Does your competent? doctor know about this from over a decade ago?- Portable Neuromodulation Stimulator device (1 posts to February 2015)
- Portable Neuromodulation Stimulator device (1 posts to February 2015)
Friday, December 5, 2025
New therapy helps speed injured worker's stroke recovery - PressReader - Portable Neuromodulation Stimulator device(PONS)
Does your competent? doctor know about this from over a decade ago?
Astrocyte-driven approach shows potential to reverse cognitive decline in Alzheimer’s
Are your doctor and hospital competent enough to get human testing going?
Astrocyte-driven approach shows potential to reverse cognitive decline in Alzheimer’s
Researchers at Baylor College of Medicine have discovered a natural mechanism that clears existing amyloid plaques in the brains of mouse models of Alzheimer's disease and preserves cognitive function. The mechanism involves recruiting brain cells known as astrocytes, star shaped cells in the brain, to remove the toxic amyloid plaques that build up in many Alzheimer's disease brains. Increasing the production of Sox9, a key protein that regulates astrocyte functions during aging, triggered the astrocytes' ability to remove amyloid plaques. The study, published in Nature Neuroscience, suggests a potential astrocyte-based therapeutic approach to ameliorate cognitive decline in neurodegenerative disease.
"Astrocytes perform diverse tasks that are essential for normal brain function, including facilitating brain communications and memory storage. As the brain ages, astrocytes show profound functional alterations; however, the role these alterations play in aging and neurodegeneration is not yet understood," said first author Dr. Dong-Joo Choi, who was at the Center for Cell and Gene Therapy and the Department of Neurosurgery at Baylor while he was working on this project. Choi currently is an assistant professor at the Center for Neuroimmunology and Glial Biology, Institute of Molecular Medicine at the University of Texas Health Science Center at Houston.
In the current study, researchers looked to identify mechanisms associated with astrocyte aging and Alzheimer's disease, focusing on Sox9, as this protein is a top regulator of multiple genes in aging astrocytes.
"We manipulated the expression of the Sox9 gene to assess its role in maintaining astrocyte function in the aging brain and in Alzheimer's disease models," said corresponding author Dr. Benjamin Deneen, professor and Dr. Russell J. and Marian K. Blattner Chair in the Department of Neurosurgery, director of the Center for Cancer Neuroscience, a member of the Dan L Duncan Comprehensive Cancer Center at Baylor and a principal investigator at the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital.
In these Alzheimer's mice, the team over expressed or eliminated Sox9 and then assessed the cognitive function of individual mice for six months, evaluating the animals' ability to recognize objects or places. At the end of the experiment, the researchers measured plaque deposition in the brains.
Compared to reducing Sox9 expression, increasing it had the opposite effect. Sox9 knockout accelerated plaque formation, reduced astrocyte complexity and decreased clearance of amyloid deposits. Overexpression reversed these trends, promoting plaque clearance, while increasing the cells' activity and complexity. Importantly, overexpression of Sox9 also preserved cognitive function in these mice, indicating that astrocytic clearance of plaques halts neurodegenerative-related cognitive decline.
The Doctor Behind Turkey's Robotic Rehab Revolution: Dr. Mustafa Corum
Will your competent? doctor and hospital learn and implement anything from his success? Oh no, they don't know about it and plan nothing. Perfect example of extreme incompetence of everyone involved!
The Doctor Behind Turkey's Robotic Rehab Revolution: Dr. Mustafa Corum
Doc. Dr. Mustafa Corum, a groundbreaking figure in Physical Medicine and Rehabilitation, has emerged as one of the leading pioneers of robot-assisted rehabilitation in Turkey and on the international stage.
Combining advanced technology with traditional therapeutic methods--particularly in the treatment of stroke, traumatic brain injury, and spinal cord damage--Dr. Corum has become a widely recognized name in the field.
A New Approach to Robotic Rehabilitation
Dr. Corum's technology-driven approach goes far beyond conventional physiotherapy techniques. His practice incorporates state-of-the-art robotic systems and virtual-reality-supported rehabilitation devices.
The systems featured in his clinic include:
? Lokomat Pro - robotic gait training system
? C-Mill VR Plus - virtual-reality-based treadmill and balance platform
? Armeo Spring - arm and upper-limb robotic therapy device
? Amadeo - robotic finger therapy system
? Erigo Pro - robotic tilt-table and early-mobilization platform
These technologies provide intensive, personalized therapy programs that aid in regaining gait, mobility, and upper-limb functions following stroke. Dr. Corum emphasizes three key principles in his method: early intervention, high-intensity therapy, and individualized programming.
Patient Stories and Remarkable Success
The patient cases treated in Dr. Corum's clinic demonstrate the tangible outcomes of this innovative approach. One notable example includes a stroke patient who traveled from Germany to Turkey. The patient arrived with severe complications, including infection and difficulty swallowing. Following a structured robotic rehabilitation program, they progressed to the point of walking indoors with support.
Dr. Corum's social media accounts also showcase real-time demonstrations of robotic therapy, offering a closer look at how these devices function during treatment sessions.
Revolutionary Impact and Turkey's Role
Dr. Corum stands at the forefront of Turkey's technological transformation in physical rehabilitation. By making robotic systems more accessible and expanding the scope of neurorehabilitation practices, he has offered renewed hope to thousands of neurological patients.
Among the key benefits of robotic rehabilitation are:
- faster recovery of motor functions,
- enhanced neuroplasticity through high-repetition movements,
- safer and more controlled therapy environments.
According to Dr. Corum, when applied at the right time and intensity, robot-assisted therapy can produce significantly better outcomes than traditional rehabilitation alone.
A Vision Beyond Turkey
Dr. Corum's ambitions extend far beyond national borders. His clinic welcomes international patients and offers comprehensive inpatient robotic rehabilitation programs operated by a multidisciplinary team of physicians, physiotherapists, occupational therapists, and speech-language pathologists.
He also contributes to the scientific community through academic publications and conference presentations. One of his recent studies focuses on a pilot randomized trial examining the effects of robot-assisted upper-extremity training.
New Study Shows Promising Advancement in Stroke Treatment That Aligns With the Philosophy Behind Anathapindika’s Detoxing Supplements
A press release, so ask your competent? doctor to vet it. and then see when your doctor and hospital will get human testing going. Inability to do that is PURE INCOMPETENCE! I take no prisoners in trying to get stroke solved, a hell of a lot of people need to be fired for not even attempting to solve stroke in the past 50 years!
New Study Shows Promising Advancement in Stroke Treatment That Aligns With the Philosophy Behind Anathapindika’s Detoxing Supplements
Anathapindika’s Supplements Are Unique in Their Focus on Detoxification. Recent Research Surrounding Stroke Recovery Could Support Their Use as Natural Brain and Body Cleansing Agents.
Fort Lauderdale, FL, Dec. 04, 2025 (GLOBE NEWSWIRE) -- A new study has shed light on how brain stem cells could play a crucial role in the growth of new brain cells. This could lead to longer recovery opportunity windows for stroke survivors and could allow for a greater chance for the recovery of brain function in stroke patients. Anathapindika Health’s founder, Dr. Intaek Lee, has brought attention to this critical area of health, simultaneously highlighting the importance of the groundbreaking new study and the way his own brand’s products support stroke recovery through targeted dietary supplementation.
A newly published study of an experimental stem cell therapy for stroke survivors from the Keck School of Medicine of USC in the US and ETH Zurich in Switzerland has found that a stem cell transplanted in mice a week after a stroke has taken place led to recovery. This is a dramatic improvement on the normal window of recovery therapy (which can be as limited as 4.5 hours).
“We need more naturally focused research, like brain stem cells and how they can play a crucial role in the recovery of brain function in stroke patients,” said Dr. Lee. Lee. He compared the new treatment to feedback he’s received for his own natural dietary supplement formulas, which focus on detoxification, adding, “That is why we’ve been excited at Anathapindika for a while now, as well. There are now at least three cases where we received feedback from our customers that they believe taking our health supplements accelerated functional recovery of stroke patients, both for ischemic stroke and brain hemorrhage cases.”
Strokes are one of the leading causes of disability and death in the United States. According to the American Stroke Association, it is the No. 5 most likely cause of death and the No. 1 cause of disability. With such significant concern surrounding the condition, any experimental support, supplement, or therapy is naturally going to garner attention.
In the case of the new study, brain stem cells are a critical component, and Dr. Lee sees a connection between this new data and his own growing set of customer success stories. “This study on the potential role of brain stem cells,” he proposed, “is in line with many of our customers’ stories who recovered even a year after the stroke damage had occurred.”
Products like Anathapindika’s Super Brain Health lean on clean, strong dosages of natural ingredients, like Lion’s mane mushroom, beet root, and Gotu Kola. These seek to nourish the brain, removing unwanted toxins and helping the body operate at full capacity. As Anathapindika continues to support natural, healthy brain activity, studies like this most recent one continue to put urgency behind finding natural and effective solutions to help stroke survivors thrive once again.
About Anathapindika Health
Anathapindika Health LLC was founded by Dr. Intaek Lee in July 2023 in Frisco, Texas, after months of product development. In May 2024, it relocated to Chesterfield, Missouri. In the past, Lee had worked as a scientist at the Yale School of Medicine for years alongside renowned Biomedical Scientist James Rothman. Lee is also a Buddhist meditation trainer. His health and wellness brand brings together his scientific acumen and spiritual passion to create informed solutions for natural health. Learn more at anathapindika.com.
CONTACT: Anathapindika Phone number: +1 945 257 7512 Email: info@anathapindika.com
NOTE: This content is not written by or endorsed by "WDAF", its advertisers, or Nexstar Media Inc.
Increased Phase Angle Reflects Improvement in Activities of Daily Living and Muscle Health in Post-Stroke Rehabilitation
Without telling us how to improve this; TOTALLY FUCKING USELESS!
Definition:
In the context of stroke, the phase angle (PhA) is a non-invasive measure of muscle quality and cellular health derived from a bioelectrical impedance analysis (BIA) test. It
reflects the integrity and function of cell membranes, indicating
cellularity, fluid distribution, and overall nutritional status. A
higher phase angle is generally associated with better cellular health
and physical function, while a low phase angle can predict poor
outcomes, such as decreased functional independence and increased
nutritional risk in stroke patients.
Increased Phase Angle Reflects Improvement in Activities of Daily Living and Muscle Health in Post-Stroke Rehabilitation
Abstract
Background: Phase angle (PhA) reflects cellular integrity and muscle quality. However, evidence is limited regarding whether an increase in PhA is associated with improvements in activities of daily living (ADL) and skeletal muscle mass. This study aimed to investigate the association between change in PhA and prognosis in terms of ADL and skeletal muscle mass in post-stroke patients undergoing rehabilitation.
Methods: This retrospective cohort study was conducted at a convalescent rehabilitation hospital in Japan. Patients with a PhA at admission below the cutoff values (4.76° for males and 4.11° for females) were included. Patients were categorized into a PhA-increase group (>0) and a non-increase group (≤0). Outcomes included the Functional Independence Measure (FIM)-motor score and skeletal muscle mass index (SMI) at discharge. Multivariate regression was used to assess associations.
Results: A total of 253 patients were included (mean age 78.0 ± 10.9 years; 51% women). The median [IQR] PhA at admission was 3.70° [3.20, 4.10], and the median change during hospitalization was 0.00° [-0.20, 0.30]. Of these, 119 patients had increased PhA and 134 did not. Change in PhA was independently associated with higher FIM-motor scores (β = 0.078, P = 0.040) and greater SMI (β = 0.454, P < 0.001) at discharge.
Conclusions: In post-stroke patients, an increase in PhA during hospitalization was associated with better functional and muscular outcomes. PhA may therefore serve as a valuable biomarker for assessing the efficacy of rehabilitation.
Keywords: Activities of daily living; Bioelectrical impedance analysis; Phase angle; Sarcopenia; Skeletal muscle mass; Stroke rehabilitation.
High-fructose diet induces depressive-like behaviors and short-term memory deficits through hippocampal neurogenesis impairment via neural stem cell dysfunction
Will your incompetent? doctor get the dietician to evaluate this and get the problem cases removed from all hospital locations? Even though this latest one is in mice?
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?Let's see how long your doctor has been incompetent!
Fructose may be fueling the formation of Alzheimer’s disease February 2023
The latest here:
High-fructose diet induces depressive-like behaviors and short-term memory deficits through hippocampal neurogenesis impairment via neural stem cell dysfunction
Abstract
Background
Neural stem cells (NSCs), crucial for brain function and repair, are disrupted by high-fructose diet (HFrD) in proliferation and survival, linking to neurogenesis impairment and neuropsychiatric risks. Mechanistic insights remain undefined.
Methods
Comprehensive behavioral assessments were conducted on HFrD mice, including the tail suspension test (TST) and sucrose preference test (SPT) for depressive-like behaviors, elevated plus maze (EPM) and open field test (OFT) for anxiety-like behaviors, as well as novel object recognition (NOR) and Morris water maze (MWM) for cognition. Hippocampal NSCs and newborn neurons were quantified by immunofluorescence, and fructose-treated NE-4C cells underwent RNA sequencing (RNA-seq) analysis coupled with measurements of proliferation, apoptosis and ferroptosis markers.
Results
HFrD mice showed depressive-like behaviors without anxiety-like behaviors, and exhibited impaired short-term memory in NOR but did not show impaired spatial memory in MWM. Decreased number of hippocampal NSCs and newborn neurons were observed, suggesting impaired neurogenesis. In vitro, fructose-treated NE-4c exhibited altered gene expression profiles, with PCA showing distinct clustering between treated and control groups. Further analysis (GO, KEGG, GSEA) indicated enrichment in energy metabolism pathways, including mitochondrial ATP synthesis (e.g., downregulated ATP5E, ATP5H). Consistently, intracellular ATP levels were elevated, indicating metabolic dysregulation. Further experiments demonstrated that high fructose promoted NSC proliferation via p53/Wnt pathways (upregulated CyclinA2, CDK1) while concurrently inducing apoptosis (BAX, P53 upregulation) and ferroptosis (reduced GPX4, elevated ROS, and lipid peroxidation).
Conclusion
This study elucidates the mechanistic link between HFrD-induced metabolic disruption and NSC dysfunction, providing novel insights into the pathogenesis of fructose-associated neuropsychiatric disorders.
Fructose may be fueling the formation of Alzheimer’s disease February 2023
The latest here:
Abstract
Background
Neural stem cells (NSCs), crucial for brain function and repair, are disrupted by high-fructose diet (HFrD) in proliferation and survival, linking to neurogenesis impairment and neuropsychiatric risks. Mechanistic insights remain undefined.
Methods
Comprehensive behavioral assessments were conducted on HFrD mice, including the tail suspension test (TST) and sucrose preference test (SPT) for depressive-like behaviors, elevated plus maze (EPM) and open field test (OFT) for anxiety-like behaviors, as well as novel object recognition (NOR) and Morris water maze (MWM) for cognition. Hippocampal NSCs and newborn neurons were quantified by immunofluorescence, and fructose-treated NE-4C cells underwent RNA sequencing (RNA-seq) analysis coupled with measurements of proliferation, apoptosis and ferroptosis markers.
Results
HFrD mice showed depressive-like behaviors without anxiety-like behaviors, and exhibited impaired short-term memory in NOR but did not show impaired spatial memory in MWM. Decreased number of hippocampal NSCs and newborn neurons were observed, suggesting impaired neurogenesis. In vitro, fructose-treated NE-4c exhibited altered gene expression profiles, with PCA showing distinct clustering between treated and control groups. Further analysis (GO, KEGG, GSEA) indicated enrichment in energy metabolism pathways, including mitochondrial ATP synthesis (e.g., downregulated ATP5E, ATP5H). Consistently, intracellular ATP levels were elevated, indicating metabolic dysregulation. Further experiments demonstrated that high fructose promoted NSC proliferation via p53/Wnt pathways (upregulated CyclinA2, CDK1) while concurrently inducing apoptosis (BAX, P53 upregulation) and ferroptosis (reduced GPX4, elevated ROS, and lipid peroxidation).
Conclusion
This study elucidates the mechanistic link between HFrD-induced metabolic disruption and NSC dysfunction, providing novel insights into the pathogenesis of fructose-associated neuropsychiatric disorders.
Study reveals fructose consumption may silently increase inflammation levels
Will your incompetent? doctor get the dietician to evaluate this and get the problem cases removed from all hospital locations?
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?
Let's see how long your doctor has been incompetent!
Fructose may be fueling the formation of Alzheimer’s disease February 2023
The latest here:
Study reveals fructose consumption may silently increase inflammation levels
Hearing Loss and Cognitive Decline in Older Adults
Do you really think your incompetent doctor in everything stroke related will know and prevent this for you?
With your risk of dementia post stroke your doctor and hospital (If competent) need to create this protocol and have dementia prevention protocols on hand.
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.`
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?
Hearing Loss and Cognitive Decline in Older Adults
Hearing loss affects an estimated 13% of adults in the United States, with prevalence roughly doubling to 27% among those aged 65 years and older.1 Among adults aged 71 and older, approximately 65% experience hearing impairment.2
Hearing loss is associated not only with social isolation, depression, and anxiety, but an accumulating body of research links hearing loss to cognitive decline and dementia.3,4 Early intervention, including the use of hearing aids, may modify this risk, underscoring the importance of timely identification and management.
Evidence Linking Hearing Impairment to Cognitive Decline
“Currently, there are numerous studies that show an association between untreated hearing loss and cognitive decline,” said Catherine Palmer, PhD, Director of Audiology, Chair, Department of Communication Sciences and Disorders, University of Pittsburgh.
In a 2023 meta-analysis, researchers observed an association between untreated hearing loss and performance on cognitive assessments such as the Mini-Mental State Examination and the Montreal Cognitive Assessment.4
International studies corroborate these findings. Research in Poland, Brazil, Canada, Japan, and France has reported links between hearing loss and cognitive decline or dementia.5-9 For example, a Polish cohort study found that mild cognitive impairment (MCI) was present in nearly 50% of participants with hearing loss compared to 26% of participants without hearing loss, with hearing loss increasing the odds of MCI by 34% (OR, 1.34; CI, 0.93-1.93).5
Further, a 2024 meta-analysis, which combined data from 50 studies encompassing more than 1.5 million participants, concluded that adult-onset hearing loss increases the risk for cognitive decline, dementia, MCI, and Alzheimer disease. The analysis further revealed a 16% increase in dementia risk for each 10-decibel worsening of hearing.10
We would do well to remind patients that all of these abilities go way beyond the ear: We hear with our brains.
Pathophysiological Mechanisms
Although mechanisms linking hearing loss and cognitive decline are still being investigated, several hypotheses have been proposed. “One theory is that hearing loss causes decreased stimulation of cognitive processing,” explained Seiji Shibata, MD, PhD, Otolaryngologist and Assistant Professor, Keck Medicine, University of Southern California. “In addition, there are a number of human and animal studies that have shown that there are structural changes in the auditory cortex associated with hearing loss.”
Kasia M Bieszczad, PhD, Associate Professor, Rutgers University, explained the hypothesis that “difficulty listening bears a burden on the brain that leads to brain dysfunction over time—this is the ‘cognitive load’ hypothesis.” There could also be an “indirect causation if hearing loss and difficulty listening lead to social isolation, and the social retraction over time—sometimes decades of isolation—leads to unhealthy brain function.”
The “common cause” hypothesis suggests that shared neurodegenerative processes may underlie both hearing loss and dementia. Dr Bieszczad explained, “I describe this as the auditory system being a ‘canary in the coal mine’ of cognitive decline.”
Clinical Screening and Assessment
Given the high prevalence of hearing loss and its associated comorbidities, the “recommendation is to get an annual hearing test by an audiologist or certified clinician for earlier detection,” Dr Shibata said. “I would also recommend getting a hearing test if a patient has been diagnosed with dementia.”
The American Academy of Otolaryngology-Head and Neck Surgery Clinical Practice Guideline for Age-Related Hearing Loss recommends screening for individuals aged 50 years and older.11 “Ideally, individuals would be screened at this time and receive a full hearing evaluation if they fail the screening,” Dr Palmer said. She emphasized that a “focus on hearing screening becoming ubiquitous in primary care and geriatric settings would support timely access to hearing care.”
Dr Bieszczad compared hearing screening to vision checks, saying, “Most people will understand what ’20/20′ means for vision, and they know their number. We might do well to promote knowing your ‘hearing number,’ and there is a great initiative on this point.”
For patients undergoing cognitive testing, Dr Palmer recommended ensuring a prior hearing assessment. “If the person has hearing loss, clinicians should, at a minimum, use an amplifier during cognitive screening or testing to account for any issues with audibility, given that most cognitive tests are delivered orally.” She continued, “Without amplification, the hearing loss may directly impact the test results, not because of cognition, but because the message wasn’t received clearly.”
Hearing Interventions and Cognitive Outcomes
“Several observational studies have reported some protection against cognitive losses in older adults who use well-fit hearing aids,” Dr Palmer said. In one meta-analysis, hearing aid use was associated with a 19% decrease in the long-term risk for cognitive decline.4
Additionally, a cross-sectional, prospective cohort study conducted in Japan found a significant negative correlation between hearing threshold and cognitive function among patients older than 55 years with hearing loss and no history of hearing aid use. In contrast, no such correlation was observed in those with hearing loss who had been using hearing aids for more than 3 years. The authors concluded that the average pure-tone audiometry hearing threshold of 38.75 dB or greater of hearing loss “may be a risk factor for cognitive decline among hearing aid non-users who are in midlife and beyond,” and that “long-term use of hearing aids may potentially reduce this risk.”7
However, in the multicenter ACHIEVE randomized controlled trial (Clinicaltrial.gov Identifier: NCT03243422) of 977 older adults, hearing aids did not reduce the progression of cognitive decline over a 3-year period.12 “But there is hope, because a subset of people that were already at higher risk for cognitive decline due to other factors, such as cardiovascular risk, did show a 48% reduction in the rate of cognitive decline if they wore hearing aids,” compared with participants in the control group, Dr Bieszczad said. “So all in all, wearing hearing aids may have an overall positive effect on hearing and brain health, but there is more to the story than hearing aids and auditory care.”12
Clinical Recommendations and Best Practices
To address hearing loss and potential cognitive risks, Dr Palmer emphasized that the “best approach is to provide well-fit hearing aids to individuals with hearing loss.”
“It is best to start using hearing aids prior to significant cognitive decline so the use is automatic and not something the individual is trying to learn when short-term memory might be impacted,” she advised. “Earlier intervention is best not only for the help it will provide but also to support long-term use.”
The US Food and Drug Administration’s 2022 approval of over-the-counter hearing aids has increased accessibility and affordability.13 However, Dr Shibata added,”In the event of moderate to severe sensorineural hearing loss, a cochlear implant has been shown to be effective towards improving cognitive function.”14
Dr Bieszczad suggested that clinicians promote the idea to patients that wearing hearing aids may help their cognitive brain health. “Some may find it a more compelling argument, and motivation, to wear hearing aids to possibly avoid dementia, rather than to ‘simply’ correct their hearing,” she explained.
Research Directions and Implications for Clinical Practice
Among the ongoing questions regarding this topic, Dr Shibata pointed to the need for further research to determine the exact mechanisms by which hearing loss may lead to dementia. “This kind of research will inform the development of new biomarkers and better neuroimaging for earlier detection and prevention.”
Dr Palmer cited the need for more research on the impact of improving hearing on the onset and progression of cognitive decline, though she emphasized the importance of not “overstating the relationship between hearing loss and cognitive decline given the current data.”15 She noted that statements from some professional groups have discussed “population-level risk, which is often misinterpreted as individual-level risk, making the risk appear larger than it may actually be.”
Considering the possibility of an indirect “common cause” in hearing impairment and cognitive decline, researchers may “gain valuable insight into what process might be using the auditory system and then invent new therapies that can be tested in the auditory system and then applied to the whole brain to ultimately slow or stop the course of general cognitive decline,” Dr Bieszczad explained. “We might also find clever ways to use the auditory brain system to uncover very early life biomarkers that could identify people at risk decades before the onset of dementia,” allowing for earlier intervention.
She concluded, “Our most sophisticated abilities as humans have so much to do with how we hear and listen in the world. We use language, sing, play music, dance, and socialize, and these are all highly sophisticated cognitive functions rooted in sound, hearing, and listening… We would do well to remind patients that all of these abilities go way beyond the ear: We hear with our brains.”
Diabetes drugs may help older adults slow frailty, suggests study
Your competent? doctor has had years to come up with a protocol to prevent frailty post stroke.
Did that occur? NO? So, you don't have a functioning stroke doctor or hospital, do you? RUN AWAY!
So, your doctor isn't up to the task of new knowledge? I'd suggest forced retirement of the doctor if your hospital is any good at all!
Diabetes drugs may help older adults slow frailty, suggests study
Cognitive Intervention Does More Than Defend Against Dementia
Now your competent? doctor has no reason not to give this to you to delay your risk of dementia post stroke. Is your doctor competent?
DOES YOUR INCOMPETENT? DOCTOR NOT HAVE THESE?
DOES YOUR DOCTOR HAVE EXACT DEMENTIA PREVENTION PROTOCOLS? NO? So, your doctor is incompetent?
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.`
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
The latest here:
Cognitive Intervention Does More Than Defend Against Dementia
Sleep, brain resilience, and blood flow improved with structured POINTER program
Three ancillary studies to the U.S. POINTER trial collectively demonstrated that a structured 2-year lifestyle intervention for older adults at increased risk of cognitive decline led to better overall health.
In main results from the U.S. POINTER trial released in July, two lifestyle interventions -- one structured, the other self-guided -- improved cognitive scores in over 2,000 older adults, said Rema Raman, PhD, of the University of Southern California in Los Angeles, who co-chaired a symposium at the Clinical Trials on Alzheimer's Disease (CTAD) annual meeting.
Both 2-year interventions in U.S. POINTER encouraged physical activity, cognitive activity, healthy diet, social engagement, and cardiovascular health monitoring, but they differed in structure, intensity, and accountability.
The mean annual increase in global cognitive scores was greater in the structured group compared with the self-guided group (P=0.008). "The structured intervention may, in our opinion, slow the cognitive aging clock by about 1 to 2 years compared to the self-guided intervention," Raman said.
At CTAD, the first results reported from the trial's ancillary studies -- POINTER-NV (neurovascular), POINTER-Neuroimaging, and POINTER-zzz (sleep) -- showed that blood pressure regulation, cognitive resilience, and sleep apnea were better with the structured intervention.
"I am very encouraged by these early findings from the U.S. POINTER ancillary studies, which offer valuable insights into the physiological mechanisms that may have contributed to the positive results of the U.S. POINTER trial," said Richard Hodes, MD, director of the NIH's National Institute on Aging, which supported the research.
"The forthcoming publications and continued analysis of this rich dataset will deepen our understanding of how multimodal interventions can support brain health," Hodes said in a statement.
POINTER-NV
The POINTER-NV study showed that the structured intervention significantly enhanced blood pressure regulation, cerebral autoregulation, and vascular elasticity while also improving functional properties of the aorta and major cerebral arteries, reported principal investigator Tina Brinkley, PhD, of the Wake Forest University School of Medicine in Winston-Salem, North Carolina.
Baroreflex sensitivity, which measures a mechanism that regulates blood pressure and ultimately drives cerebral blood flow, was a key outcome. In the structured intervention group, baroreflex sensitivity improved by 1.177 ms/mm Hg (95% CI 0.634-1.720) over 2 years, representing a 14% increase, Brinkley said. In the self-guided group, the change in baroreflex sensitivity was not significant.
The findings indicate that a structured multidomain lifestyle intervention can improve the body's ability to regulate blood pressure, which is crucial for proper brain blood flow to the brain, Brinkley said.
POINTER-Neuroimaging
In POINTER-Neuroimaging, participants with high-risk profiles -- those who had low baseline hippocampal volume or entorhinal tau accumulation in the brain -- had greater cognitive benefits from the structured versus the self-guided intervention (P=0.006).
Amyloid status did not appear to affect the cognitive benefit of the intervention. "This means that people with amyloid build-up experienced the same benefits from the intervention as those without amyloid," said Susan Landau, PhD, of the University of California Berkeley, who led the ancillary study.
The structured and self-guided groups did not differ overall on 2-year changes in amyloid, tau, hippocampal volume, or white matter hyperintensity volume, Landau noted. However, the structured intervention showed a protective effect on cognitive function, reducing the effect of entorhinal tau as it accumulated, she said. A 4-year extension study to follow these biomarkers is underway.
POINTER-zzz
In POINTER-zzz, participants had sleep assessments at baseline, 12 months, and 24 months. At baseline, 63% had least mild sleep apnea, reported Laura Baker, PhD, also of the Wake Forest University School of Medicine.
Home-based sleep testing revealed that, over 2 years, the structured intervention group had a reduction of one to two respiratory disturbance events per hour relative to the self-guided group. In the structured group, the mean 2-year reduction in the apnea-hypopnea index (AHI) from baseline was 1.759 (95% CI -2.554 to -0.965). In the self-guided group, the difference was not significant.
The structured intervention benefit on AHI was consistent across several key subgroups and tended to be stronger for people with more severe baseline sleep apnea, Baker noted. These improvements in sleep-disordered breathing are clinically meaningful and may confer additional neuroprotective benefits, she said.
Data about other metrics, including sleep fragmentation, are still being analyzed.
Overall, the ancillary study findings suggest that "the U.S. POINTER lifestyle intervention with structured support has substantial and significant health benefits beyond improving cognition, and the benefits are in areas known to lower risk of cognitive decline and dementia," observed Maria Carrillo, PhD, chief science officer of the Alzheimer's Association in Chicago, which supported the trial.
"Bottom line, we now have a more comprehensive picture of how the U.S. POINTER intervention affects brain health, and overall health, too," she added.
The U.S POINTER trial was supported by the Alzheimer's Association. The National Institute on Aging of the NIH supported the POINTER ancillary studies.
Brinkley had no disclosures.
Landau reported relationships with the NIH, Eisai, IMPACT-AD, Johnson & Johnson, ATRI, the Alzheimer's Association, and Shenzhen Bay Lab.
Baker had no disclosures.
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