Sarah C. Conner, MPH; Japyandra J. Himali, PhD; et al: “Circulating Cortisol and Cognitive and Structure Brain Measures: The Framingham Heart Study.” Neurology October 24, 2018

Stress May Affect Memory and Brain Size

A State of the Union Gesture, February 5, 2019

Gum Disease Could Be a Contributing Factor of Alzheimer’s Disease

“AFTER decades of disappointment, we may have a new lead on fighting Alzheimer’s disease. Compelling evidence that the condition is caused by a bacterium involved in gum disease could prove a game-changer in tackling one of medicine’s biggest mysteries, and lead to effective treatments or even a vaccine.

“As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimer’s constitutes some 70 per cent of these cases (see “What is Alzheimer’s disease”), yet we don’t know what causes it. The condition, which results in progressive loss of memory and cognitive function, usually over a decade or so, is devastating both to those who have it and to their loved ones.

“The condition often involves the accumulation of two types of proteins – called amyloid and tau – in the brain. As these are among the earliest physical signs of the disease, the leading hypothesis since 1984 has been that the condition is caused by the defective control of these proteins, especially amyloid, which accumulates to form large, sticky plaques in the brain.

“The bulk of research into understanding and treating Alzheimer’s has centered on this ‘amyloid hypothesis.’ Huge sums of money have been invested in experiments involving mice genetically modified to produce amyloid, and in developing drugs that block or destroy amyloid proteins, or sometimes degraded tangles of tau.

“It has become clear that this approach isn’t working. In 2018 alone, the US National Institutes of Health spent $1.9 billion on Alzheimer’s research. But according to a recent study, the failure rate of drug development for Alzheimer’s has been 99 per cent.

“Some have begun to question the amyloid hypothesis. The lack of results has been compounded by the discovery that people – including some in their 90s with exceptional memories – can have brain plaques and tangles without having dementia. In a review of the research to date last year, Bryce Vissel at the University of Technology Sydney, Australia, concluded that there isn’t sufficient data to suggest that ‘amyloid has a central or unique role in Alzheimer’s.’

“In 2016, researchers discovered that amyloid seems to function as a sticky defense against bacteria. They found that the protein can act as an anti-microbial compound that kills bacteria, and when they injected bacteria into the brains of mice engineered to make Alzheimer’s proteins, plaques developed round bacterial cells overnight.

“At the time, the team said it still believed that amyloid itself went on to cause the brain damage of Alzheimer’s, not bacteria. But a spate of subsequent studies have looked at microbes. Bacteria have been found in the brains of people who had Alzheimer’s when they were alive. But it hasn’t been clear whether the bacteria caused the disease or were simply able to enter brains damaged by Alzheimer’s.

“Multiple teams have been researching Porphyromonas gingivalis, the main bacterium involved in gum disease, which is a known risk factor for Alzheimer’s. So far, teams have found that P. gingivalis invades and inflames brain regions affected by Alzheimer’s; that gum infections can worsen symptoms in mice genetically engineered to have Alzheimer’s; and that it can cause Alzheimer’s-like brain inflammation, neural damage and amyloid plaques in healthy mice.

“A whole new hypothesis: ‘When science converges from multiple independent laboratories like this, it is very compelling,’ says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco. Now researchers from Cortexyme and several universities have reported finding the two toxic enzymes that P. gingivalis uses to feed on human tissue in 99 and 96 per cent of 54 human Alzheimer’s brain samples taken from the hippocampus – a brain area important for memory (Science Advances, doi.org/gftvdt). These protein-degrading enzymes are called gingipains, and they were found in higher levels in brain tissue that also had more tau fragments and thus more cognitive decline.

“The team also found genetic material from P. gingivalis in the cerebral cortex – a region involved in conceptual thinking – in all three Alzheimer’s brains they looked for it in. ‘This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains co-localising with plaques,’ says Sim Singhrao at the University of Central Lancashire, UK, who wasn’t involved in the study. Her team has previously found that P. gingivalis actively invades the brains of mice with gum infections.

“When Lynch and her colleagues looked at brain samples from people without Alzheimer’s, they saw that some had P. gingivalis and protein accumulations, but at low levels. We already know that amyloid and tau can accumulate in the brain for 10 or 20 years before Alzheimer’s symptoms begin. This, says the team, shows that P. gingivalis doesn’t get into the brain as a result of Alzheimer’s – but could be the cause.

“When the team gave P. gingivalis gum disease to mice, it led to brain infection, amyloid production, tangles of tau protein and neural damage in the regions and nerves normally affected by Alzheimer’s. This suggests causation, says Lynch.

“She adds that P. gingivalis fulfils an updated set of criteria for attributing a disease to a particular pathogen. These conditions are named Koch’s postulates, after Robert Koch, a founder of the germ theory of disease.

‘The study does address most of Koch’s postulates,’ says Robert Genco of the University at Buffalo, New York. ‘Future studies need to be in humans to be convincing.’

“We don’t know how P. gingivalis gets into the brain, but there are plausible routes it could take. Your mouth normally hosts a diverse and relatively stable community of bacteria, but when dental plaque builds under the edge of your gums, it can form inflamed pockets in which P. gingivalis can thrive and release toxins.

“This inflammation can lead to chronic periodontitis and tooth loss, and some studies have shown that people with fewer teeth are more likely to have dementia. The inflammation and toxins caused by P. gingivalis damage the lining of your mouth, which may make it possible for oral bacteria to enter the bloodstream and then other organs. Even if you don’t have gum disease, transient damage to your mouth lining from eating or tooth-brushing can let mouth bacteria into your blood, says Lynch.

“As to how P. gingivalis might cause dementia after it arrives in the brain, there are two clear possibilities. It may trigger the release of amyloid, the brain’s method of trying to contain the infection, and this may then kill neurons.

“Hope for treatments: The speed at which damage accumulates is a key factor in the disease. Although many people harbour P. gingivalis in their mouths, only some develop Alzheimer’s. Because it can be decades before Alzheimer’s symptoms appear, whether a person develops the condition could come down to how much damage occurs before they die of other causes.

“The blood-brain barrier should protect your brain from microbes, but P. gingivalis can invade white blood cells and the cells lining blood vessels, so might cross it that way. It may also invade cranial nerves near the mouth, then spread from cell to cell towards the brain over a period of years.

“Or P. gingivalis may directly damage the brain. We already know that Alzheimer’s involves inflammation, an excessive immune response that ends up killing neurons instead of protecting them. P. gingivalis is known to cause inflammation in gum tissue, and it may do so in the brain as well. In response to the new findings, David Reynolds of the Alzheimer’s UK charity said he is dubious that P. gingivalis causes Alzheimer’s, because of the evidence showing that a person’s genes play a crucial role in the disease.

“‘Strong genetic evidence indicates that factors other than bacterial infections are central to the development of Alzheimer’s, so these new findings need to be taken in the context of this existing research,’ he said in a statement. But a bacterial hypothesis for Alzheimer’s doesn’t conflict with genetic evidence. The human body’s propensity for inflammation can vary according to genetic variations that affect our immune systems, and this may influence how much damage P. gingivalis induces in a brain.

“The biggest genetic risk factor for Alzheimer’s is a variant of the gene that makes the ApoE immune protein. Last year, a team in Sweden found that the gingipains released by P. gingivalis break up the ApoE protein into fragments, cleaving it at the site of a particular amino acid within the protein, and that these fragments may harm nerves. The ApoE4 variant of this protein contains more of this amino acid, suggesting that the reason people who make this variant are at a higher risk of developing Alzheimer’s may be because harmful levels of ApoE protein fragments build up more quickly in their brains than in those of other people.

“‘Alzheimer’s strikes people who accumulate gingipains and damage in the brain fast enough to develop symptoms during their lifetimes,’ says Lynch. She says her team’s findings are a ‘universal hypothesis of pathogenesis,’ fully explaining the causes of Alzheimer’s disease. But Vissel warns that Alzheimer’s is a complex disease. ‘The answer is unlikely to be one-cause-fits-all. We need to keep open eyes.’

“However, the new study is ‘very exciting,’ he says. ‘Alzheimer’s is so common in people at advanced age that I think it can only be either some intrinsic property of the brain, or an infection.’

“If this new hypothesis of Alzheimer’s is borne out, the good news is that it could lead to effective treatments for the condition. Although there is plenty you can do to reduce your risk of gum disease, Cortexyme is hoping it can stop or even reverse Alzheimer’s using molecules it has developed that block gingipains. The firm found that giving some of these to mice with P. gingivalis infections reduced brain infection, halted amyloid production, lowered brain inflammation and even rescued damaged neurons. ‘This provides hope of treating or preventing Alzheimer’s disease one day,’ says Singhrao.

“Cortexyme reported last year that the best of its gingipain blockers had passed initial safety tests in people, and entered the brain. It also seemed to improve symptoms in participants with Alzheimer’s. The firm will launch a larger trial later this year.

“The company also plans to test the drug against gum disease itself. Efforts to fight that have led a team in Melbourne to develop a vaccine for P. gingivalis that started tests in 2018. A vaccine for gum disease would be welcome – and if it also stops Alzheimer’s the impact could be enormous.

It is early days for this new hypothesis, and if the pursuit of amyloid-busting drugs over the past few decades has taught us anything, says Vissel, it is that a complex disease may not have a simple mechanism.

“Even if P. gingivalis is confirmed as a cause of Alzheimer’s, we don’t know yet whether it will turn out to be the only cause or one of several factors contributing to the disease. ‘This paper is very important,’ says George Perry at the University of Texas at San Antonio. ‘The view that pathogens might be one of several paths leading to Alzheimer’s disease fits my current thoughts of amyloid and tau being critical brain responses to injury, instead of the initiators.’

“That, he says, is why years of efforts to treat Alzheimer’s by removing those proteins have seen few results: they are symptoms of the disease, not its cause. ‘This is a further turning point in the understanding that infections and inflammation can be at the heart of Alzheimer’s disease.’”

We may finally know what causes Alzheimer’s – and how to stop it by Debora MacKenzie