Could dream manipulation help us solve real life problems?

 

Your competent? doctor should have been all over this by creating lucid dreaming protocols! With lucid dreaming you can see action observation of your own movements. I would do running.  The rest of the article is behind a paywall.

Your doctor should have been familiar with galantamine for a decade already

• galantamine (5 posts to August 2013)

A drug's weird side effect lets people control their dreams

The latest here:

Could dream manipulation help us solve real life problems?

The organisation of the Periodic Table, Paul McCartney's song Yesterday, and the main scenes in Mary Shelley's Frankenstein reportedly all sprang from insights that arose during dreams. Some studies have also strengthened the idea that spontaneously dreaming of a problem you're facing can lead to creative solutions.

However, evidence that deliberately manipulating dreams can foster creative problem-solving has been lacking, write the authors of a recent paper in the Neuroscience of Consciousness. In their study, though, Karen R Konkoly at Northwestern University and colleagues report findings that suggest that indeed it can.

The researchers recruited 20 participants who reported having a lucid dream at least once per month. During a lucid dream, the sleeper reports being aware that they are dreaming, and they can often influence or even control the content of their dreams.  

On two separate occasions, a week apart, each participant came into the lab for an overnight sleep study. They arrived at around 10pm, and attempted a series of difficult brain-teaser type puzzles until there were four left that they just couldn't solve. Importantly for the study, during each puzzle, the team played a specific eight to twelve-second long snippet of sound, and they made sure that the participants had learned which soundtrack went with which test.

The participant then went to sleep in the lab. While they slept, their brain activity and other physiological signals, including eye movements and muscle activity, were monitored using polysomnography.

At 4am, an experimenter woke them and used a method called Targeted Lucidity Reactivation to try to encourage lucid dreaming during their next bout of REM sleep. This technique involves pairing specific sounds with a lucid state of mind as the individual allows themself to fall asleep. When the polysomnography signals indicated that they had entered REM sleep, the researchers used TLR sound signals to try to trigger a lucid dream, then played the soundtracks to two of their four unsolved puzzles.

After the team finished presenting the cues or when the REM period ended, whichever was sooner, they woke the participant and asked them if they had heard the sound cues or anything that related to the puzzles during their dream, before allowing them to fall back to sleep. At 9am that morning, the participants were then given four minutes to work on each of the four unsolved puzzles again.

When the team analysed the data, they found that while many of the participants did not experience a lucid dream, three quarters dreamed about elements of unsolved puzzles, or ideas relating to those puzzles, at some point during the night. Also, when this happened, these particular puzzles were solved far more often the following morning. In fact, after waking, the participants solved 42% of puzzles that had appeared in some way during dreams, compared with 17% of the puzzles that had not.

The study does suffer from a few drawbacks. One is that it tested only one particular type of creativity: identifying one correct response from many alternatives. Also, all the participants were lucid dreamers; it's possible that this group has some quality that may make them respond differently to dream manipulations than those of us who don't lucid dream.

Another shortcoming is that the study can't prove that dreaming about a puzzle directly increased the chance of a creative solution. It's possible that when a participant was more interested in a particular puzzle, they were not only more likely to dream about it, but they also thought about it more before and after waking, and this waking activity might have helped them to solve it.

Still, the findings "support the conclusion that dreaming in REM sleep can contribute to creative problem solving," the team writes. And the study does demonstrate a method to influence the content of a person's dreams. They now plan to use this 'targeted memory reactivation' to explore in more detail the roles of REM dreams not just for problem-solving but also in emotional regulation as well as broader types of learning.

Read the paper in full:
Schredl, M., & Erlacher, D. (2007). Self-Reported Effects of Dreams on Waking-Life Creativity: An Empirical Study. The Journal of Psychology, 141(1), 35–46. https://doi.org/10.3200/jrlp.141.1.35-46

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Galantamine for dementia due to Alzheimer's disease and mild cognitive impairment

 

 Your competent? doctor should have been familiar with galantamine for a decade already. Did your doctor do one damn thing with it?  NO?  So, you don't have a functioning stroke doctor, do you?

• galantamine (9 posts to August 2013)

Galantamine for dementia due to Alzheimer's disease and mild cognitive impairment

• Amanda Wei Yin Lim
• Lon Schneider
• Clement Loy

Authors' declarations of interest

Version published: 05 November 2024 Version history

https://doi.org/10.1002/14651858.CD001747.pub4

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Abstract

available in

English

Español

فارسی

Background

Dementia leads to progressive cognitive decline, and represents a significant health and societal burden. Its prevalence is growing, with Alzheimer's disease as the leading cause. There is no cure for Alzheimer's disease, but there are regulatory‐approved pharmacological interventions, such as galantamine, for symptomatic relief. This review updates the 2006 version.

Objectives

To assess the clinical effects, including adverse effects, of galantamine in people with probable or possible Alzheimer's disease or mild cognitive impairment, and to investigate potential moderators of effect.

Search methods

We systematically searched the Cochrane Dementia and Cognitive Improvement Group's Specialised Register on 14 December 2022 using the term 'galantamine'. The Register contains records of clinical trials identified from major electronic databases (including CENTRAL, MEDLINE, and Embase), trial registries, grey literature sources, and conference proceedings. We manually searched reference lists and collected information from US Food and Drug Administration documents and unpublished trial reports. We imposed no language restrictions.

Selection criteria

We included double‐blind, parallel‐group, randomised controlled trials comparing oral galantamine with placebo for a treatment duration exceeding four weeks in people with dementia due to Alzheimer's disease or with mild cognitive impairment.

Data collection and analysis

Working independently, two review authors selected studies for inclusion, assessed their quality, and extracted data. Outcomes of interest included cognitive function, change in global function, activities of daily living, functional disability, behavioural function, and adverse events. We used a fixed‐effect model for meta‐analytic synthesis, and presented results as Peto odds ratios (OR) or weighted mean differences (MD) with 95% confidence intervals. We used Cochrane's original risk of bias tool (RoB 1) to assess the risk of bias in the included studies.

Main results

We included 21 studies with a total of 10,990 participants. The average age of participants was 74 years, and 37% were male. The studies' durations ranged from eight weeks to two years, with 24 weeks being the most common duration. One newly included study assessed the effects of galantamine at two years, and another newly included study involved participants with severe Alzheimer's disease.

Nineteen studies with 10,497 participants contributed data to the meta‐analysis. All studies had low to unclear risk of bias for randomisation, allocation concealment, and blinding. We judged four studies to be at high risk of bias due to attrition and two due to selective outcome reporting.

Galantamine for dementia due to Alzheimer's disease

We summarise only the results for galantamine given at 8 to 12 mg twice daily (total galantamine 16 mg to 24 mg/day), assessed at six months. See the full review for results of other dosing regimens and assessment time points.

There is high‐certainty evidence that, compared to placebo, galantamine improves: cognitive function, as assessed with the Alzheimer's Disease Assessment Scale – Cognitive Subscale (ADAS‐cog) (MD‐2.86, 95% CI ‐3.29 to ‐2.43; 6 studies, 3049 participants; minimum clinically important effect (MCID) = 2.6‐ to 4‐point change); functional disability, as assessed with the Disability Assessment for Dementia (DAD) scale (MD 2.12, 95% CI 0.75 to 3.49; 3 studies, 1275 participants); and behavioural function, as assessed with the Neuropsychiatric Inventory (NPI) (MD ‐1.63, 95% CI ‐3.07 to ‐0.20; 2 studies, 1043 participants) at six months. Galantamine may improve global function at six months, as assessed with the Clinician's Interview‐Based Impression of Change plus Caregiver Input (CIBIC‐plus) (OR 1.58, 95% CI 1.36 to 1.84; 6 studies, 3002 participants; low‐certainty evidence). Participants who received galantamine were more likely than placebo‐treated participants to discontinue prematurely (22.7% versus 17.2%) (OR 1.41, 95% CI 1.19 to 1.68; 6 studies, 3336 participants; high‐certainty evidence), and experience nausea (20.9% versus 8.4%) (OR 2.89, 95% CI 2.40 to 3.49; 7 studies, 3616 participants; high‐certainty evidence) during the studies. Galantamine reduced death rates at six months: 1.3% of participants in the galantamine groups had died compared to 2.3% in the placebo groups (OR 0.56, 95% CI 0.33 to 0.96; 6 studies, 3493 participants; high‐certainty evidence).

Galantamine for mild cognitive impairment

We summarise results, assessed at two years, from two studies that gave participants galantamine at 8 to 12 mg twice daily (total galantamine 16 mg to 24 mg/day). Compared to placebo, galantamine may not improve cognitive function, as assessed with the expanded ADAS‐cog for mild cognitive impairment (MD ‐0.21, 95% CI ‐0.78 to 0.37; 2 studies, 1901 participants; low‐certainty evidence) or activities of daily living, assessed with the Alzheimer's Disease Cooperative Study – Activities of Daily Living scale for mild cognitive impairment (MD 0.30, 95% CI ‐0.26 to 0.86; 2 studies, 1901 participants; low‐certainty evidence). Participants who received galantamine were probably more likely to discontinue prematurely than placebo‐treated participants (40.7% versus 28.6%) (OR 1.71, 95% CI 1.42 to 2.05; 2 studies, 2057 participants) and to experience nausea (29.4% versus 10.7%) (OR 3.49, 95% CI 2.75 to 4.44; 2 studies, 2057 participants), both with moderate‐certainty evidence. Galantamine may not reduce death rates at 24 months compared to placebo (0.5% versus 0.1%) (OR 5.03, 95% CI 0.87 to 29.10; 2 studies, 2057 participants; low‐certainty evidence).

Results from subgroup analysis and meta‐regression suggest that an imbalance in discontinuation rates between galantamine and placebo groups, together with the use of the 'last observation carried forward' approach to outcome assessment, may potentially bias cognitive outcomes in favour of galantamine.

Authors' conclusions

Compared to placebo, galantamine (when given at a total dose of 16 mg to 24 mg/day) slows the decline in cognitive function, functional ability, and behaviour at six months in people with dementia due to Alzheimer's disease. Galantamine probably also slows declines in global function at six months. The changes observed in cognition, assessed with the ADAS‐cog scale, were clinically meaningful. Gastrointestinal‐related adverse events are the primary concerns associated with galantamine use in people with dementia, which may limit its tolerability. Although death rates were generally low, participants in the galantamine groups had a reduced risk of death compared to those in the placebo groups. There is no evidence to support the use of galantamine in people with mild cognitive impairment. 

Galantamine combined with cognitive rehabilitation on post-stroke cognitive impairment: a proof-of-concept study

 Ask your competent? doctor if this is enough to recover your  lost 5 cognitive years from your stroke? No answer, you need to fire that doctor.

Galantamine combined with cognitive rehabilitation on post-stroke cognitive impairment: a proof-of-concept study

Mélanie Planton

,

Federico Nemmi

,

Berengère Pages

,

Jean-François Albucher

,

Nicolas Raposo

,

Lola Danet

, show all

Received 05 Mar 2024, Accepted 20 Sep 2024, Published online: 03 Oct 2024

• Cite this article
• https://doi.org/10.1080/02699052.2024.2409355
• CrossMark

 

ABSTRACT

Purpose

We conducted a proof-of-concept study to evaluate the effects of galantamine treatment versus placebo combined to cognitive rehabilitation (CR) after stroke.

Materials and methods

In this 12-week, double blinded, randomized, controlled trial, patients were assigned to either combined approach of galantamine and CR (G-CR) or placebo and CR (P-CR). Primary outcome was the proportion of patients who crossed over from vascular cognitive disorder (VCD) to no-VCD at 12 weeks. Secondary outcomes included changes in cognition, mood, quality of life and the N-back fMRI paradigm, assessed at baseline, 6 and 12 weeks and after an 8-week washout period.

Results

Ten patients were allocated to G-RC group, 12 to the P-RC group. After 12 weeks, 40.1% of all patients converted to no-VCD with similar proportions between groups. Both groups showed improvements in episodic and working memory, executive and quality of life after 6 weeks of CR. Decreased depression and anxiety were noted, and all benefits persisted after the washout period. An interaction effect was observed in the right parietal lobule during the N-back task.

Conclusions

Interventions lead to improved cognition and distinct cortical reorganization without being able to establish correlation between neural changes and behavioral measures.

Effect of high-frequency (5Hz) rTMS stimulating left DLPFC combined with galantamine on cognitive impairment after ischemic stroke and serum homocysteine and neuron-specific enolase

 Your doctor should have been familiar with galantamine for a decade already

• galantamine (5 posts to August 2013)

And with these positive effects your doctor should immediately create a protocol on this!

Effect of high-frequency (5Hz) rTMS stimulating left DLPFC combined with galantamine on cognitive impairment after ischemic stroke and serum homocysteine and neuron-specific enolase

Guojin HuLi ZhangXiuli Sun^*Lin Wang^*Qian XuQin LiWei HuangYao Xiao

• Department of Geriatric Rehabilitation, Shanghai Second Rehabilitation Hospital, Shanghai, China

Objective: To investigate the efficacy of high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) combined with galantamine in patients with cognitive impairment after stroke and its effect on serum homocysteine (Hcy) and neuron-specific enolase (NSE) levels.

Methods: A total of 90 patients with cognitive impairment after the first ischemic stroke were enrolled. They were randomly divided into rTMS+ cognitive rehabilitation group, Galantamine + cognitive rehabilitation group, and rTMS+ Galantamine + cognitive rehabilitation group. All groups received routine medical treatment and limb rehabilitation treatment. The rTMS stimulation site was the left dorsolateral prefrontal cortex (left DLPFC), the magnetic stimulation frequency was 5 Hz, the magnetic stimulation intensity was 80% of the motor threshold level, and 3,000 pulses were given every day. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Fugl-Meyer scale, and modified Barthel index, as well as rehabilitation scale and serum NSE and Hcy were evaluated before and after treatment (after 4 weeks).

Results: After 4 weeks of treatment, the scores of MMSE, MoCa scale, Fugl-Meyer scale, and modified Barthel index in the three groups were significantly higher than those before treatment (all p < 0.05), while the serum NSE and Hcy levels of the three groups were decreased. rTMS+ Galantamine + cognitive rehabilitation group had higher scale scores, and the difference between the three groups was statistically significant compared with the other two groups (all p < 0.05).

Conclusion: Cognitive rehabilitation combined with HF-rTMS and galantamine could improve the cognitive function of patients to the greatest extent, promote the recovery of physical activity, improve the self-care ability of daily life, and effectively reduce the serum HCY and NSE levels in patients with cognitive impairment after stroke. No randomized controlled trials of similar combination treatments have been reported. The better therapeutic effect may be related to the fact that galantamine combined with repetitive transcranial magnetism can activate the brain cholinergic system more extensively, promote brain neural remodeling through long-term potentiation and inhibit local neuroinflammatory responses in brain injury.

1 Introduction

Post-stroke cognitive impairment (PSCI), especially post-stroke dementia, seriously affects patients’ functional recovery, daily activities, and social functioning. PSCI is an independent risk factor affecting the prognosis of stroke. Professor Hachinski’s survey published in “Stroke” in 2006 showed that as many as 64% of stroke patients have varying degrees of cognitive impairment, and 1/3 will develop obvious dementia (1). A systematic review of epidemiological characteristics of post-stroke cognitive impairment in China in 2013 showed that the incidence rates of PSCI and post-stroke dementia (PSD) within 3 months after stroke were 56.6 and 23.2%, respectively (2). Compared with those without dementia, physical function of PSCI patients, their mental health status, and social functioning undergo more significant decline. Also, their functional independence is weakened, social participation ability is worsened, life satisfaction drastically decreases, and the 5-year survival rate is significantly lowered (3, 4). PSCI also seriously hinders the improvement of patients’ motor function, psychological state, self-care ability, and ability to participate in social activities and reduces life expectancy.

In recent years, non-invasive brain stimulation technology has developed rapidly, among which repetitive transcranial magnetic stimulation (rTMS) technology has received the greatest attention from researchers. rTMS acts on the central nervous system, mainly the brain, through a pulsed magnetic field, changing the membrane potential of neurons in the cerebral cortex, causing them to generate induced currents, affecting intramembrane metabolism and neural electrical activity, and inducing a series of physiological and biochemical changes. As a result, this technology has been widely investigated in recent years, producing positive effects on depression, cognitive impairment, post-stroke movement disorders, aphasia, etc. (5–7).

rTMS alters the excitability of cortical and subcortical neurons. Among them, high-frequency (>1 Hz) stimuli produce excitatory effects, and low-frequency (≤1 Hz) stimuli produce inhibitory effects. rTMS can act on synapses to produce long-term potentiation or long-term inhibitory effects and promote the excitation or inhibition of cortical neural circuits. Moreover, the physiological effects are persistent (8).

A large amount of available data indicates that TMS technology has a very unique role in the rehabilitation treatment of dementia, including degenerative dementias such as Alzheimer’s disease, as well as secondary dementias (mainly caused by vascular factors). Transcranial magnetic field can not only predict the risk of dementia in the brain, but also improve cognitive function by stimulating treatment to activate cholinergic neural pathways and promote brain injury remodeling. Existing transcranial magnetic studies have shown that patients with vascular dementia have increased motor cortex excitability (decreased resting motor threshold), which is consistent with patients with Alzheimer’s disease (9, 10). This may be part of a mechanism to compensate for plasticity after neuron loss and/or ischemic injury in the brain, with increased excitability helping to protect cognitive function. Abnormal resting motor threshold can be used as a “neurophysiological boundary point” to distinguish patients with normal cognition, non-demented vascular cognitive impairment, and vascular dementia (11). At the same time, the short-latency input inhibition measured by transcranial magnetic can reflect the function of cholinergic circuit in the central nervous system, which is closely related to cognitive function. Although there are some conflicting data in vascular dementia studies (12–14), this may be related to the variable location of subcortical infarctions in patients with vascular cognitive impairment and the significant differences in the distribution and extent of cholinergic denervation caused by them. Nevertheless, short latency inhibition holds great promise in the diagnosis and prognosis of different dementia processes and in the identification of acetylcholinesterase inhibitors for the treatment of sensitive individuals (15).

Transcranial magnetic therapy has a pleiotropic effect, although in a small number of experiments, the effects of high-frequency rTMS on mood, cognition, cortical microcircuits, neurotrophic/growth factors, and cerebral blood flow were not detected. This may be related to the selection of stimulus intensity, total pulse number, test sample size, sex selection, and the unclear mechanism of how ischemic brain injury affects plasticity induced by transcranial magnetic stimulation (16).

At present, there are many studies on the clinical application of rTMS in the treatment of post-stroke dementia, and gratifying results have been achieved (17, 18). Cha et al. (19) performed high-frequency transcranial magnetic therapy in patients with PSCI and assessed cognitive and emotional abilities at 2 and 14 weeks of treatment. The results showed that after rTMS treatment, the cognitive function of the patients was improved, and the proinflammatory cytokines in peripheral blood were decreased. These improvements lasted for three months. The meta-analysis by Li et al. (18) showed that the left dorsolateral prefrontal cortex of PSCI patients was stimulated by high-frequency rTMS, and the number symbol test, Rivermead behavioral memory test and the patients’ attention were significantly improved.

Galantamine hydrobromide is a second-generation cholinesterase inhibitor, initially used for the treatment of AD, which is highly selective for AChE in the central nervous system. It mainly inhibits cholinesterase at the synaptic cleft between the presynaptic membrane and the posterior membrane of brain cholinergic nerve cells, delays the degradation of acetylcholine, increases the content of available acetylcholine, stimulates and improves the function of the remaining acetylcholine receptors (20). The same time, after oral administration of Galantamine, the nicotinic cholinergic receptors in patients with vascular dementia can be regulated to a certain extent (allosteric regulation), and this change can promote a large amount of cholinergic nervous system in patients, releasing acetylcholine, promote its central nervous system into an excited state, and correct its memory and cognitive dysfunction. This unique dual action is beneficial for improving cognitive deficits in dementia patients.

Studies have shown that Galantamine has a good curative effect on patients with vascular dementia. In 2007, Auchus et al. (21) conducted a randomized, double-blind, and placebo-controlled clinical study involving multiple countries. Their results showed that the Galantamine group had significantly improved cognitive function and executive ability compared to the placebo group. In terms of improving activities of daily living, there was little difference between the two groups. The meta-analysis conducted by Yu-Dan et al. (22) showed that the treatment with donepezil and galantamine could significantly improve the Alzheimer’s disease cognitive scale (ADAS cog) score in patients with vascular dementia, with mild adverse reactions and high safety.

The treatment of PSCI requires early screening and detection and timely comprehensive intervention. Comprehensive intervention includes intervention and prevention of known risk factors, drug treatment, and rehabilitation. In addition, the recovery of cognitive function after stroke depends on repairing damaged nerve cells and cortical reconstruction, and intensive cognitive training can accelerate the process of cortical reconstruction. There is no ideal method for the treatment of PSCI, and the current treatment methods have poor efficacy. We attempted to combine high-frequency repetitive transcranial magnetic stimulation and galantamine oral therapy on the basis of cognitive rehabilitation therapy for PSCI patients, achieving better efficacy than the control group. The following report is presented.

More at link.

Alzheimer's Supplements Fail Compared With Generic Drugs

 

 Well! You're on your own with supplements, better start your own testing lab.

The supplements in the US have zero guarantee of purity or efficacy due to the fucking stupidity of the US Congress passing the Dietary Supplement Health and Education Act of 1994 (DSHEA).

Alzheimer's Supplements Fail Compared With Generic Drugs

Prescription galantamine drugs were labeled accurately, but dietary supplements were not

by Judy George, Deputy Managing Editor, MedPage Today February 23, 2024

Galantamine sold as prescription generic drugs was labeled accurately and free of contamination, but galantamine sold as dietary supplements was not, an analysis showed.

Across 10 brands of dietary supplements, the actual quantity of galantamine -- a plant alkaloid with anticholinergic effects used to treat Alzheimer's dementia -- was anywhere from 2% to 110% of the labeled quantity, reported Pieter Cohen, MD, of Cambridge Health Alliance in Massachusetts, and colleagues in a JAMA research letter.

In contrast, the amount of galantamine in 11 brands of generic drugs ranged from 97.5% to 104.2% of the labeled content.

Moreover, three of the over-the-counter dietary supplements were contaminated with Bacillus cereus sensu stricto, which may suggest a lack of appropriate quality control during manufacturing, the researchers noted.

"What we found was a striking difference between the products," Cohen noted in an email to MedPage Today.

"Generic galantamine aced the tests. The amount of galantamine listed on the label accurately represented the amount of galantamine in the pills and, importantly, no bacterial contamination was found," he said.

"The galantamine dietary supplements, on the other hand, almost universally failed our tests: 90%, or 9 out of the 10 brands, had an inaccurate amount of galantamine on the label and, disturbingly, 30%, 3 out of 10 brands, were also contaminated with bacteria that could, if consumed at higher levels, cause diarrheal illnesses."

Galantamine is derived from botanical sources including narcissus and snowdrops. Prescription galantamine (Razadyne) was approved in 2001 and several generic brands are now sold. The cholinesterase inhibitor is indicated for mild to moderate dementia in Alzheimer's and has been shown to decrease the risk of severe dementia.

Galantamine appears to be ineffective in treating mild cognitive impairment or preventing dementia, but the supplement is marketed for a variety of cognitive conditions.

"When sold as a dietary supplement, manufacturers claim galantamine can improve memory, initiate lucid dreams, and improve 'cognitive acuity,' but what's actually in those bottles of galantamine and how that compares to prescription galantamine is not known," Cohen said.

In June 2023, Cohen and co-authors purchased all dietary supplements available on Amazon that were labeled with galantamine as an ingredient and carried a supplement facts panel (to ensure the product was marketed as a dietary supplement). The supplements were bought online in the U.S.

In September 2023, they purchased all generic immediate-release formulations of galantamine available in the U.S. Generic drugs were labeled as containing 4, 8, and 12 mg of galantamine per tablet or capsule.

The contents of all products were reconstituted in water and analyzed for the presence of galantamine. The researchers also assessed the products for possible contamination with microorganisms.

Overall, 100% of the generic drugs and only one supplement (10%) contained a quantity of galantamine that was within 10% of the quantity declared on the label.

Clinicians should query patients with memory concerns about their use of dietary supplements and advise patients not to use galantamine supplements, Cohen and colleagues said.

"For patients with Alzheimer's disease, use of galantamine supplements instead of generic galantamine may adversely affect their care," they pointed out.

"Furthermore, the sale of inaccurately labeled galantamine supplements promoted for nonspecific memory and other cognitive problems is concerning given the lack of proven efficacy, potential drug-drug interactions, and adverse effects, including nausea, vomiting, dizziness, bradycardia, and syncope," they added.

The study has several limitations, the researchers acknowledged. Galantamine supplements were purchased at one time point only and findings might not apply to products available at other times. Whether results are generalizable to other substances like niacin, potassium, or iron that also are available as either supplements or drugs isn't known, they added.

"Our study raises a troubling question: Are the laws regulating dietary supplements in the U.S. adequate to ensure the quality of the many active drugs sold directly to U.S. consumers as supplements?" Cohen asked. "We think not."

• Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

Cohen reported receiving grants from Consumers Union and PEW Charitable Trust and personal fees from UpToDate and the CDC outside the submitted work.

Co-authors had no disclosures to report.

Primary Source

JAMA

Source Reference: Cohen PA, et al "Accuracy of labeling of galantamine generic drugs and dietary supplements" JAMA 2024; DOI: 10.1001/jama.2024.0328.

A drug's weird side effect lets people control their dreams

Your competent? doctor should have been all over this. With lucid dreaming you can see action observation of your own movements. I would do running.  The rest of the article is behind a paywall.

Your doctor should have been familiar with galantamine for a decade already

• galantamine (5 posts to August 2013)

A drug's weird side effect lets people control their dreams

By Alice Klein

16 August 2018 , updated 17 August 2018

An Alzheimer’s treatment boosts lucid dreaming

harry + lidy/Plainpicture

Have you ever wanted to fly? A drug that helps people control their dreams could let you try it from the comfort of your own bed.

A small number of people naturally have lucid dreams, meaning they can recognise when they’re dreaming and steer the storyline they experience. Some others can learn to induce them using cognitive techniques.

The practice is most commonly used to pursue fantasies like flying, but it may also help to overcome fears and nightmares, says Benjamin Baird at …

Article amended on 17 August 2018

A description of galantamine side effects was added.

Multi-year study shows galantamine slows progression of Alzheimer’s dementia

You'll have to ask your competent? doctor if they did ANYTHING AT ALL with this earlier research.

Galantamine Slashes Heart Attacks and Death August 2013 

Razadyne For Alzheimer's(galantamine) Improves Thinking & Lengthens Life June 2015 

Randomized Placebo-Controlled Trial of Methylphenidate or Galantamine for Persistent Emotional and Cognitive Symptoms Associated with PTSD and/or Traumatic Brain Injury September 2015 

Rehabilitative Success After Brain Trauma by Augmenting a Subtherapeutic Dose of Environmental Enrichment With Galantamine November 2017

The latest here:

Multi-year study shows galantamine slows progression of Alzheimer’s dementia

Cholinesterase inhibitors provided moderate but persistent benefits in patients with Alzheimer’s dementia, including a lower risk for death, according to data published in Neurology.

However, galantamine was the only the cholinesterase inhibitor (ChEI) that demonstrated a significant reduction in the risk for severe dementia.

Researchers found that cholinesterase inhibitors had a modest but persistent benefit for patients with Alzheimer’s dementia, particularly galantamine. Source: Adobe Stock

“ChEIs are a group of drugs recommended for the treatment of AD, but their effects on cognition have been debated and few studies have investigated their long-term effects,” Maria Eriksdotter, MD, head of the department of neurobiology, care sciences and society at the Karolinska Institutet in Sweden, told Healio Neurology. “We wanted to follow patients who are on treatment with ChEI for longer times since patients with AD live for many years with the disease.”

Eriksdotter and colleagues examined data from patients diagnosed with mild to advanced stage Alzheimer’s dementia who were enrolled the Swedish Dementia Registry between 2007 to 2017.

The study compared 11,652 AD patients who were started on ChEIs within 3 months of their dementia diagnosis — either donepezil, rivastigmine or galantamine — and 5,836 AD patients who did not take ChEIs.

During a mean follow up of 5 years, the researchers found ChEI use correlated with a 27% reduced risk for death (0.73; 95% CI, 0.69-0.77) compared with patients who did not take ChEIs. Among the three ChEIs, galantamine was linked with the highest reduction in the risk for death (HR = 0.71; 95% CI, 0.65-0.76) compared with donepezil (HR = 0.78; 95% CI, 0.74-0.83) and rivastigmine (HR = 0.86; 95% CI, 0.8-0.93). Galantamine also reduced the risk for severe dementia (HR = 0.69; 95% CI 0.47-1) and demonstrated the greatest impact on cognitive decline, measured on the Mini-Mental State Examination (0.18 MMSE points/year; 95% CI 0.07-0.28). It had a modulatory effect on nicotine receptors as well, according to Eriksdotter, but she said that finding requires further study.

During the study period, 255 patients developed severe dementia and 35% died. The researchers noted that patients who did not take ChEIs tended to be older and had more comorbidities and medications. ChEI use overall was associated with higher MMSE scores at each visit, they said (0.13 MMSE points/year; 95% CI, 0.06-0.2). Among those on treatment, 62% of patients took donepezil, 21% galantamine and 17% rivastigmine. The overall mortality rate for ChEI users was lower compared with nonusers (105.78/1,000 person-years vs. 136.93/1,000 person-years).

“What did surprise me is not that the cognitive benefits were modest (that has been shown for up to 1 year before) but that these cognitive benefits persisted for such a long time, up to 5 years.” Eriksdotter said. “That is very encouraging from a clinical perspective for a chronic and progressive disease as AD. Our results provide strong support to treat people with AD with ChEIs, but we also show that the therapeutic effect lasts for a long time (ie, the ChEIs should be used long term).”

 

Rehabilitative Success After Brain Trauma by Augmenting a Subtherapeutic Dose of Environmental Enrichment With Galantamine

Sounds like this might be useful for stroke also so followup with human testing is needed.  Of course you will have to ask your doctor what the environment enrichment protocol is for your rehab.

Rehabilitative Success After Brain Trauma by Augmenting a Subtherapeutic Dose of Environmental Enrichment With Galantamine

Show all authors

Patricia B. de la Tremblaye, PhD, Jody L. Wellcome, Benjamin Wells de Witt, MD, ...

First Published November 12, 2017 Research Article

Download PDF	Article information

Abstract

Background. Environmental enrichment (EE) confers benefits after traumatic brain injury (TBI) when provided daily for > 6 hours, but not 2 or 4 hours, which more accurately reflects the daily amount of clinical rehabilitation. The lack of benefit with sub-therapeutic EE suggests that augmentation with galantamine (GAL), which enhances cognition after TBI, may be indicated to confer benefits.  
Objective. To test the hypothesis that 2 and 4 hours of EE paired with GAL will provide benefits comparable to 24 hours of EE alone. Moreover, all EE groups will perform better than the standard (STD)-housed GAL group.  
Methods. Anesthetized rats received a TBI or sham injury and then were randomized to receive intraperitoneal injections of GAL (2 mg/kg) or saline vehicle (VEH; 1 mL/kg) beginning 24 hours after surgery and once daily while receiving EE for 2, 4, or 24 hours. Motor and cognitive assessments were conducted on postoperative days 1-5 and 14-19, respectively.  
Results. Motor function was significantly improved in the TBI + 24-hour EE group versus the TBI + STD + VEH and TBI + STD + GAL groups (P < .05). Cognitive performance was enhanced in all EE groups as well as in the TBI + STD + GAL versus TBI + STD + VEH (P < .05). Moreover, the 2- and 4-hour EE groups receiving GAL did not differ from the 24-hour EE group (P > .05) and performed better than GAL alone (P < .05).  
Conclusions. The findings support the hypothesis and have clinical relevance because, often, only brief rehabilitation may be available in the clinic and, thus, augmenting with a pharmacotherapy such as GAL may lead to outcomes that are significantly better than either therapy alone.

Randomized Placebo-Controlled Trial of Methylphenidate or Galantamine for Persistent Emotional and Cognitive Symptoms Associated with PTSD and/or Traumatic Brain Injury

Your doctor will need to create a followup study on this. Or a study sponsored by our fucking failures of stroke associations.

Randomized Placebo-Controlled Trial of Methylphenidate or Galantamine for Persistent Emotional and Cognitive Symptoms Associated with PTSD and/or Traumatic Brain Injury`

McAllister TW¹, Zafonte R², Jain S³, Flashman LA⁴, George MS⁵, Grant GA⁶, He F³, Lohr JB⁷, Andaluz N⁸, Summerall L⁹, Paulus MP¹⁰, Raman R³, Stein MB^11,12.

Author information

Abstract

We report findings from a 12-week randomized double-blind placebo-controlled trial of methylphenidate or galantamine to treat emotional and cognitive complaints in individuals (N=32) with a history of PTSD, TBI, or both conditions. In this small pilot study, methylphenidate treatment was associated with clinically meaningful and statistically significant improvement compared to placebo on the primary outcome, a measure of cognitive complaints (Ruff Neurobehavioral Inventory - Postmorbid Cognitive Scale), as well as on the secondary outcomes reflecting postconcussive (Rivermead Postconcussive Symptom Questionnaire) and posttraumatic stress symptoms (Posttraumatic Stress Disorder Checklist). Treatment was well tolerated. These results suggest the need for a larger RCT to replicate and confirm these findings. Design considerations for such a trial should include the need for multiple sites to facilitate adequate recruitment and extension of the treatment and follow-up periods.Neuropsychopharmacology accepted article preview online, 11 September 2015. doi:10.1038/npp.2015.282.

Razadyne For Alzheimer's(galantamine) Improves Thinking & Lengthens Life

WHOM is going to sponsor the research on this to see if it improves cognitive thinking for stroke survivors? Or are the ASA and NSA going to continue to sit on their asses again? ARE YOU WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM?

Razadyne For Alzheimer's(galantamine) Improves Thinking & Lengthens Life 

 The treatment group also had significantly lesser cognitive decline measured by the change from baseline in the Mini Mental Status Evaluation (MMSE) at month 24 of the study, compared to the group treated with placebo.
 

Galantamine Slashes Heart Attacks and Death

For your doctor to analyze and report back to you.

Galantamine Slashes Heart Attacks and Death

A new study has found that subjects taking the highest recommended doses of cholinesterase inhibitors (ChEIs)—including donepezil (at 10 mg/day), rivastigmine (at 6 mg/day), and galantamine (at 24 mg/day)—had significantly lower levels of myocardial infarction (MI, aka heart attack) or significantly reduced risk of death from any cause.¹ The research was conducted at Karolinska University Hospital, Stockholm, Sweden where over 7000 subjects (mean age 79 years) from the Swedish Dementia Registry with the diagnoses of Alzheimer’s dementia or Alzheimer’s mixed dementia since 2007 were followed for a mean period of 503 days. In the study, those who used ChEI, compared to those who did not, experienced:

• 38% lower risk of heart attack
• 26% lower risk of death from stroke and other cardiovascular diseases
• 36% lower risk of death from any cause

More at link.