Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,831 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Showing posts with label alzheimers research. Show all posts
Showing posts with label alzheimers research. Show all posts
Alcohol may not affect the Alzheimer’s-damaged brain in one single way—instead, its impact appears to depend on which type of brain change is already present, according to new research from Texas A&M University.
The findings complicate the widely held assumption that alcohol simply worsens Alzheimer’s-related decline across the board. Instead, the study found that alcohol interacted with two of the disease’s hallmark features—amyloid-beta plaques and tau tangles—in opposite ways.
Two Proteins, Two Different Reactions
Alzheimer’s disease is marked by two main types of abnormal protein buildup in the brain: amyloid-beta, which forms sticky plaques between brain cells, and tau, which forms tangles inside them. Scientists have long studied both, but rarely examined how alcohol interacts with each separately.
The research team set out to do exactly that. They focused on the corticostriatal circuit, a brain pathway that helps control decision-making and behavioral flexibility—the ability to adjust behavior when circumstances change. This function is often impaired in both addiction and Alzheimer’s disease.
Using animal models representing amyloid-beta pathology and tau pathology separately, the researchers tracked how chronic alcohol exposure changed communication within this circuit.
An Unexpected Reversal
Scientists initially expected alcohol to push each model further in the direction its existing pathology was already headed. Amyloid-beta pathology is typically linked to abnormal increases in brain cell activity, while tau pathology is usually linked to reduced communication between cells. The researchers therefore predicted alcohol would increase circuit activity in the amyloid-beta model and decrease it in the tau model.
Instead, they found the opposite. In animals with amyloid-beta pathology, alcohol reduced communication in the corticostriatal circuit. In animals with tau pathology, alcohol increased it. The same substance produced reversed effects depending on which type of pathology was present.
“The key point for non-experts is not that our study proves alcohol causes Alzheimer’s disease,” the researchers toldNewsweek, in a joint statement. “Rather, it suggests that alcohol can meaningfully affect vulnerable brain circuits, and that those effects depend on which Alzheimer’s-related changes are already present. People who are concerned about their brain health or Alzheimer’s risk may wish to be cautious about alcohol and follow their doctor’s advice.
(This will be your doctor's advice; NO thinking required!
“More broadly, our findings raise new questions about how alcohol, Alzheimer’s-related brain changes, and the brain’s immune responses influence one another—and how alcohol might shape brain-circuit function and the progression of the disease.”
Why It Matters
The findings add to growing evidence that Alzheimer’s disease is not one uniform condition. Differences in disease stage, the specific pathology involved, genetics and lifestyle factors may all shape how a person’s brain responds to outside influences such as alcohol.
That distinction could eventually matter for how doctors think about risk. A blanket warning about alcohol and dementia may be too simple, the researchers suggest, if the underlying brain pathology changes how alcohol acts on neural circuits in the first place.
Dr. Amy Swift, psychiatrist and deputy chief medical officer at Silver Hill Hospital, told Newsweek: “Integrating these nuanced insights into clinical decision-making may be particularly valuable for patients who continue to struggle with alcohol use after receiving a diagnosis of Alzheimer’s disease and related dementia. As our understanding of the underlying mechanisms evolves, treatment approaches should likewise adapt to reflect these biological and phenotypic differences, ultimately supporting more individualized, evidence-informed patient care.”
Ask your competent? doctor for the EXACT LIMITS on your alcohol consumption if you're doing it(like me) to increase your social connections and thus prevent dementia! NO answer or just a blank stare; INCOMPETENCE! Fire them!
Summary: A new study focused on the corticostriatal circuit, a critical neural pathway governing decision-making, goal-directed behavior, and behavioral flexibility. Using animal models representing isolated features of the disease, the team discovered that alcohol dramatically reduces communication in the presence of amyloid-beta, but significantly amplifies circuit communication in the presence of tau. This unexpected divergence proves that everyday exposures can interact with pre-existing biological conditions in entirely non-linear ways.
Key Facts
The Cognitive Overlap: Behavioral flexibility is heavily impaired in both substance addiction and early-stage Alzheimer’s disease. This operational overlap prompted the Wang lab to investigate whether alcohol use alters the specific brain circuits targeted during early dementia progression.
The Additive Assumption Upended: Because amyloid-beta pathology naturally causes abnormal spikes in neural activity and tau causes depressed communication, researchers assumed alcohol would act as a simple additive risk factor, pushing each condition further in its existing path. Instead, alcohol triggered the exact opposite pattern.
The Amyloid Suppression: In animal models characterized by amyloid-beta accumulation, alcohol exposure severely decreased signaling communication across the corticostriatal pathway.
The Tau Amplification: In stark contrast, when applied to models defined by tau protein tangles, alcohol exposure sharply increased signaling communication within the exact same brain highway.
Microglia Immune Disruption: Beyond altering circuit-level communication, the study revealed that alcohol actively interferes with microglia, the resident immune cells of the brain. In the amyloid-dominated models, alcohol disrupted the microglia’s ability to clean up and respond to toxic amyloid buildup.
Rejecting Uniform Profiles: These findings emphasize that Alzheimer’s disease is not a uniform condition. Because human patients carry completely different ratios of amyloid and tau depending on their genetics, lifestyle, and disease stage, a person’s neurological response to alcohol will vary significantly based on their unique internal pathology.
Source: Texas A&M
Alcohol use has been associated with an increased risk of cognitive decline and dementia. But new research from the Texas A&M University Naresh K. Vashisht College of Medicine at Texas A&M Health suggests the relationship between alcohol and Alzheimer’s disease is more complicated than previously thought.
Instead of affecting all Alzheimer’s-related brain changes in the same way, alcohol interacted differently with amyloid-beta-related and tau-related pathology in animal models, two key pathological processes involved in Alzheimer’s disease.
Alcohol exposure triggers opposite signaling behaviors within the brain’s corticostriatal circuit depending on the presence of amyloid-beta or tau protein hallmarks, shattering the long-standing medical assumption that lifestyle risk factors induce a uniform additive effect on dementia progression. Credit: Neuroscience NewsThe study was led by postdoctoral research associate Dr. Yufei Huang in the lab of Dr. Jun Wang, professor in the Department of Neuroscience and Experimental Therapeutics. The researchers focused on how alcohol affects brain circuits that are important for behavioral flexibility, or the ability to adjust behavior when situations change. This ability often becomes impaired in both addiction and Alzheimer’s disease.
“We started thinking about whether the same circuits involved in flexibility and adaptation might also be important in Alzheimer’s disease,” Huang said.
The team studied a brain circuit called the corticostriatal circuit, which helps control decision-making and behavioral flexibility. When this circuit does not work properly, people may struggle to adapt to new information or changing environments.
To test the effects of alcohol, the researchers used animal models that represent different Alzheimer’s-related pathological features. One model was based on amyloid-beta, a protein that forms plaques in the brain. The other was based on tau, a protein that forms tangles inside brain cells.
What they found surprised them.
Alcohol affected communication differently in the corticostriatal circuit, a major neural pathway involved with goal-directed behaviors. In animal models with amyloid-beta pathology, alcohol reduced communication in the circuit. In those with tau pathology, alcohol increased communication in the same circuit. In other words, the same exposure led to opposite effects depending on the type of Alzheimer’s-related change present.
“This finding was a complete surprise to us,” Huang said. “We expected alcohol to worsen both conditions in a similar way, but that was not what we saw.”
The researchers explained that amyloid-beta and tau affect the brain differently. Amyloid-beta pathology is often associated with abnormal increases in neural activity, whereas tau pathology is frequently linked to decreased communication between brain cells.
Based on these known differences, the team initially expected alcohol to push each model further in its existing pathological direction—increasing circuit communication in the amyloid-beta model and decreasing it in the tau model. Instead, alcohol produced the opposite pattern, reducing communication in the amyloid-beta model while increasing it in the tau model.
“The results were almost the opposite of what we expected,” Huang said. “To us, this highlights an important principle in biology: Combining two risk factors does not always produce a simple additive effect.”
The study adds to a growing understanding that Alzheimer’s disease is not a single, uniform condition. Different people may have different combinations of disease stage, pathology, genetics and lifestyle factors, which could influence how the brain responds to outside factors such as alcohol.
“This is important because Alzheimer’s disease is not a uniform condition,” Huang said. “People may differ in disease stage, type of brain changes, genetics and lifestyle factors.”
The study also highlights an unexpected link between Alzheimer’s research and addiction science. The Wang lab has long studied how substances like alcohol affect brain circuits involved in learning and decision-making. Those studies showed that substance use can lead to long-term changes in brain flexibility, which is also affected early in Alzheimer’s disease.
That overlap led researchers to ask whether alcohol might also influence Alzheimer’s-related brain changes.
Beyond effects on brain signaling, the study also found that alcohol may interfere with immune cells in the brain, especially in the amyloid model. These immune cells, called microglia, help maintain brain health and respond to disease-related changes such as amyloid accumulation.
“Alcohol not only altered brain circuit function but also appeared to disrupt immune cell responses in the brain,” Huang said. “This may be one way alcohol contributes to Alzheimer’s-related brain dysfunction.”
While the study was done in animal models, the researchers say the findings raise important questions for human health. Alcohol may not affect everyone with Alzheimer’s risk in the same way. People who already have early disease-related brain changes, or who carry genetic risk factors, may respond differently to alcohol exposure.
The team hopes future studies will look at alcohol use in people alongside brain biomarkers such as amyloid, tau and inflammation markers. This could help clarify whether alcohol has different or stronger effects in people who are already in the early stages of Alzheimer’s disease.
For now, the study adds to a growing understanding that brain health is shaped by a combination of biology, environment and lifestyle. Alcohol, rather than having a single effect on the brain, may interact with existing conditions in ways that are more complex than once thought.
Ultimately, the researchers say the goal is not only to understand Alzheimer’s disease better, but also to better understand how everyday exposures may shape brain health over time.
Funding: This research was supported by funding from the National Institute on Alcohol Abuse and Alcoholism (NIAAA/NIH; U01AA025932, R01AA027768, and R01AA030293) and the Texas A&M University Division of Research Targeted Proposal Teams (TPT) funding program.
Key Questions Answered:
Q: Why did scientists expect alcohol to affect amyloid-beta and tau proteins in the exact same way?
A: Traditionally, air pollution, high blood pressure, and alcohol use have been treated as generic risk factors that simply worsen brain health across the board. Because both amyloid plaques and tau tangles are toxic to brain tissue, researchers naturally assumed that adding alcohol to the mix would act like pouring gasoline on a fire, speeding up the damage uniformly. Discovering that alcohol actually dials down brain communication in one model while winding it up in the other was a complete biological surprise.
Q: What is behavioral flexibility, and why is this specific brain circuit so important?
A: Behavioral flexibility is your brain’s ability to smoothly change its strategy or choices when your environment shifts. The corticostriatal circuit is the primary brain highway that controls this decision-making process. When this circuit is damaged or altered, individuals get “stuck” in repetitive loops and struggle to process new information. Because this flexibility breaks down very early in both alcohol addiction and Alzheimer’s disease, understanding how they intersect is crucial to protecting adult cognitive health.
Q: Does this mean alcohol could actually be good for certain types of Alzheimer’s patients?
A: Absolutely not. While alcohol caused an unexpected surge in communication within the tau model, an abnormal spike in signaling can be just as toxic and damaging to brain networks as a drop in communication. Dr. Yufei Huang stresses that the real takeaway is that combining two different health risks doesn’t produce a simple, predictable outcome. Instead of showing that alcohol is beneficial, the study proves that everyday lifestyle exposures interact with our unique internal biology in highly complex, unpredictable ways.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this Alzheimer’s disease research news
Author: Laura Tolentino Source: Texas A&M Health Contact: Laura Tolentino – Texas A&M Health Image: The image is credited to Neuroscience News
Because acknowledging it would have resulted in vast pressure to do the trial. It is much cheaper to not release the report. The company doesn't care about anyone's health, profit is the only concern.
A
team of researchers inside Pfizer made a startling find in 2015: The
company's blockbuster rheumatoid arthritis therapy Enbrel, a powerful
anti-inflammatory drug, appeared to reduce the risk of Alzheimer's
disease by 64 per cent.
The results were from an analysis of
hundreds of thousands of insurance claims. Verifying that the drug would
actually have that effect in people would require a costly clinical
trial - and after several years of internal discussion, Pfizer opted
against further investigation and chose not to make the data public, the
company confirmed.
Alzheimer's cause plaques between nerve cells in the brain.
Researchers
in the company's division of inflammation and immunology urged Pfizer
to conduct a clinical trial on thousands of patients, which they
estimated would cost $US80 million, to see if the signal contained in
the data was real, according to an internal company document obtained by
The Washington Post.
"Enbrel could potentially safely
prevent, treat and slow progression of Alzheimer's disease,'' said the
document, a PowerPoint slide show prepared for review by an internal
Pfizer committee in February 2018.
The
company said it decided during its three years of internal reviews that
Enbrel did not show promise for Alzheimer's prevention because the drug
does not directly reach brain tissue. It deemed the likelihood of a
successful clinical trial to be low. A synopsis of its statistical
findings prepared for outside publication, it says, did not meet its
"rigorous scientific standards".
Science was the sole determining factor against moving forward, company spokesman Ed Harnaga said.
Pfizer
said it opted against publication of its data because of its doubts
about the results. It said publishing the information might have led
outside scientists down an invalid pathway.
Pfizer's
deliberations, which previously have not been disclosed, offer a rare
window into the frustrating search for Alzheimer's treatments inside one
of the world's largest drug companies. Despite billions spent on
research, Alzheimer's remains a stubbornly prevalent disease with no
effective prevention or treatment.
Some
outside scientists disagree with Pfizer's assessment that studying
Enbrel's potential in Alzheimer's prevention is a scientific dead end.
Rather, they say, it could hold important clues to combating the disease
and slowing cognitive decline in its earliest stages.
Pfizer did
share the data privately with at least one prominent scientist, but
outside researchers believe Pfizer also should at least have published
its data, making the findings broadly available to researchers.
"Of
course they should. Why not?'' said Rudolph Tanzi, a leading
Alzheimer's researcher and professor at Harvard Medical School and
Massachusetts General Hospital.
"It would benefit the scientific
community to have that data out there,'' said Keenan Walker, an
assistant professor of medicine at Johns Hopkins who is studying how
inflammation contributes to Alzheimer's. "Whether it was positive data
or negative data, it gives us more information to make better informed
decisions.''
Internal
discussions about possible new uses of drugs are common in
pharmaceutical companies. In this case, Pfizer's deliberations show how
decisions made by industry executives - who are ultimately accountable
to shareholders - can have an impact well beyond corporate board rooms.
As
its Enbrel deliberations ended early last year, Pfizer was getting out
of Alzheimer's research. It announced in January 2018 that it would be
shutting down its neurology division, where Alzheimer's treatments were
explored, and laying off 300 employees.
The company says it was not worth pursuing the results.Credit:AP
Drug
companies often are criticised for extending the patent life of a drug -
and winning new profits - by merely tweaking a drug's molecule or
changing the method of delivery into the body. But it is a "heavy lift''
for a company to win regulatory approval to use a drug for a completely
different disease, said Robert Field, a professor of law and health
care management at Drexel University.
"Our patent laws do not
provide the appropriate incentives,'' Field said. Drug therapy for early
Alzheimer's "would be a godsend for American patients, so we should be
doing everything we can as a country to encourage development of
treatments. It's frustrating that there may be a missed opportunity.''
As
Enbrel's life cycle winds down, Pfizer has introduced a new rheumatoid
arthritis drug, Xeljanz, that works differently from Enbrel. Pfizer is
putting its marketing muscle behind the new treatment. While Enbrel
revenue is shrinking, Xeljanz revenue is growing. The Xeljanz patent
expires in 2025 in the United States and 2028 in Europe, according to
Pfizer's public disclosures. The drug is on track to make Pfizer
billions more each year for the foreseeable future.
Drug companies
frequently have been pilloried for not fully disclosing negative side
effects of their drugs. What happens when the opposite is the case? What
obligation does a company have to spread potentially beneficial
information about a drug, especially when the benefits in question could
improve the outlook for treating Alzheimer's, a disease that afflicts
at least 500,000 new US patients per year?
A
medical ethics expert argued that Pfizer has a responsibility to
publicise positive findings, although it is not as strong as an
imperative to disclose negative findings.
"Having acquired the
knowledge, refusing to disclose it to those who might act upon it hides a
potential benefit, and thereby wrongs and probably harms those at risk
of developing Alzheimer's by impeding research,'' said Bobbie Farsides,
professor of clinical and biomedical ethics at Brighton and Sussex
Medical School in London.
Compare to stroke. In the last 40 years of stroke research has there been any successes? tPA is a failure at 12% full recovery. Survivors could run this much much better that all these Drs. and PhDs.
Isn't this exactly what our stroke leadership should be doing? Putting together a strategy to solve stroke and then get funding for that? Stroke right now is a management problem not a medical problem. There are thousands of research trials needing followup that can solve stroke. We need leadership that understands that concept. We don't need fucking lazy press releases and prevention crap.
High-profile investors led by billionaires Bill Gates and Leonard Lauder are throwing their weight behind a “venture philanthropy vehicle” offering more than $30 million in grants for new biomarkers and early diagnostic tests for Alzheimer’s disease.
In collaboration with the Alzheimer’s Drug Discovery Foundation, the new Diagnostics Accelerator will aim to back promising research that may not guarantee an immediate commercial return—hoping to take more risks than a traditional VC fund, while also focusing on products being developed for market, over basic science research.
One of the main bottlenecks in Alzheimer’s drug development has been a lack of validated biomarkers to diagnose patients noninvasively, monitor progression or reveal subgroups that may benefit from specific therapies in clinical trials.
“Like in cancer today, using the biomarker-specific model of precision medicine, we will be able to predict more accurately which treatment and prevention strategies will work in different at-risk populations of people who have Alzheimer’s disease or other forms of dementia,” said Howard Fillit, founding executive director and chief science officer of the ADDF.
Currently, the only way to definitively diagnose the disease is through an autopsy; tests of cognitive decline need to rule out other possible causes. Positron emission tomography scans can be used to detect amyloid plaque deposits in the brain, but the technology is not widely available and carries high radiation exposure.
"The significance of biomarkers in Alzheimer's disease research is underscored by recent FDA guidelines that recognize the critical role of biomarkers in drug development, and shift the research definition of the early stages of the disease to include biomarkers, even before clinical symptoms become apparent," Fillit added.
The $30 million in grants, provided over the next three years, will be available globally to existing biotech companies and new spinouts as mission-related investments—as well as to academic medical centers, universities and nonprofits, with industry partnerships being encouraged.
“If any of the projects backed by Diagnostics Accelerator succeed, our share of the financial windfall goes right back into the fund,” Gates wrote in a post on his blog.
The venture philanthropy model splits the difference between public investments aimed at advancing cutting-edge research, and VC firms hunting for projects with the largest possible returns, Gates said. While there has been promising research in the field, the lack of a commercial market has meant that very few companies are trying to translate that work into a product.
“It’s a bit of a chicken and egg problem,” he wrote. “It’s hard to come up with a game changing new drug without a cheaper and less invasive way to diagnose patients earlier. But most people don’t want to find out if they have the disease earlier when there’s no way to treat it.”
The former Microsoft chief and Lauder, chairman emeritus of the Estee Lauder group of cosmetics companies and co-founder of the ADDF, provided the accelerator’s initial funding alongside other philanthropists including the Dolby family and the Charles and Helen Schwab Foundation.
Last November, Gates announced his first, personal investment in Alzheimer’s research, committing $50 million to the U.K.-based Dementia Discovery Fund. The money was given separately from the Bill and Melinda Gates Foundation, and he described how the disease has afflicted a number of his family members.
At the time, Gates listed early detection and diagnostics among his top funding priorities in Alzheimer’s, alongside developing a better scientific understanding of the disease process, diversifying the drug pipeline, increasing clinical trial recruitment and improving the use of research data.
You'll need this. So if your hospital is so incompetent they are not following and implementing Alzheimers prevention research into protocols then you will need to find one that does. It is all up to YOU, your doctor and hospital have not been following research for decades.
Sanford Burnham Prebys Medical Research Institute (SBP) researchers have published two new studies in Neuron that describe how TREM2, a receptor found on immune cells in the brain, interacts with toxic amyloid beta proteins to restore neurological function. The research, performed on mouse models of Alzheimer's disease, suggests boosting TREM2 levels in the brain may prevent or reduce the severity of neurodegenerative disorders including Alzheimer's disease.
"Our first paper identifies how amyloid beta binds to TREM2, which activates neural immune cells called microglia to degrade amyloid beta, possibly slowing Alzheimer's disease pathogenesis," says Huaxi Xu, Ph.D., professor and director of SBP's Neuroscience Initiative, Jeanne and Gary Herberger Leadership Chair in Neuroscience Research and senior author of the study. "The second study shows that increasing TREM2 levels renders microglia more responsive and reduces Alzheimer's disease symptoms."
Alzheimer's disease affects more than 47 million people worldwide, a number expected to grow as the population ages. One of the hallmarks of the disease is the accumulation of amyloid plaques that form between neurons and interfere with brain function. Many drug companies have been working for years to reduce amyloid beta production to thwart Alzheimer's-;but with minimal success.
"TREM2 offers a potential new strategy," says Xu. "Researchers have known that mutations in TREM2 significantly increase Alzheimer's risk, indicating a fundamental role for this particular receptor in protecting the brain. This new research reveals specific details about how TREM2 works, and supports future therapeutic strategies to strengthen the link between amyloid beta and TREM2, as well as increasing TREM2 levels in the brain to protect against pathological features of the disease."
Xu led the first study (TREM2 is a receptor for β-amyloid which mediates microglial function), showing that TREM2 binds quite specifically to amyloid beta. In particular, it connects with amyloid beta oligomers (proteins that bind together to form a polymer), which are the protein's most toxic configuration. Without TREM2, microglia were much less successful at binding to, and clearing out, amyloid beta.
Further investigation showed that removing TREM2 downregulated microglial potassium ion channels, impairing the electrical currents associated with the activation of these immune cells. In addition, TREM2 turned on a number of mechanisms associated with the amyloid beta response in microglia.
The second study (TREM2 Gene Dosage Increase Reprograms Microglia Responsivity and Ameliorates Pathological Phenotypes in Alzheimer's Disease Models), a collaboration led by with X. William Yang, M.D., Ph.D., professor in Jane and Terry Semel Institute for Neuroscience and Human Behavior, and Department of Psychiatry & Biobehavioral Sciences at David Geffen School of Medicine at UCLA, added TREM2 to a mouse model with aggressive Alzheimer's disease. They found that the added TREM2 signaling stopped disease progression and even restored cognitive function.
"These studies are important because they show that in addition to rescuing the pathology associated with Alzheimer's disease, we are able to reduce the behavioral deficits with TREM2," says Xu. "To our knowledge this provides convincing evidence that minimizing amyloid beta levels alleviates Alzheimer's disease symptoms." As they learn more about how TREM2 modulates the amyloid signals that put microglia to work, the Xu lab and other researchers have their work cut out for them.
"It could be beneficial in early stages to activate microglia to eat up amyloid beta," says Xu, "but if you over-activate them, they may release an overabundance of cytokines (causing extensive inflammation) damaging healthy synaptic junctions as a side-effect from overactivation."
Still, the ability to use the brain's existing immune mechanisms to clear amyloid offers intriguing possibilities.
"Going after microglia, rather than amyloid beta generation, may be a new research avenue for Alzheimer's disease," says Xu. "We could use brain immune cells to solve what's becoming a public health crisis."
