Tag: cognition

Neupro may reduce cognitive dysfunction among patients with Alzheimer’s disease

On By A.P.In UncategorizedLeave a comment

The dopaminergic agonist Neupro appeared to improve frontal cognitive functions and activities of daily living among patients with mild to moderate Alzheimer’s disease, according to study results published in JAMA Network Open.

“Some early attempts have been carried out using dopaminergic drugs, such as L-dopa or selegiline, in samples of patients with Alzheimer’s disease at different stages of the disease, with some controversial results,” Giacomo Koch, MD, PhD, of the department of behavioral and clinical neurology at Santa Lucia Foundation Scientific Institute for Research, Hospitalization and Healthcare in Rome, and colleagues wrote. “More recently, experimental studies in animal models of Alzheimer’s disease showed that dopaminergic agonists may reduce amyloid deposition and improve memory and that the degeneration of dopaminergic neurons in the ventral tegmental area contributes to memory deficits. It has also been shown that in the early stages of Alzheimer’s disease, dopaminergic agonists improve cholinergic transmission and cortical plasticity likely by acting on the dopaminergic projections over the frontal cortex.”

This prior evidence suggested novel implications for therapies based on dopaminergic stimulation among patients with mild to moderate Alzheimer’s disease, according to the investigators. Thus, they sought to determine whether dopaminergic agonist therapy would affect cognitive functions among this patient population.

In the current phase 2, monocentric, randomized, double-blind, placebo-controlled trial conducted in Italy and funded by the Alzheimer’s Drug Discovery Foundation, Koch and colleagues enrolled 94 patients (mean age, 73.9 years) with mild to moderate Alzheimer’s disease between September 2017 and December 2018. The intervention comprised use of a Neupro (rotigotine, UCB) 2 mg transdermal patch for 1 week, followed by a 4 mg patch for 23 weeks among 47 patients or a placebo transdermal patch for 24 weeks among 47 patients. Change from baseline on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale served as the primary end point. Secondary end points included changes in Frontal Assessment Battery, Alzheimer’s Disease Cooperative Study-Activities of Daily Living and Neuropsychiatric Inventory scores. The researchers used transcranial magnetic stimulation combined with electroencephalography to evaluate prefrontal cortex activity.

A total of 78 patients completed the study. Results showed rotigotine compared with placebo had no significant effect on the primary end point, with an estimated mean change in Alzheimer’s Disease Assessment Scale-Cognitive Subscale score of 2.92 (95% CI, 2.51-3.33) among the rotigotine group and 2.66 (95% CI, 2.31-3.01) among the placebo group. The researchers reported significant estimated mean changes for the secondary outcomes between groups for Alzheimer Disease Cooperative Study-Activities of Daily Living score, which was 3.32 (95% CI, 4.02 to 2.62) among the rotigotine group and 7.24 (95% CI, 7.84 to 6.64) among the placebo group. Frontal Assessment Battery score was 0.48 (95% CI, 0.31-0.65) among the rotigotine group and 0.66 (95% CI, 0.80 to 0.52) among the placebo group. Koch and colleagues observed no longitudinal change in Neuropsychiatric Inventory scores for either group. Neurophysiological analysis of electroencephalography results revealed increased prefrontal cortical activity among the rotigotine group but not the placebo group. Patients in the rotigotine group were more likely to experience adverse events than the placebo group, and 11 patients dropped out compared with five, respectively.

“This study provides novel evidence that drugs acting on the dopaminergic system may be helpful to improve cognitive functions related to the frontal lobe activity,” Koch told Healio Psychiatry. “We hope that this research will expand Alzheimer’s disease therapy to drugs acting on different neurotransmission systems, such as the dopaminergic one, in addition to the cholinergic drugs.”

https://www.healio.com/news/psychiatry/20200715/neupro-may-reduce-cognitive-dysfunction-among-patients-with-alzheimers-disease?utm_source=ADDF&utm_campaign=e9d85ea654-EMAIL_CAMPAIGN_2019_11_18_10_21_COPY_01&utm_medium=email&utm_term=0_cc5f9da121-e9d85ea654-97060793

Children with less sleep experience increased depression and anxiety, and decreased cognitive performance

On By A.P.In UncategorizedLeave a comment

Shorter sleep duration among children was associated with increased risk for depression, anxiety, impulsive behavior and poor cognitive performance, according to study findings published in Molecular Psychiatry.

“Sleep disturbances are common among children and adolescents around the world, with approximately 60% of adolescents in the United States receiving less than 8 hours of sleep on school nights,” Jianfeng Feng, PhD, of the department of computer science at University of Warwick in the UK, told Healio Psychiatry. “An important public health implication is that psychopathology in both children and their parents should be considered in relation to sleep problems in children. Further, we showed that brain structure is associated with sleep problems in children and that this is related to whether the child has depressive problems.”

According to Feng and colleagues, the present study is the first large-scale research effort to analyze sleep duration in children and its impact on psychiatric problems including depression, brain structure and cognition. They analyzed measures related to these areas using data from the Adolescent Brain Cognitive Development Study, which included structural MRI data from 11,067 individuals aged 9 to 11 years.

The researchers found that depression, anxiety and impulsive behavior were negatively correlated with sleep duration. Dimensional psychopathology in participants’ parents was correlated with short sleep duration in the children. Feng and colleagues noted that the orbitofrontal cortex, prefrontal and temporal cortex, precuneus and supramarginal gyrus were brain areas in which higher volume was correlated with longer sleep duration. According to longitudinal data analysis, psychiatric problems, particularly depressive problems, were significantly associated with short sleep duration 1 year later. Moreover, they found that depressive problems significantly mediated these brain regions’ effect on sleep. Higher volume of the prefrontal cortex, temporal cortex and medial orbitofrontal cortex were associated with higher cognitive scores.

“Our findings showed that 53% of children received less than 9 hours of sleep per night,” Feng said. “More importantly, the behavior problems total score for children with less than 7 hours of sleep was 53% higher on average and the cognitive total score was 7.8% lower on average than for children with 9 to 11 hours of sleep. We hope this study attracts public attention to sleep problems in children and provides evidence for governments to develop advice about sleep for children.” – by Joe Gramigna

https://www.healio.com/psychiatry/depression/news/online/%7B7440e93a-fe6a-4154-88f4-a5858d16c4cb%7D/children-with-less-sleep-experience-increased-depression-anxiety-decreased-cognitive-performance

Scientists reverse cognitive symptoms in a mouse model of Down Syndrome

On By A.P.In UncategorizedLeave a comment

By Kristin Houser

Down syndrome is a cognitive disability that can affect a person’s memory or ability to learn — intellectual impairments researchers traditionally thought were untreatable and irreversible.

But now, researchers from the University of California San Francisco and Baylor College of Medicine say they’ve reversed the impairments in mouse models of Down syndrome — potentially foreshadowing an ethically-fraught future in which doctors can do the same for humans with the condition.

All people with Down syndrome share one thing in common: an extra copy of chromosome 21. For that reason, much of the research on Down syndrome has focused on genetics.

But for this new study, published Friday in the prestigious journal Science, researchers focused on the protein-producing cells in the brains of mice with Down syndrome. That led them to the discovery that the animals’ hippocampus regions produced 39 percent less protein than those of typical mice.

Further study led the researchers to conclude that the presence of an extra chromosome likely prompted the animals’ hippocampal cells to trigger the integrated stress response (ISR), which decreased protein production.

“The cell is constantly monitoring its own health,” researcher Peter Walter said in a press release. “When something goes wrong, the cell responds by making less protein, which is usually a sound response to cellular stress. But you need protein synthesis for higher cognitive functions, so when protein synthesis is reduced, you get a pathology of memory formation.”

By blocking the activity of PKR, the enzyme that prompted the ISR in the mouse model’s hippocampal cells, the researchers found they could not only reverse the decreased protein production but also improve the animals’ cognitive function.

Of course, just because something works in mice doesn’t mean it’ll work in humans.

However, when the researchers analyzed postmortem brain tissue samples of people with Down syndrome, they found evidence that the ISR had been activated. They also obtained a tissue sample from a person with Down syndrome who only had the extra copy of chromosome 21 in some of their cells — and those cells were the only ones with ISR activated.

“We started with a situation that looked hopeless,” Walter said. “Nobody thought anything could be done. But we may have struck gold.”

https://futurism.com/neoscope/scientists-reverse-cognitive-deficiets-of-down-syndrome-mice

Thanks to Kebmodee for bringing this to the It’s Interesting community.

How we think as children may be linked to our cognitive performance at age 70

On By A.P.In UncategorizedLeave a comment

Our thinking skills in childhood could offer a glimpse into how our minds might work at the age of 70, according to a study spanning decades.

The research started in 1946, when 502 8-year-olds, who were born in the U.K. in the same week, took tests to measure their thinking and memory skills. The participants took cognitive tests again between the ages of 69 and 71.

The participants also had scans, including a positron emission tomography (PET) scan that detects amyloid-beta plaques in the brain. These sticky collections of protein are linked to Alzheimer’s disease.

The study, published in the journal Neurology, shows those with the highest test scores in childhood were more likely to have high scores later in life. Kids in the top 25 percent had a greater chance of being in that same quartile at 70.

Educational attainment and socioeconomic status also appeared to make a difference. Those who were college-educated scored around 16 percent better in tests than those who left school before they hit 16. Participants who had a white-collar job were able to remember, on average, 12 details from a short story, versus 11 if they had a manual job. Overall, women did better than men when their memory and thinking speed were tested.

Participants who were found to have amyloid-beta plaques in their brains, meanwhile, scored lower on cognitive tests. In one assessment where participants had to find the missing pieces in five geometric shapes, those with the plaque got 23 out of 32 problems correct, versus 25 for those without the plaques.

Dr. Jonathan M. Schott of University College London commented: “Finding these predictors is important because if we can understand what influences an individual’s cognitive performance in later life, we can determine which aspects might be modifiable by education or lifestyle changes like exercise, diet or sleep, which may, in turn, slow the development of cognitive decline.

“Our study found that small differences in thinking and memory associated with amyloid plaques in the brain are detectable in older adults even at an age when those who are destined to develop dementia are still likely to be many years away from having symptoms.”

Earlier this year, Schott and his team published a separate study in the journal The Lancet Neurology that showed having high blood pressure in a person’s mid-30s was linked to higher levels of blood vessel damage in the brain, as well as shrinkage of the organ.

Professor Tara Spires-Jones from the UK Dementia Research Institute at the University of Edinburgh, who did not work on the new study, told Newsweek the findings add to other studies that suggest our genetics, as well as environmental factors, play a role in how we maintain our thinking skills as we age.

“However, this does not mean that all of your brain power during aging is determined during childhood,” she said. “There is good scientific evidence from this study and many others that keeping your brain and body active are likely to reduce your risk of developing Alzheimer’s disease, even as adults.”

Learning, socializing and exercise can all help, she said.

“One way this works is by building new connections between brain cells, called synapses. Synapses are the building blocks of memory, so building up a robust network of synapses, sometimes called ‘brain reserve’ is thought to be the biology behind the finding that more education is associated with a lower risk of dementia and age-related cognitive decline,” explained Spires-Jones.

Spires-Jones suggested amyloid-beta plaques might be linked with lower tests scores in the study because they build up and damage the connections between brain cells, called synapses, impairing brain function.

“Amyloid plaques are also widely thought to initiate a toxic cascade that leads to dementia in Alzheimer’s disease, including the build-up and spread of another pathology called ‘tangles,'” she said.

She said the study was “very strong” but limited because observational studies can’t explain the links that emerge, and the participants were all white so the results might not relate to other populations.

“It will be important in future work to try and understand the biological underpinnings for the associations between childhood intelligence and better cognitive ability during aging,” she said.

https://www.newsweek.com/dementia-aging-study-brains-tests-1468657

Researchers implant a memory into a bird’s brain

On By A.P.In UncategorizedLeave a comment

by ABBY OLENA

Animals learn by imitating behaviors, such as when a baby mimics her mother’s speaking voice or a young male zebra finch copies the mating song of an older male tutor, often his father. In a study published today in Science, researchers identified the neural circuit that a finch uses to learn the duration of the syllables of a song and then manipulated this pathway with optogenetics to create a false memory that juvenile birds used to develop their courtship song.

“In order to learn from observation, you have to create a memory of someone doing something right and then use this sensory information to guide your motor system to learn to perform the behavior. We really don’t know where and how these memories are formed,” says Dina Lipkind, a biologist at York College who did not participate in the study. The authors “addressed the first step of the process, which is how you form the memory that will later guide [you] towards performing this behavior.”

“Our original goals were actually much more modest,” says Todd Roberts, a neuroscientist at UT Southwestern Medical Center. Initially, Wenchan Zhao, a graduate student in his lab, set out to test whether or not disrupting neural activity while a young finch interacted with a tutor could block the bird’s ability to form a memory of the interchange. She used light to manipulate cells genetically engineered to be sensitive to illumination in a brain circuit previously implicated in song learning in juvenile birds.

Zhao turned the cells on by shining a light into the birds’ brains while they spent time with their tutors and, as a control experiment, when the birds were alone. Then she noticed that the songs that the so-called control birds developed were unusual—different from the songs of birds that had never met a tutor but also unlike the songs of those that interacted with an older bird.

Once Zhao and her colleagues picked up on the unusual songs, they decided to “test whether or not the activity in this circuit would be sufficient to implant memories,” says Roberts.

The researchers stimulated birds’ neural circuits with sessions of 50- or 300-millisecond optogenetic pulses over five days during the time at which they would typically be interacting with a tutor but without an adult male bird present. When these finches grew up, they sang adult courtship songs that corresponded to the duration of light they’d received. Those that got the short pulses sang songs with sounds that lasted about 50 milliseconds, while the ones that received the extended pulses held their notes longer. Some song features—including pitch and how noisy harmonic syllables were in the song—didn’t seem to be affected by optogenetic manipulation. Another measure, entropy, which approximates the amount of information carried in the communication, was not distinguishable in the songs of normally tutored birds and those that received 50-millisecond optogenetic pulses, but was higher in the songs of birds who’d received tutoring than in the songs of either isolated birds or those that received the 300-millisecond light pulses.

While the manipulation of the circuit affected the duration of the sounds in the finches’ songs, other elements of singing behavior—including the timeline of vocal development, how frequently the birds practiced, and in what social contexts they eventually used the songs—were similar to juveniles who’d learned from an adult bird.

The researchers then determined that when the birds received light stimulation at the same time as they interacted with a singing tutor, their adult songs were more like those of birds that had only received light stimulation, indicating that optogenetic stimulation can supplant tutoring.

When the team lesioned the circuit before young birds met their tutors, they didn’t make attempts to imitate the adult courtship songs. But if the juveniles were given a chance to interact with a tutor before the circuit was damaged, they had no problem learning the song. This finding points to an essential role for the pathway in forming the initial memory of the timing of vocalizations, but not in storing it long-term so that it can be referenced to guide song formation.

“What we were able to implant was information about the duration of syllables that the birds want to attempt to learn how to sing,” Roberts tells The Scientist. But there are many more characteristics birds have to attend to when they’re learning a song, including pitch and how to put the syllables in the correct order, he says. The next steps are to identify the circuits that are carrying other types of information and to investigate the mechanisms for encoding these memories and where in the brain they’re stored.

Sarah London, a neuroscientist at the University of Chicago who did not participate in the study, agrees that the strategies used here could serve as a template to tease apart where other characteristics of learned song come from. But more generally, this work in songbirds connects to the bigger picture of our understanding of learning and memory, she says.

Song learning “is a complicated behavior that requires multiple brain areas coordinating their functions over long stretches of development. The brain is changing anyway, and then on top of that the behavior’s changing in the brain,” she explains. Studying the development of songs in zebra finches can give insight into “how maturing neural circuits are influenced by the environment,” both the brain’s internal environment and the external, social environment, she adds. “This is a really unique opportunity, not just for song, not just for language, but for learning in a little larger context—of kids trying to understand and adopt behavioral patterns appropriate to their time and place.”

W. Zhao et al., “Inception of memories that guide vocal learning in the songbird,” Science, doi:10.1126/science.aaw4226, 2019.

https://www.the-scientist.com/news-opinion/researchers-implant-memories-in-zebra-finch-brains-66527?utm_campaign=TS_DAILY%20NEWSLETTER_2019&utm_source=hs_email&utm_medium=email&utm_content=77670023&_hsenc=p2ANqtz-87EBXf6eeNZge06b_5Aa8n7uTBGdQV0pm3iz03sqCnkbGRyfd6O5EXFMKR1hB7lhth1KN_lMxkB_08Kb9sVBXDAMT7gQ&_hsmi=77670023

Playing video games may increase your brain’s gray matter and improve how it communicates

On By A.P.In UncategorizedLeave a comment

According to the results of a study published in Nature, gaming could possibly increase the volume of gray matter in the brain.
Researchers recently studied the insular cortex regions of frequent gamers and those who didn’t play video games as regularly.
The study found a correlation between playing action video games and increased gray matter volume in the brain.

Do you ever feel you could do with polishing up on your cognitive skills?

Well, according to the results of a study published in Nature, gaming could possibly be the way forward.

Researchers from the Chinese University of Electronic Science and Technology and the Australian Macquarie University in Sydney joined forces, and recently found a correlation between playing action video games and increased gray matter volume in the brain.

How video games stimulate the gray matter in your brain

The focus of the team’s research was on the insular cortex, a part of the cerebral cortex folded deep in the brain that has been the subject of very few studies to date.

It’s thought that a large part of linguistic processing takes place in this region of the brain, and that other processes relating to taste and smell, compassion and empathy, and interpersonal experiences are also managed here.

The study looked at 27 regular video game players described in the study as “Action Video Game experts” as well as 30 amateurs who played less frequently and didn’t perform as well in games.

The participants in the “expert” group were all recognised participants of regional or national championships of League of Legends and Dota 2. Using an MRI scanner, the scientists took detailed pictures of the participants’ insular cortices.

“By comparing AVG experts and amateurs, we found that AVG experts had enhanced functional connectivity and gray matter volume in insular subregions,” wrote the research team.

Gaming actually promotes networking within the brain

The gray matter in your brain is part of your central nervous system and essentially controls all your brain’s functions.

It follows that better connectivity in this region will lead to faster thought processes and correspondingly higher intelligence.

If you want to improve your cognitive performance, you don’t necessarily have to resort to hours of video games; sports and art-based recreation are just two among many activities that promote connectivity in the brain.

However it does mean that those who still like to sit in front of their console from time to time no longer need to feel guilty about being sat in front of a screen — after all, it is exercise — just for the brain.

https://www.businessinsider.com/video-games-may-increase-your-brains-gray-matter-2018-12

Researchers discovery an independent role for astrocytes in cognition

On By A.P.In UncategorizedLeave a comment

The majority of the cells in the brain are no neurons, but Glia (from “glue”) cells, that support the structure and function of the brain. Astrocytes (“start cells”) are star-shaped glial cells providing many supportive functions for the neurons surrounding them, such as the provision of nutrients and the regulation of their chemical environment. Newer studies showed that astrocytes also monitor and modulate neuronal activity. For example, these studies have shown that astrocytes are necessary for the ability of neurons to change the strength of the connections between them, the process underlying learning and memory, and indeed astrocytes are also necessary for normal cognitive function. However, it is still unknown whether astrocytic activity is only necessary, or is it may also be sufficient to induce synaptic potentiation and enhance cognitive performance.

In a new study published in Cell, two graduate students, Adar Adamsky and Adi Kol, from Inbal Goshen’s lab, employed chemogenetic and optogenetic tools that allow specific activation of astrocytes in behaving mice, to explore their role in synaptic activity and memory performance. They found that astrocytic activation in the hippocampus, a brain region that plays an important role in memory acquisition and consolidation, potentiated the synaptic connections in this region, measured in brain slices. Moreover, in the intact brain, astrocytic activation enhanced hippocampal neuronal activity in a task-dependent way: i.e. only during when it was combined with memory acquisition, but not when mice were at their home cage with no meaningful stimuli. The ability of astrocytes to increase neuronal activity during memory acquisition had a significant effect on cognitive function: Specifically, astrocytic activation during learning resulted in enhanced memory in two memory tests. In contrast, direct neuronal activation in the hippocampus induced a non-selective increase in activity (during learning or in the home cage), and thus resulted in drastic memory impairment.

The results suggest that the memory enhancement induced by astrocytic activation during learning is not simply a result of a general increase in hippocampal neuronal activity. Rather, the astrocytes, which sense and respond to changes in the surrounding neuronal activity, can detect and specifically enhance only the neuronal activity involved in learning, without affecting the general activity. This may explain why general astrocytic activation improves memory performance, whereas a similar activation of neurons impairs it.

Memory is not a binary process (remember/don’t remember); the strength of a memory can vary greatly, either for the same memory or between different memories. Here, we show that activating astrocytes in mice with intact cognition improves their memory performance. This finding has important clinical implications for cognitive augmentation treatments. Furthermore, the ability of astrocytes to strengthen neuronal communication and improve memory performance supports the claim that astrocytes are able to take an active part in the neuronal processes underlying cognitive function. This perspective expands the definition of the role of astrocytes, from passive support cells to active cells that can modulate neural activity and thus shape behavior.

Link: https://www.cell.com/cell/pdf/S0092-8674(18)30575-0.pdf

https://elsc.huji.ac.il/content/article-month-june-2018-goshens-lab

Meditation and Music Boost Memory and Cognition

On By A.P.In UncategorizedLeave a comment

Two simple mind-body practices improved cognition and helped reverse perceived memory loss in older adults with subjective cognitive decline, in a pilot study published in the Journal of Alzheimer’s Disease.

Researchers randomly assigned 60 older adults with subjective cognitive decline—a strong predictor of Alzheimer’s disease—to a program of either beginner meditation (Kirtan Kriya) or music listening over 6 months. For the first 3 months, participants were directed to practice their intervention 12 minutes daily. For the remaining 3 months, participants were told to engage in their intervention at their discretion.

At 3 months, both the meditation and music listening groups showed marked and significant improvements in subjective memory function and objective cognitive performance, researchers found. What’s more, the substantial gains were maintained or improved at 6 months.

Brain Games Linked to Delayed Cognitive Decline in Elderly

“Findings of this preliminary randomized controlled trial suggest practice of meditation or music listening can significantly enhance both subjective memory function and objective cognitive performance in adults with subjective cognitive decline,” researchers concluded, “and may offer promise for improving outcomes in this population.”

Researchers had previously found that both interventions also improved sleep, mood, stress, well-being, and quality of life—with gains particularly pronounced in participants who practiced meditation. In that study, too, improvements were maintained or improved 3 months after baseline.

—Jolynn Tumolo

References

Innes KE, Selfe TK, Khalsa DS, Kandati S. Meditation and music improve memory and cognitive function in adults with subjective cognitive decline: a pilot randomized controlled trial. Journal of Alzheimer’s Disease. 2017;56:899-916.

Meditation and music may help reverse early memory loss in adults at risk for Alzheimer’s disease [press release]. Lansdale, PA: IOS Press; January 23, 2017.

Science confirms link between slow walking and cognitive decline

On By A.P.In Uncategorized2 Comments

Older people with a slow walking pace are at increased risk of cognitive decline and dementia, according to a new meta-analysis.

“In light of its characteristics of safety, cost-effectiveness, and ease to test and interpret, walking pace may be an effective indicator of the development of cognitive decline and dementia in older people,” Dr. Minghui Quan of Shanghai University of Sport in China and colleagues write in their report, published online December 6 in the Journal of Gerontology: Medical Sciences.

Past research has linked walking pace to cognitive dysfunction, but the size of the association and whether there is a dose-response relationship has not been studied systematically, the researchers state. To investigate, they reviewed 17 prospective studies of walking pace. Seven looked at cognitive decline, seven at dementia, and three studies included both outcomes.

The 10 studies of cognitive decline included nearly 10,000 participants, while the 10 studies with dementia as an outcome included more than 14,000. The slowest walkers had an 89% higher risk of cognitive decline (95% confidence interval, 1.54 – 2.31), but there was no linear relationship between walking pace and cognitive decline risk.

Dementia risk was 66% higher in individuals with the slowest walking pace versus those with the fastest pace (95% CI, 1.43 – 1.92). Three studies included data on dose-response relationship, and found a relative risk of cognitive decline of 1.13 for each decimeter/second drop in walking pace (95% CI, 1.08 – 1.18).

Walking pace may be an indicator of cognitive function for many reasons, Dr. Quan and colleagues note. For example, walking pace is associated with muscle strength, and muscle loss has been tied to inflammation, oxidative stress and other factors related to cognitive function.

Walking is not an automatic activity, they add, but “requires a seamless coordination of several neurologic systems including motor, sensory, and cerebellar activities.” Slow walking pace could also contribute to physical inactivity, they add, which in turn is associated with cognitive decline and dementia.

“Since a randomized clinical trial on walking pace and cognitive function may not be feasible due to practical considerations, future well-designed, large-scale, prospective cohort studies are needed to determine the age-, sex-, and population-specified cutoff values for walking pace, in order to enhance the effectiveness and efficiency of this early indicator of cognitive decline and dementia,” Dr. Quan and colleagues conclude.

New treatment protocol shows promise of improving cognition in patients with Alzheimer’s disease

On By A.P.In Alzheimer's disease, DementiaLeave a comment

Ten patients with early Alzheimer’s disease or its precursors showed improvement in memory after treatment with Metabolic Enhancement for NeuroDegeneration (MEND), a programmatic and personalized therapy protocol.

Researchers described results from the small trial, which used quantitative MRI and neuropsychological testing of participants before and after treatment, in the study published online in Aging.

“ The magnitude of the improvement is unprecedented,” researchers wrote, “providing additional objective evidence that this programmatic approach to cognitive decline is highly effective.”

Before starting the program, the 10 participants had well-defined mild cognitive impairment, subjective cognitive impairment, or had been diagnosed with Alzheimer’s disease. Their subsequent treatment consisted of a complex, 36-point therapeutic personalized program that included comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry.

Researcher Dale Bredesen, MD, a professor at the Buck Institute for Research on Aging and at the Easton Laboratories for Neurodegenerative Disease Research at UCLA, Los Angeles, believes the protocol’s broader-based approach is key to its apparent success in reversing cognitive decline.

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well — the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much,” Dr. Bredesen said. “We think addressing multiple targets within the molecular network may be additive, or even synergistic, and that such a combinatorial approach may enhance drug candidate performance as well.”

Tests showed some participants “going from abnormal to normal,” Dr. Bredesen said.

In Aging , researchers describe the impact of MEND on all 10 patients, including:
•A 66-year-old man whose neuropsychological testing was compatible with a diagnosis of mild cognitive impairment. After 10 months on the MEND protocol, his hippocampal volume increased from the 17 th percentile for his age to the 75 th percentile, with an associated absolute increase in volume of nearly 12%.
•A 69-year-old entrepreneur with 11 years of progressive memory loss. After 22 months on the protocol, he showed marked improvements in all categories of neuropsychological testing, with long-term recall increasing from the 3 rd to 84 th percentile.
•A 49-year-old woman in the early stages of cognitive decline who, after 9 months on the protocol, no longer showed evidence on quantitative neuropsychological testing of cognitive decline.

Plans for larger studies are under way.

“Even though we see the far-reaching implications of this success,” Dr. Bredesen said, “we also realize that this is a very small study that needs to be replicated in larger numbers at various sites.”

http://www.psychcongress.com/article/mend-protocol-reverses-memory-loss-alzheimer%E2%80%99s-disease-27858