Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,432 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.
I consider the WSO a TOTAL JOKE! Nothing they are doing will get survivors 100% recovered! Hope their experience with stroke after they become the 1 in 4 per WHO that has a stroke! is appropriate comeuppance for their current failures to solve stroke!
A UTHealth Houston neurologist was among a group of two dozen health care(NOT RECOVERY!) professionals from across the globe who developed an international certification program designed to improve rehabilitation care(NOT RECOVERY!) among stroke survivors.
Sean Savitz, MD, professor of neurology at McGovern Medical School at UTHealth Houston and director of the UTHealth Houston Institute for Stroke and Cerebrovascular Diseases, served as co-senior author on the paper announcing the certification program, which was published in the International Journal of Stroke.
More than 12 million people suffer a stroke each year, according to the World Stroke Organization, which developed the new certification through the guidance of international experts.
"So much has been done over decades to improve care(NOT RECOVERY!) of patients in hospitals in the emergency department, but the next stage is what happens to them after they're discharged from the hospital. There hasn't been as much attention paid to this area," said Savitz, who chairs the World Stroke Organization Rehabilitation Committee and holds the Frank M. Yatsu, MD, Chair in Neurology at McGovern Medical School.
The World Stroke Organization Rehabilitation Certification Program will be available to all countries and is focused on improving rehabilitation care(NOT RECOVERY!) in low- and middle-income countries. The program is modeled after the World Stroke Organization Stroke Center Certification, which commenced in 2021 and focuses on acute stroke care(NOT RECOVERY!).
Under the new program, health care(NOT RECOVERY!) entities can qualify for certifications based on three different tiers. To become certified, entities will be evaluated across 55 criteria that address service-level indicators, such as clear documentation, quality improvement and continuing education, as well as patient-level indicators, especially for different impairments.
"You need to have multidisciplinary teams that are providing care(NOT RECOVERY!) to the patient. You have to have people who represent different disciplines of rehab—occupational therapy, physical therapy, speech therapy, for example," Savitz said. "We talk about aerobic exercise, strength training and task-specific training, and how specific impairments such as difficulty swallowing should be evaluated and treated."
The World Stroke Organization anticipates that health care(NOT RECOVERY!) entities can apply for certification beginning in October. The rollout of the program comes after the criteria were assessed at 15 different centers in six countries.
Additional authors with UTHealth Houston include Emily A. Stevens, pOTD, an occupational therapist at the UTHealth Houston Institute for Stroke and Cerebrovascular Diseases.
Elizabeth A. Lynch, Ph.D., an associate professor at Flinders University in Australia, was also a co-senior author on the paper.
More information
International Journal of Stroke Jessica Nolan et al, World Stroke Organization (WSO) rehabilitation certification program, International Journal of Stroke (2026). DOI: 10.1177/17474930261463019
If they were truly good at stroke they would tell us EXACT RECOVERY RESULTS! But instead they tell us about 'care'! I consider that an admission of failure in getting survivors recovered. And this is one of the networks where I live.
The McLaren Stroke Network, which provides timely and potentially lifesaving care(NOT RECOVERY! during stroke emergencies, has again earned national recognition for the exceptional care(NOT RECOVERY! delivered across its network of hospital sites.
The American Heart Association/American Stroke Association recognized several McLaren Stroke Network hospital-based program with its Get With The Guidelines® – Stroke distinctions, reflecting those programs’ consistent adherence to the latest evidence-based care(NOT RECOVERY! guidelines and their commitment to improving patient outcomes.
Through the McLaren Stroke Network, emergency and neurology care(NOT RECOVERY! teams across the span of the system follow established protocols designed to quickly — though efficiently and thoroughly — identify stroke symptoms and confirm the diagnosis through advanced imaging, and connect patients with stroke specialists for timely treatment decisions.
McLaren Bay Region
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Target: Type 2 Diabetes Honor Roll
McLaren Central Michigan
Get With The Guidelines® – Stroke GOLD PLUS Get With The Guidelines® – Rural Stroke GOLD
McLaren Flint
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Plus Target: Type 2 Diabetes Honor Roll Advanced Therapy
McLaren Greater Lansing
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Plus Target: Type 2 Diabetes Honor Roll
McLaren Lapeer Region
Get With THe Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Target: Type 2 Diabetes Honor Roll Get With The Guidelines® – Rural Stroke SILVER
McLaren Macomb
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Plus Target: Type 2 Diabetes Honor Roll Advanced Therapy
McLaren Northern Michigan
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Plus Target: Type 2 Diabetes Honor Roll
McLaren Oakland
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Target: Type 2 Diabetes Honor Roll
McLaren Port Huron
Get With The Guidelines® – Stroke GOLD PLUS Target: Stroke Honor Roll Elite Target: Type 2 Diabetes Honor Roll
McLaren Thumb Region
Get With The Guidelines® – Rural Stroke SILVER
The McLaren Stroke Network features unique 24/7 access to stroke-trained and experienced neurointerventional physician, telehealth consultation capabilities, and established pathways for advanced therapies such as IV tPA clot-busting treatment and thrombectomy when clinically appropriate.
By linking community hospitals with higher-level stroke resources and transfer processes, the network helps ensure patients receive the right level of care(NOT RECOVERY! as quickly as possible, close to home whenever appropriate.
A stroke occurs when blood flow in the brain is interrupted, depriving it of oxygen and requiring immediate medical intervention to reestablish that blood flow.
Strokes are the fifth leading cause of death in the United States—globally, it is the second leading cause of death—and the leading cause of adult disability. There are approximately 800,000 stroke annual in the US, with more than 600,000 of those being first-time strokes.
High blood pressure, high cholesterol, smoking, obesity, and diabetes are all leading risk factors for stroke, and one in every three Americans currently lives with one of these risk factors.
To view the locations and learn the capabilities of the McLaren Stroke Network, visit mclaren.org/stroke.
About McLaren Health Care McLaren Health Care, headquartered in Grand Blanc, Michigan, is a $6.9 billion, fully integrated health care(NOT RECOVERY! delivery system committed to quality, evidence-based patient care(NOT RECOVERY! and cost efficiency. The McLaren system includes 12 hospitals across the state, ambulatory surgery centers, imaging centers, a 730-member employed primary and specialty care(NOT RECOVERY! physician network, commercial and Medicaid HMOs covering more than 242,000 Michigan lives, home health, infusion and hospice providers, pharmacy services, a clinical laboratory network, and a wholly owned medical malpractice insurance company. McLaren operates Michigan’s largest network of cancer centers and providers, anchored by the Karmanos Cancer Institute, a National Cancer Institute-designated comprehensive cancer center. McLaren has 20,000 full-, part-time and contracted employees and more than 93,000 network providers throughout Michigan. Learn more at mclaren.org.
What further research will your competent?
doctor initiate to figure out how to successfully prevent cognitive
decline? Oh sorry; YOUR DOCTOR PLANS ON DOING NOTHING, RIGHT!
You are finding out now that you don't have a functioning stroke doctor/hospital even after unsuccessfully getting you 100% recovered! THAT IS DOCTOR FAILURE!
High-dose DHA successfully
reached the brains of older adults at increased risk of Alzheimer's
disease, but the two-year clinical trial found no improvements in memory
or brain structure, challenging assumptions that greater omega-3
delivery alone can slow cognitive decline.
A clinical trial published in eBioMedicine
found that high-dose docosahexaenoic acid (DHA) supplementation
successfully increased brain DHA levels in older adults at risk of
dementia, including those carrying the APOE ε4 Alzheimer's risk variant.
However, despite reaching the brain, the supplement did not improve
cognitive performance or brain structure over two years, raising new
questions about how DHA is used within the brain.
Why APOE ε4 alters brain DHA metabolism
DHA is a fatty acid that is part of the nerve cell membrane, playing a
key role in synaptic function and modulating neuroinflammation. Its
levels tend to be lower in the presence of dementia-linked changes like
amyloid deposition and cognitive decline, and in patients with
late-onset Alzheimer's disease (AD).
The APOE ε4 gene variant is the strongest genetic risk factor for AD.
Previous research suggests it is associated with accelerated DHA
catabolism and lower plasma and cerebrospinal fluid DHA levels in people
with AD dementia compared with non-carriers.
Observational studies have suggested modest associations between
higher omega-3 intake and lower risk of cognitive decline, but
randomized trials have produced inconsistent results. Of 24 randomized
trials in people without dementia, only five reported positive cognitive
effects following DHA supplementation. Conversely, no improvement was
seen in patients with AD.
Thus, two important questions remain unanswered: is early
intervention necessary in patients with low omega-3 levels before
dementia sets in, and are higher doses required to ensure adequate brain
uptake? Previous imaging studies suggest that younger cognitively
healthy carriers have increased brain DHA incorporation, which may
reflect greater DHA demand, compared to non-carriers. This has not been
studied in older adults prior to the onset of dementia.
In the current study, researchers investigated whether high-dose DHA
supplementation could effectively raise brain DHA levels and potentially
support cognitive and structural brain health in older adults with low
dietary omega-3 intake before dementia develops.
Testing high-dose DHA before dementia develops
The investigators conducted a randomized, double-blind,
placebo-controlled trial that enrolled 365 adults without dementia, aged
55–80 years, with low DHA intake and at least one dementia risk factor
at baseline. Participants received either 2 g/day of DHA or a placebo
for 24 months.
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The
mean participant age was 66 years, with 58% being female. Approximately
47% of the participants were APOE ε4 carriers, and 39% were Hispanic.
The participants were first classified by willingness to undergo a
lumbar puncture (LP) to obtain cerebrospinal fluid (CSF) for analysis.
The two groups were assessed for the CSF DHA: arachidonic acid (AA)
ratio after six months, which reflects the extent to which DHA is
delivered to the brain. Various brain volumes were also assessed.
Increased DHA delivery
The 365 participants were divided into two arms: 181 in the LP
arm and 184 in the non-LP arm. In both arms, DHA supplementation
significantly increased the CSF DHA/AA ratio at six months compared with
placebo, indicating successful delivery of DHA to the brain. There was
also a 17% increase in CSF DHA. The red cell omega-3 index also
increased from 4.9% to 11%.
The increases in DHA delivery to the brain and in the red cells were
independent of APOE ε4 status. This suggests that the gene variant did
not influence this process.
However, APOE ε4 non-carriers showed greater improvement in cognitive
scores than carriers, with a mean improvement of 3.8 and 1.6 in the two
groups, respectively, regardless of treatment group. Importantly, the
study demonstrates that inadequate brain delivery is unlikely to explain
the disappointing results of previous DHA supplementation trials,
because high-dose supplementation successfully increased CNS DHA levels.
The authors hypothesize that simply improving DHA delivery to the
brain may not be sufficient to enhance cognitive function, given the
enzymatic catabolism of DHA within synaptic membranes, which are crucial
for cognitive processing.
There was no difference in brain volumes or in cognitive performance
over the whole study period between the intervention and control groups.
Adverse events were comparable between groups, and the treatment was
generally safe and well-tolerated.
Strengths and limitations
The sample included White and Hispanic participants with a high
proportion of APOE ε4 carriers. The low baseline omega-3 intake, CSF DHA
measurement, and multiple outcome assessments, coupled with a stringent
trial design, were among the study’s strengths.
However, it had several limitations. The participants were relatively
young, well-educated, and at an early stage of disease, which might
have limited their ability to detect treatment effects over just 24
months.
The study showed a relatively high dropout rate at 38%. Most of this
was related to the coronavirus disease 2019 (COVID-19) pandemic. The
consequent reduction in sample size might have affected its ability to
detect smaller effects on cognitive function or brain structure. Those
who dropped out of the study were more likely to be Hispanic, to have
lower education levels and baseline cognitive scores, and to have lower
plasma DHA concentrations than those who completed the study, which
might have affected the generalizability of the findings.
The study used a single supplement, but the authors point out that
this could be insufficient in the face of multiple disease processes
affecting neuronal health and DHA metabolism in the brain. This is even
more true when the participants have vascular risk factors like
hypertension and physical inactivity, all of which need to be addressed
simultaneously.
The current study included only cognitively healthy individuals, but
future studies may benefit from testing supplementation in individuals
who already have biochemical signs of early neurodegeneration, such as
elevated biomarkers (phosphorylated tau in blood, advanced imaging
markers) or more granular neuropsychological testing to detect small
changes in executive function. This would improve the detection of
treatment changes. A longer follow-up may also be necessary.
Conclusion
The findings show that high-dose DHA supplementation can
substantially increase brain DHA levels within six months in older
adults at risk of dementia, regardless of APOE ε4 status. Conversely,
this did not translate into observable improvements in cognition or
brain structure over 24 months.
These results suggest that high DHA intake alone may not be
sufficient to improve cognitive outcomes or preserve brain structure in
relatively healthy older adults over a 2-year period, despite adequate
brain delivery. They also imply that APOE ε4 carriers experience normal
DHA delivery to the brain before dementia, despite the dysregulation in
established dementia reported in prior research.
Future research should focus on examining DHA metabolism in the brain
rather than on additional supplementation trials. Because brain DHA
delivery was successfully achieved without improving cognition, future
work should focus on how DHA is processed and used within brain cells
rather than simply increasing DHA intake.
Yassine, H. N., Pour, S. G., Juarez, M., et al. (2026). CNS target
engagement of high-dose DHA supplementation in older adults at risk for
dementia: a randomised, double-blind, placebo-controlled trial. eBioMedicine. DOI: https://doi.org/10.1016/j.ebiom.2026.106316. https://www.thelancet.com/journals/EBIOM/article/PIIS2352-3964(26)00198-2/fulltext
In the past stroke rehabilitation plans were centered on helping patients relearn movement by practicing tasks correctly and through repetition. Occupational therapists helped to guide patients toward proper movement patterns and worked to minimize errors that may slow recovery.
Stroke rehabilitation continues to evolve with advances in robotic rehabilitation and recent research has challenged the fundamental therapy assumption that fewer mistakes during rehabilitation lead to better outcomes. In fact, this research shows that the opposite may actually be true. Error augmentation actually amplifies errors rather than trying to eliminate them. This may help stroke survivors recover motor function more effectively by accelerating the brain’s natural learning processes. The continued advancement of robotics, artificial intelligence, and sensor technologies are innovating the frontiers in stroke rehabilitation.
Errors enhance learning
Trial and error is an important part of the learning process. When humans learn to walk, ride a bicycle, or play a musical instrument, the brain continuously compares intended movement with actual movement and makes adjustments based on the difference. This motor learning process is driven by error signals.
When a person has a stroke, the brain’s ability to process and correct movement patterns can become impaired. Traditional rehabilitation attempts to compensate for this impairment by guiding patients toward correct movements through repetitive practice and physical assistance. This can be helpful in recovery, but it can also reduce the error signals that are important in neuroplasty, the brain’s ability to reorganize and form new neural connections.
Instead of trying to minimize mistakes, error augmentation deliberately exaggerates movement errors so patients can more clearly perceive the gap between intended and actual performance. The brain is then prompted to adapt more aggressively, strengthening motor learning and accelerating the recovery process. Error Augmentation primarily engages implicit motor learning mechanisms, allowing the nervous system to adapt instinctively and automatically rather than relying on conscious cognitive strategies. This promotes more natural and durable motor recovery by leveraging the brain’s innate capacity for sensorimotor adaptation.
Robotics and error augmentation
Advances in robotic rehabilitation have helped clinicians to apply error augmentation consistently in therapeutic settings. Robotic exoskeletons, upper-limb rehabilitation devices, and sensor-driven therapy platforms can precisely track patient movements in real time. These systems can detect subtle deficits and introduce controlled resistance or visual distortions that amplify errors during rehabilitation exercises.
If during therapy a patient veers off course several times while reaching for an object, a robotic system may intentionally exaggerate that deviation. The increased error becomes more noticeable, encouraging the patient to make stronger corrective adjustments. Importantly, the perturbations are intentionally subtle, engaging the brain’s implicit motor learning mechanisms so that adaptation occurs instinctively and automatically rather than through conscious cognitive effort. These robotic systems continuously monitor performance and adapt the level of error augmentation to match the patient’s capabilities and stage of recovery, providing a personalized rehabilitation experience that can be more effective than manual therapy alone.
Artificial intelligence and stroke rehabilitation
Artificial intelligence is now touching nearly every industry and is now moving into stroke rehabilitation as it is expanding the potential of error augmentation. Modern rehabilitation platforms are now using AI to analyze movement patterns, identify compensatory behaviors, and personalize therapy interventions in real time. They also further personalize a rehabilitation plan by determining when a patient may benefit from additional challenges, when increased support is necessary, and how error augmentation should be adjusted throughout the recovery process. Each patient recovers from a stroke differently and this adaptive approach offers a more individualized approach. AI-enabled rehabilitation systems provide crucial patient data that will help clinicians learn what would work best for each patient.
Recovery and compensation
One challenge that needs to be addressed in stroke rehabilitation is distinguishing between compensation and recovery. Patients sometimes figure out shortcuts that allow them complete tasks despite impairments that still remain. These compensatory strategies can help them perform tasks and achieve independence, but they also can limit long-term neurological recovery.
Error augmentation supports patients and allows them to work with underlying motor deficits rather than avoid them. When errors are made more visible, patients are then able to develop more normal movement patterns and even strengthen damaged neural pathways. This is a clear shift from helping patients move despite their limitations to actually helping them regain their lost abilities if possible.
The future of stroke rehabilitation
While error augmentation is not a replacement for traditional rehabilitation approaches, when used as part of a personalized therapy plan, it can effectively and quickly help patients achieve independence.
This technology addresses critical challenges in stroke rehabilitation such as slow recovery times, plateaued progress and limited motor recovery.
Future rehabilitation programs may combine AI and data-driven approaches such as:
● Robotic therapy systems
● AI-driven personalization
● Wearable sensors
● Home-based rehabilitation platforms
● Real-time performance analytics
● Error augmentation techniques
Combined with traditional therapies, these emerging technologies have the potential to make rehabilitation more intensive, more personalized, and ultimately more effective. When a patient is highly engaged in their therapy, the higher chances of success.
As hospitals and clinicians seek better ways to address the growing number of stroke-related disabilities, therapy plans that support the brain’s natural learning mechanisms will become increasingly useful.
The future of stroke rehabilitation is not about preventing patient mistakes, but actually highlighting the mistakes that are made, in order to enhance the brain’s miraculous capacity to adapt and recover. The errors can actually increase independence.
In a population-based cohort of 1,865 older adults followed for a mean of 8.4 years, greater adherence to a dietary pattern with lower inflammatory potential was associated with significantly lower dementia risk among individuals with elevated Alzheimer disease (AD) and neurodegeneration biomarkers, including phosphorylated tau at threonine 217 (p-tau217), neurofilament light chain (Nfl), and glial fibrillary acidic protein (GFAP).
The findings, published in JAMA Network Open, suggest that anti-inflammatory dietary habits may help reduce dementia risk even in people with underlying AD-related pathology.
“To our knowledge, this study is the first to show that diet quality may modify the relationship between AD pathology or broader neurobiological and dementia risks… healthy dietary patterns may delay dementia onset, including AD-related dementia, and prolong a dementia-free life even in individuals with possible underlying AD pathology.” wrote Anja Mrhar, Karolinska Institutet and Stockholm University, Stockholm, Sweden, and colleagues. “This distinction is notable, as it is well known that the presence of AD pathology increases dementia risk but does not inevitably lead to its clinical manifestation.”
For the study, the researchers analysed data from 1,865 dementia-free adults aged ≥60 years enrolled in the Swedish National Study on Aging and Care. Participants were followed for up to 15.9 years, with dietary adherence assessed repeatedly over 6 years using 3 dietary patterns: the Alternate Mediterranean Diet (AMED), the Alternative Healthy Eating Index (AHEI), and a reversed Empirical Dietary Inflammatory Index (rEDII). Baseline blood levels of AD and neurodegeneration biomarkers were measured, and investigators examined how diet quality influenced subsequent dementia risk across different biomarker levels.
During follow-up, 240 participants developed dementia. Higher adherence to the anti-inflammatory rEDII dietary pattern was associated with significantly lower dementia risk among individuals with elevated biomarker levels, reducing risk by 21% to 29% depending on the biomarker assessed. In contrast, the protective associations of the Mediterranean-style and healthy eating diets were generally observed only among participants with lower biomarker levels. Similar results were seen for AD-related dementia, suggesting that reducing dietary inflammation may be particularly beneficial for people already showing biological signs of AD disease and neurodegeneration.
“These results reinforce the importance of dietary interventions for dementia, not only for the general population but also for individuals already at elevated disease risk, and support the development of precision public health strategies and personalised dietary recommendations in clinical practice,” the authors concluded. “Future studies should confirm these associations in more diverse populations and identify the specific foods and nutrients driving the observed benefits.”
Scientists believe they have identified a key mechanism behind the spread of Alzheimer’s disease through the brain, a discovery that could open the door to new treatments aimed at slowing the condition rather than simply clearing away toxic proteins after damage is done.
Researchers at the University of Utah Health found that a brain protein called Arc, which normally helps neurons communicate with one another, may be inadvertently helping the disease spread. The protein appears to carry toxic Tau—a hallmark of Alzheimer’s—out of damaged brain cells and into healthy ones.
“For decades, research has focused on the toxic buildup of Tau inside neurons; this study reframes the problem by showing how Tau may exploit the brain’s own communication machinery, specifically the Arc protein and its extracellular vesicle system, to spread between cells,” Missling said.
He added that the discovery “underscores how normal synaptic signaling proteins can become hijacked in disease, blurring the line between physiological and pathological communication,” and that targeting this transport system might one day help slow or contain Alzheimer’s spread rather than trying to eliminate Tau entirely.
How Tau Hitches a Ride
Alzheimer’s disease is driven by the buildup of Tau, a protein that clumps into sticky tangles inside neurons, disrupting their internal machinery and eventually killing them. As Tau spreads to new regions of the brain, memory loss and cognitive decline worsen.
To understand how this spread happens, researchers compared mice with Alzheimer’s-like disease to mice that also lacked the Arc protein. They found Arc plays an essential role in moving Tau between cells.
Normally, Arc packages itself into tiny structures called extracellular vesicles, which shuttle between neurons carrying important cellular signals. But the study found that toxic Tau can hitch a ride inside these same vesicles, using Arc to travel from a diseased neuron into a healthy one, where it can trigger new tangles to form.
When Arc was removed from the mice, the vesicles carried far less Tau, and the disease no longer spread effectively between neurons.
A Protective Role Complicates the Picture
The results were not entirely straightforward. Arc also appears to do the positive job of helping neurons survive longer in the early stages of disease by allowing them to expel excess toxic Tau.
That finding suggests simply blocking Arc altogether may not be the answer. Instead, researchers believe future treatments should focus on preventing the Tau-carrying vesicles from entering healthy neurons, while still allowing damaged cells to expel their toxic waste.
The team also detected extracellular vesicles containing both Arc and Tau in human brain tissue, suggesting the same process could be at work in people. Researchers caution that significant further study, especially on humans, is needed before the findings could lead to any treatment, but they say the discovery offers a promising new target for future therapies aimed at slowing, rather than eliminating, the disease’s spread through the brain by intercepting Tau containing extracellular vesicles after they leave diseased neurons, before they reach healthy ones.
Instead of having to monitor this post stroke why not have your competent? doctor GIVE YOU EXACT PREVENTION PROTOCOLS? The problem has been known for years and your incompetent? doctor has done nothing to solve that?
Your risk of dementia, has your doctor
told you of this? Your doctor is responsible for preventing this! Is
s/he willing to prevent this?
Anyone who’s lost a loved one to Alzheimer's disease may be worried about noticing symptoms in themselves.
Alzheimer's takes a terrible toll. It’s the most common cause of dementia — abnormal brain changes that lead to memory loss, impaired thinking skills and confusion.
Patients become unable to learn, remember and recognize family.
The biggest risk factor is age, followed by family history, says Mary Sano, Ph.D., professor of psychiatry and director of the Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York.
She’s a neuropsychologist — a specialist who focuses on the brain and behavior. A patient may be referred to a neuropsychologist for an evaluation when they, their family or their doctors notice a change in behavior that could signal dementia.
People with cognitive decline may be unaware of the disease in themselves, a condition known as anosognosia. But they may notice important clues in early stages of brain changes.
“I think everyone as they age is probably attentive to cognitive impairment,” Sano tells TODAY.com.
“A very common thing can be that people really do feel a difference that others aren't aware of or don't acknowledge. I see that very often in participants. They say, ‘I'm just not doing this as well,’ or, ‘I feel foggy when I'm trying to do something.’”
Knowing what she knows, here are the Alzheimer’s disease symptoms she pays attention to in her own life:
Missing Periods of Time
Not being able to figure out: What did I do for breakfast this morning? What routine did I follow this morning?
“That can be a problem,” Sano notes.
Staci Marklin, a 47-year-old Tennessee woman diagnosed with early-onset Alzheimer's disease, says she was “having instances where it felt like things were just gone,” including when her 3-year-old son was born.
“Once someone asked me my son's date of birth, and I had no idea,” Marklin told Buzzfeed.
Hearing Concern from Others
The "most important thing" is being open to hearing a concern from others, since Alzheimer’s disease symptoms are often identified by someone else, Sano says.
“Be open to the fact that someone says, ‘I don't think you're doing this as well as you used to,’” she advises.
Accept it as someone noticing a change that's worthy of getting checked out, she adds.
For example, other people commenting that you’re repeating yourself or asking the same question over and over again might be cause for concern.
Misplacing Things in Odd Places
There are common stories of someone putting their keys in the refrigerator or another inappropriate place, Sano notes.
“My experience is when those things are happening, many more things have happened before that,” she says.
Being More Anxious or Upset
Not being able to find your keys or your phone provokes unusual anxiety.
“Sometimes people can have an awareness of that, and are particularly irritable or anxious around their own performance,” Sano says.
“That might indicate that, in fact, they have this worry about some change that they can't articulate, and it's worthy of conversation with a physician.”
Forgetting to Pay Bills
“That can be a very important sign,” Sano says. “I think that's probably the biggest kind of problem.”
How to Get Help
If you’re worried, talk with a friend, family member or another trusted person in your circle and ask if they’ve also noticed changes.
If any of your symptoms are acknowledged by someone else, it’s worthy of a medical evaluation, Sano advises. Tell your doctor about your concerns.
You can be referred to a neuropsychologist for standardized cognitive testing and more.
“If I have someone whose testing is normal, but they really insist that there's something different, they can then be recommended for biological testing and see if there is evidence of Alzheimer's pathology,” Sano says.
Two blood tests were approved by the U.S. Food and Drug Administration in 2025 to help diagnose or rule out Alzheimer’s disease.
One can be used in a primary care setting and is designed to rule out the presence of amyloid plaques, a hallmark sign of Alzheimer’s disease. The sticky plaques can cause brain cells to die, so checking for amyloid in the brain helps doctors find out whether Alzheimer’s is the potential cause, according to the National Institutes of Health.
The other test is used for early detection of amyloid plaques. Both are for people 55 years old and older who have symptoms of the disease.
Can Alzheimer's Disease Be Prevented?
That's not been shown, but lifestyle factors may play a role in improving cognitive status, Sano says.
If your competent? doctor can't figure out how to get dendritic branching/neurite outgrowth and axon pathfinding to work to connect up gray matter again then maybe this could work.
A team at Northwestern University has printed artificial neurons from molybdenum disulfide (MoS₂) — a semiconducting mineral — on flexible plastic that produce spiking waveforms closely matching biological action potentials in shape, width, and timing. When delivered to living Purkinje cells in mouse cerebellar tissue, the artificial spikes drove the cells to fire — the first demonstration that a printed device can produce electrical signals a real brain cell accepts and responds to.
The result, recently published in Nature Nanotechnology, could lay groundwork for a new generation of neural interfaces — prosthetic limbs that deliver realistic sensation, spinal cord bridges that relay motor commands, and benchtop disease models with tunable parameters.
“There’s this white space — organic devices are too slow, metal oxides are too fast — and biology lives in between,” said Mark C. Hersam, PhD, the study’s senior author and Walter P. Murphy Professor of Materials Science and Engineering at Northwestern University in Evanston, Illinois.
An array of printed artificial neurons on flexible polyimide held by tweezers to show the substrate bending.
“We got these devices working at that timescale,” he said, “and when you have the right timescale and the right spike shape, you can directly interface with living cells.”
How do printed neural interfaces compare with metal oxide devices?
What limits long-term stability of MoS2 neural circuits?
Which cerebellar diseases could benefit from tunable circuit models?
Engineers Interface With Neuroscientists
The collaboration began not in biology but in electrical engineering. Hersam’s National Science Foundation grant aimed to build computing hardware that mimics the brain’s energy efficiency. The human brain runs on about 20 watts, whereas modern AI training runs on megawatts — a millionfold difference — and is extravagantly wasteful and potentially harmful to the environment.
The grant’s challenge: build computing hardware that mimics the brain’s efficiency.
“Most of the artificial neurons in the literature, if you actually look at their spiking profiles, they look more like a sine wave or just an oscillator, not a sharp action potential,” Hersam said. “They don’t achieve things like bursts of spikes, which is one of the things we demonstrate.”
Meghana Holla, PhD
But to mimic the brain, Hersam needed people who study it. He teamed up with Indira M. Raman, PhD, a neurophysiologist in the Department of Neurobiology at Northwestern University, and her lab. Her doctoral students, Spencer Brown, PhD, and Meghana Holla, PhD, visited Hersam’s lab to see what the engineers were up to.
The engineers in Hersam’s lab showed them the device output, with waveforms spiking at 3000 times per second, much too fast to mimic a neural cell. Purkinje cells may be among the fastest-firing neurons in the brain, but they only reach about 100 spikes per second.
“That’s not a neuron,” Brown, an incoming assistant professor of neuroscience at Brandeis University in Waltham, Massachusetts, recalled. “They can’t do that.”
The artificial neuron’s output (blue) overlaid with a living Purkinje cell’s action potential (red). Both spikes match closely in shape and duration, completing within about 2 milliseconds.
Over the following year, both fields discovered they used identical terminology, such as long-term potentiation, memory, and synapse weight, to mean different things.
Spencer Brown, PhD
“We thought we were talking about the same things, but we weren’t,” Brown said.
Brown and Holla provided “ground truth”: Each spike had to last between a fraction of a millisecond and a few milliseconds, matching a real action potential.
And the firing rate — the number of spikes per second — had to fall between single digits and low hundreds, not the thousands the engineers’ devices had been producing.
The engineers took the neuroscientists’ advice and successfully reconfigured the circuit to match.
The Glue That Makes Artificial Neurons Fire
The artificial neurons are built from a liquid, a custom ink formulated for a specialized printer. MoS2, a semiconducting mineral, is peeled into flakes that are just a few atoms thick and suspended in ethanol. Without that suspension, the flakes clump together and settle out.
To keep them suspended, the researchers add ethylcellulose, a polymer derived from wood pulp, which coats each MoS2 flake and holds it apart from its neighbors, kind of like glue. The resulting ink is a stable suspension of semiconductor particles in solvent, and it flows through an aerosol jet printer that deposits it as a fine mist onto flexible plastic.
An aerosol jet printer deposits molybdenum disulfide ink onto flexible plastic. The nozzle sprays the ink as a fine mist, printing rows of artificial neurons without a cleanroom.
The ethylcellulose scaffolding is essential for the artificial neurons to communicate like a network. When the printed film is baked at 350 °C, the ethylcellulose partially decomposes into carbon residue that settles into tiny, nanometer-sized gaps between flakes to form conductive bridges. Once fabricated, the device operates at room temperature.
Then comes what’s called electroforming. The first time a large current passes through the device, it doesn’t flow evenly. Some pathways are slightly more conductive, such as wherever carbon residue accumulated more thickly, or wherever flakes overlapped. The more conductive pathways carry more current, and more current generates more heat. That heat decomposes more polymer residue into carbon along the same route, making it more conductive and drawing still more current toward it.
Mark C. Hersam, PhD
The result is a single dominant channel — a filament — burned through the thickness of the film. “This occurs in a spatially inhomogeneous manner, leading to the formation of a conductive filament…all the current constricted into a narrow region,” said Hersam.
The filament has two states: hot and conducting, or cool and nonconducting.
On its own, that’s just a switch. What turns it into something that fires like a neuron is the circuit around it.
“This is a random network of flakes with gaps of a few nanometers,” said Vinod K. Sangwan, PhD, co-corresponding author and research associate professor of materials science and engineering at Northwestern University. “You cannot have atoms going from one place to another across that vacuum. The only mechanism left is thermal.”
In the full artificial neuron, the printed switch sits alongside a capacitor, which is a component that stores electrical charge. A steady input current slowly charges the capacitor, the way a biological neuron gradually accumulates signals from its neighbors.
The filament heats up and becomes conductive, and the capacitor rapidly discharges through it. That sudden discharge is the spike — a sharp, fast voltage pulse. Then the filament cools, the switch resets, and the capacitor begins slowly charging again. The cycle repeats: slow accumulation, sudden firing, reset.
And because the filament heats and cools on a millisecond timescale, the spikes fall within the same timing window as a real neuronal action potential.
How Real Brain Cells Respond to Artificial Neurons
Holla, who completed her PhD in Raman’s lab and is now a postdoctoral researcher studying memory at New York University in New York City, designed and ran experiments in mouse cerebellar slices. She positioned a stimulation electrode on the parallel fibers, the main pathway that excites Purkinje cells, and a recording electrode on the Purkinje cells themselves.
She played recordings of the artificial neurons’ waveforms into the tissue through a standard stimulation electrode at four different speeds: 7, 60, 218, and 740 spikes per second.
At every speed below 200 spikes per second, the Purkinje cells fired in response. The strongest results came at 60 spikes per second, where each artificial spike lasted 0.7 milliseconds, which is fast enough to trigger the cell but brief enough to avoid flooding the tissue with unnecessary current.
Above 200 spikes per second, the cells stopped responding. They simply cannot fire that fast. The team included the 740-spikes-per-second condition on purpose to directly challenge the many engineering groups building artificial neurons that operate at those speeds. “We had to show them [740 spikes] wasn’t sufficient,” Brown said. “You can’t work that fast.”
“You can see the living neurons respond to our artificial neuron,” Hersam said. But he is careful to note a caveat: The printed artificial neurons were not touching the brain tissue. The waveforms they generated were recorded and then played back into the slice through standard laboratory stimulation equipment.
The next step is to prove the printed device itself can interface with living tissue.
Clinical Possibilities
Ian Gaudet, PhD, a neuroscientist at Florida Atlantic University in Boca Raton, Florida, who was not involved in the study, sees multiple clinical possibilities from this work.
Ian Gaudet, PhD
“I’ve been waiting for [work like this] for years,” Gaudet said. “The signals coming off of these devices are the right shape, the right speed, and the right language for real neurons to be properly affected by them.”
The printed artificial neuron, he argues, is like a translator, converting digital information into electrical patterns neurons accept as input. And in prosthetic limbs, it could replace the rectangular pulses that give amputees a buzzing sensation with signals that peripheral nerves evolved to receive. A crude approximation of sensation could become something much closer to the real feeling.
“The idea would be to have this system where you’re controlling your prosthetic limb and you are feeling your prosthetic limb using the existing neuronal systems of your peripheral nervous system,” Gaudet said.
In spinal cord injury, it could convert decoded motor intentions into biologically shaped signals that motor neurons below a lesion treat as natural commands.
“If you can make that signal seamless,” Gaudet said, “people with spinal cord injuries could walk again one day.”
But where these artificial neurons may prove most valuable first is not as replacements for any damaged brain tissue but as test models. Researchers could build a small artificial cerebellar circuit on a benchtop, configure each element to fire like a different cell type, then deliberately break it to change the firing rate, and, in turn, simulate Purkinje cell loss in spinocerebellar ataxia.
Or one could remove an element to model a cerebellar stroke to see what happens — a disease model that could lead to novel treatments.
“You can turn this on, or turn this off,” Gaudet explained. “What happens if we mimic the patterns that we see in people who have a certain disease?”
Gaudet suggests researchers may use these devices as a physical disease model with real electrical dynamics.
What the Artificial Neuron Cannot Do
Hersam’s next goal is a small circuit — perhaps 10 artificial neurons — where each one fires differently, and together they accomplish what would require thousands of conventional transistors.
“Silicon achieves complexity by having billions of identical devices,” Hersam said. “The brain is the opposite. It’s heterogeneous. The complexity is at the device level.”
But Gaudet sees a gap no circuit design can yet fill: Biological neurons grow new connections and prune old ones, strengthening pathways that are used and weakening those that aren’t. Hersam’s lab’s printed neurons — or any other neuromorphic technology that mimics neuronal dynamics — can’t achieve that level of complexity yet.
