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Study Links Muscle Loss to Alzheimer’s Risk - Neuroscience News
A study of 621 older adults found that those with smaller temporalis muscles were 60% more likely to develop dementia and experienced greater cognitive and brain volume decline over nearly six years.
This Common Device Can Slow Cognitive Decline, Trial Shows | MedPage Today
Numerous studies have linked hearing loss with future dementia risk, but the nature of that association, and particularly whether it was causal, has not been clear. In the Lancet paper, Lin and colleagues explained that several theories have been advanced for how hearing loss might exacerbate cognitive decline: coping with it might increase a person's "cognitive load," alter brain structure, and/or discourage "engagement in social and cognitively stimulating activities."
Clearance of protein linked to Alzheimer's controlled by circadian cycle: Ability of immune system to destroy Alzheimer's-related protein oscillates with daily circadian rhythm -- ScienceDaily
"Circadian regulation of immune cells plays a role in the intricate relationship between the circadian clock and Alzheimer's disease," said Jennifer Hurley, an expert in circadian rhythms, and associate professor of biological science at Rensselaer Polytechnic Institute. "This tells us a healthy sleep pattern might be important to alleviate some of the symptoms in Alzheimer's disease, and this beneficial effect might be imparted by an immune cell type called macrophages/microglia."
Researchers identify potential new means of slowing neurodegenerative diseases -- ScienceDaily
The normal function of Hsp90 is to support healthy cellular processes, but oxidation can have profound effects on the three-dimensional structure of a protein such as Hsp90, altering its function, Franco said.
"By understanding the ways that oxidation modifies the Hsp90 structure, and how the oxidized protein works in the cells, we can look for drugs that bind to the modified structure of Hsp90 and stop its toxic function without affecting the activity of normal Hsp90 in healthy tissues," she said. "That means such drugs should have minimal to no side effects."
Alzheimer’s: Inflammatory markers are conspicuous at an early stage: Evidence of damage and also neuroprotective processes long before symptoms of dementia manifest -- ScienceDaily
n recent years, it has become evident that the brain's immune system and related inflammatory processes -- also known as "neuroinflammation" -- significantly contribute to the development of Alzheimer's disease. In view of this, the scientists analyzed various immunological biomarkers that are characterized by good detectability in the cerebrospinal fluid and reproducible results. "It was already known that these markers indicate immune processes in the context of Alzheimer's disease. However, how these markers relate to brain volume, cognitive performance and other parameters had not been studied as comprehensively as we have now," explains Prof. Michael Heneka, who led the current study during his long-time tenure at DZNE and UKB. Since the beginning of this year, he has been director of the Luxembourg Centre for Systems Biomedicine.
"We have found that some of these inflammatory markers are conspicuous even when there are no symptoms of dementia yet," Heneka says. "Based on the data we have so far, we can't specify the lead time at this point. But my estimate is that it is at least ten to twenty years."
Brain tissue inflammation is key to Alzheimer's disease progression
For the first time ever, the researchers showed in living patients that neuroinflammation—or activation of the brain's resident immune cells, called microglial cells—is not merely a consequence of disease progression; rather, it is a key upstream mechanism that is indispensable for disease development.
A diet of essential amino acids could keep dementia at bay: Consuming Amino LP7, a specific combination of essential amino acids, could inhibit the development of dementia, shows a study from Japan -- ScienceDaily
In a recent study published in Science Advances, Japanese researchers showed that a low protein diet can accelerate brain degeneration in mouse models of Alzheimer's disease. More importantly, they found that Amino LP7 -- a supplement containing seven specific amino acids -- can slow down brain degeneration and dementia development in these animals. Their work expands on previous studies, which have demonstrated the effectiveness of Amino LP7 in improving cognitive function.
Wiggling worms suggest link between vitamin B12 and Alzheimer's -- ScienceDaily
"The read-out is black or white -- the worms are either moving or they are not," Tanis said. "When we gave vitamin B12 to the worms that were vitamin B12 deficient, paralysis occurred much more slowly, which immediately told us that B12 was beneficial. The worms with B12 also had higher energy levels and lower oxidative stress in their cells."
Brain changes following traumatic brain injury share similarities with Alzheimer's disease: Using MRIs and machine learning, researchers mapped comparable degenerative changes in gray and white matter of the brain -- ScienceDaily
In multiple brain areas of both TBI and Alzheimer's participants, the researchers found reduced cortical thickness when compared to the healthy controls. Cortical thickness is roughly correlated with brain age and its thinning is often associated with reductions in attention, memory and verbal fluency, as well as with decreased ability to make decisions, integrate new information and adapt one's behavior to new situations, among other deficits.
"These findings are the first to suggest that cognitive impairment following a traumatic brain injury is useful for predicting the magnitude of Alzheimer's-like brain degradation," said study author Andrei Irimia, an assistant professor of gerontology, neuroscience and biomedical engineering at the USC Leonard Davis School of Gerontology and the USC Viterbi School of Engineering. "The results may help health professionals to identify TBI victims who are at greater risk for Alzheimer's disease."
Using MRIs, the study identified significant similarities between TBI and Alzheimer's disease in how the brain's gray and white matter degrade after injury. In gray matter -- the part of the brain that contains neuron cell bodies and their short-range connections -- the most extensive similarities were in areas involved in memory (temporal lobes) and decision-making (orbitofrontal cortices).
Flickering light mobilizes brain chemistry that may fight Alzheimer's -- ScienceDaily
n 2016, researchers discovered that light flickering at 40 Hz mobilized microglia in mice afflicted with Alzheimer's to clean up that junk. The new study looked for brain chemistry that connects the flicker with microglial and other immune activation in mice and exposed a surge of 20 cytokines -- small proteins secreted externally by cells and which signal to other cells. Accompanying the cytokine release, internal cell chemistry -- the activation of proteins by phosphate groups -- left behind a strong calling card.
"The phosphoproteins showed up first. It looked as though they were leading, and our hypothesis is that they triggered the release of the cytokines," said Singer, who co-led the new study and is an assistant professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory.
In Alzheimer's research, scientists reveal brain rhythm role -- ScienceDaily
In 2016, Tsai and colleagues showed that Alzheimer's disease model mice exposed to a light flickering at 40 Hz for an hour a day for a week had significantly less buildup of amyloid and tau proteins in the visual cortex, the brain region that processes sight, than experimental control mice did. Amyloid plaques and tangles of phosphorylated tau are both considered telltale hallmarks of Alzheimer's disease.
But the study raised new questions: Could GENUS prevent memory loss? Could it prevent the loss of neurons? Does it reach other areas of the brain? And could other senses be stimulated for beneficial effect?
The new studies addressed those questions. In March, the team reported that sound stimulation reduced amyloid and tau not only in the auditory cortex, but also in the hippocampus, a crucial region for learning and memory. GENUS-exposed mice also performed significantly better on memory tests than unstimulated controls. Simultaneous light and sound, meanwhile, reduced amyloid across the cortex, including the prefrontal cortex, a locus of cognition.
Can Anticoagulants Prevent Alzheimer's?
After receiving dabigatran for 1 year, the mice had no memory loss, and there was no reduction in cerebral circulation. Dabigatran also reduced typical AD symptoms, including cerebral inflammation, blood vessel injury, and amyloid protein plaques.
Can Anticoagulants Prevent Alzheimer's?
In the new study, long-term anticoagulation therapy with dabigatran (Pradaxa, Boehringer Ingelheim) inhibited thrombin and abnormal deposition of fibrin in a mouse model of AD.
After receiving dabigatran for 1 year, the mice had no memory loss, and there was no reduction in cerebral circulation. Dabigatran also reduced typical AD symptoms, including cerebral inflammation, blood vessel injury, and amyloid protein plaques.
For the first time walking patterns identify specific types of dementia -- ScienceDaily
For the study, researchers analysed the walk of 110 people, including 29 older adults whose cognition was intact, 36 with Alzheimer's disease and 45 with Lewy body dementia.
The participants took part in a simple walking test at the Gait Lab of the Clinical Ageing Research Unit, an NIHR-funded research initiative jointly run by Newcastle Hospitals NHS Foundation Trust and Newcastle University.
Participants moved along a walkway -- a mat with thousands of sensors inside -- which captured their footsteps as they walked across it at their normal speed and this revealed their walking patterns.
People with Lewy body dementia had a unique walking pattern in that they changed how long it took to take a step or the length of their steps more frequently than someone with Alzheimer's disease, whose walking patterns rarely changed.
When a person has Lewy body dementia, their steps are more irregular and this is associated with increased falls risk. Their walking is more asymmetric in step time and stride length, meaning their left and right footsteps look different to each other.
Scientists found that analysing both step length variability and step time asymmetry could accurately identify 60% of all dementia subtypes -- which has never been shown before.
Diet's effect on gut bacteria could play role in reducing Alzheimer's risk -- ScienceDaily
In a small pilot study, the researchers identified several distinct gut microbiome signatures -- the chemicals produced by bacteria -- in study participants with mild cognitive impairment (MCI) but not in their counterparts with normal cognition, and found that these bacterial signatures correlated with higher levels of markers of Alzheimer's disease in the cerebrospinal fluid of the participants with MCI.
Through cross-group dietary intervention, the study also showed that a modified Mediterranean-ketogenic diet produced changes in the gut microbiome and its metabolites that correlated with reduced levels of Alzheimer's markers in the members of both study groups.
The Startling Link Between Sugar and Alzheimer's - The Atlantic
Melissa Schilling, a professor at New York University, performed her own review of studies connecting diabetes to Alzheimer’s in 2016. She sought to reconcile two confusing trends. People who have type 2 diabetes are about twice as likely to get Alzheimer’s, and people who have diabetes and are treated with insulin are also more likely to get Alzheimer’s, suggesting elevated insulin plays a role in Alzheimer’s. In fact, many studies have found that elevated insulin, or “hyperinsulinemia,” significantly increases your risk of Alzheimer’s. On the other hand, people with type 1 diabetes, who don’t make insulin at all, are also thought to have a higher risk of Alzheimer’s. How could these both be true?
Schilling posits this happens because of the insulin-degrading enzyme, a product of insulin that breaks down both insulin and amyloid proteins in the brain—the same proteins that clump up and lead to Alzheimer’s disease. People who don’t have enough insulin, like those whose bodies’ ability to produce insulin has been tapped out by diabetes, aren’t going to make enough of this enzyme to break up those brain clumps. Meanwhile, in people who use insulin to treat their diabetes and end up with a surplus of insulin, most of this enzyme gets used up breaking that insulin down, leaving not enough enzyme to address those amyloid brain clumps.
Gamma wave - Wikipedia
A number of experiments conducted by Rodolfo Llinás supports a hypothesis that the basis for consciousness in awake states and dreaming is 40-Hz oscillations throughout the cortical mantle in the form of thalamocortical iterative recurrent activity. In two papers entitled "Coherent 40-Hz oscillation characterizes dream state in humans” (Rodolfo Llinás and Urs Ribary, Proc Natl Acad Sci USA 90:2078-2081, 1993) and "Of dreaming and wakefulness” (Llinas & Pare, 1991), Llinás proposes that the conjunction into a single cognitive event could come about by the concurrent summation of specific and nonspecific 40-Hz activity along the radial dendritic axis of given cortical elements, and that the resonance is modulated by the brainstem and is given content by sensory input in the awake state and intrinsic activity during dreaming. According to Llinás’ hypothesis, known as the thalamocortical dialogue hypothesis for consciousness, the 40-Hz oscillation seen in wakefulness and in dreaming is proposed to be a correlate of cognition, resultant from coherent 40-Hz resonance between thalamocortical-specific and nonspecific loops. In Llinás & Ribary (1993), the authors propose that the specific loops give the content of cognition, and that a nonspecific loop gives the temporal binding required for the unity of cognitive experience.
Why visual stimulation may work in fight against Alzheimer's: Mouse study - Neuroscience News
Tsai’s original study on the effects of flickering light showed that visual stimulation at a frequency of 40 hertz (cycles per second) induces brain waves known as gamma oscillations in the visual cortex. These brain waves are believed to contribute to normal brain functions such as attention and memory, and previous studies have suggested that they are impaired in Alzheimer’s patients.
Tsai and her colleagues later found that combining the flickering light with sound stimuli — 40-hertz tones — reduced plaques even further and also had farther-reaching effects, extending to the hippocampus and parts of the prefrontal cortex. The researchers have also found cognitive benefits from both the light- and sound-induced gamma oscillations.
In their new study, the researchers wanted to delve deeper into how these beneficial effects arise. They focused on two different strains of mice that are genetically programmed to develop Alzheimer’s symptoms. One, known as Tau P301S, has a mutated version of the Tau protein, which forms neurofibrillary tangles like those seen in Alzheimer’s patients. The other, known as CK-p25, can be induced to produce a protein called p25, which causes severe neurodegeneration. Both of these models show much greater neuron loss than the model they used for the original light flickering study, Tsai says.
The researchers found that visual stimulation, given one hour a day for three to six weeks, had dramatic effects on neuron degeneration. They started the treatments shortly before degeneration would have been expected to begin, in both types of Alzheimer’s models. After three weeks of treatment, Tau P301S mice showed no neuronal degeneration, while the untreated Tau P301S mice had lost 15 to 20 percent of their neurons. Neurodegeneration was also prevented in the CK-p25 mice, which were treated for six weeks.
The F.D.A. vs. Personal Genetic Testing | The New Yorker
A fifty-five-year-old who is confused and depressed and learns that he carries two copies of the risk gene and stands an eighty-per-cent chance of getting Alzheimer’s might reach for a gun, which is the kind of scenario that some genetic counsellors worry about.
Two types of drugs you may want to avoid for the sake of your brain - Harvard Health
Taking an anticholinergic for the equivalent of three years or more was associated with a 54% higher dementia risk than taking the same dose for three months or less.
Melatonin in Synaptic Impairments of Alzheimer's Disease. - PubMed - NCBI
It is reported that both the melatonin deficit and synaptic impairments are present in the very early stage of AD and strongly contribute to the progress of AD. In the mammalian brains, the effects of melatonin are mainly relayed by two of its receptors, melatonin receptor type 1a (MT1) and 1b (MT2). To have a clear idea on the roles of melatonin in synaptic impairments of AD, this review discussed the actions of melatonin and its receptors in the stabilization of synapses, modulation of long-term potentiation, as well as their contributions in the transmissions of glutamatergic, GABAergic and dopaminergic synapses, which are the three main types of synapses relevant to the synaptic strength. The synaptic protective roles of melatonin in AD treatment were also summarized. Regarding its protective roles against amyloid-β neurotoxicity, tau hyperphosphorylation, oxygenation, inflammation as well as synaptic dysfunctions, melatonin may be an ideal therapeutic agent against AD at early stage.
Antidepressants and bladder medicines linked to dementia in landmark study -- ScienceDaily
"We studied patients with a new dementia diagnosis and looked at what anticholinergic medication they were prescribed between four and 20 years prior to being diagnosed.
"We found that people who had been diagnosed with dementia were up to 30 per cent more likely to have been prescribed specific classes of anticholinergic medications. And the association with dementia increases with greater exposure to these types of medication.
"What we don't know for sure is whether the medication is the cause. It could be that these medications are being prescribed for very early symptoms indicating the onset of dementia.
Trace elements of lithium in drinking water linked to longer life in Alzheimer's patients -- ScienceDaily
"We found counties that had above the median level of lithium in tap water (40 micrograms per litre) experienced less increases in Alzheimer's disease mortality over time, whereas counties below that median level had even higher increases in Alzheimer's deaths over time," says Fajardo.
The frequency of obesity and Type 2 diabetes also went down when the drinking water contained similar lithium levels, the researchers found.
Fajardo says he and his team focused on Texas because data on lithium levels were "freely available."
Previous studies have demonstrated lithium's ability to protect against Alzheimer's disease, obesity and diabetes.
Alzheimer's gene neutralized by exercise
Dr. Noordsy noted one particularly remarkable study in which researchers compared patients with and without the ApoE gene, which is linked strongly to late-onset Alzheimer's disease.
In the study, patients who were ApoE-negative showed similarly low mean cortical binding potential, related to plaque buildup in the brain, regardless of whether they exercised or not.
But although ApoE-positive individuals (n = 39) had values that were substantially higher, the ApoE-positive patients who exercised (n = 13) had values similar to those who did not carry the gene (Arch Neurol 2012;69:636-643).
"You could look at these results and rightfully say physical exercise neutralizes your risk for developing Alzheimer's disease if you're ApoE positive," Dr. Noordsy said.
Is It Time To Test Presidents For Dementia?
"Donald Trump at the time of his inauguration was older than half of our deceased former presidents at the age when they died," says Dr. Jacob Appel, a Mt. Sinai School of Medicine psychiatrist who has studied the health of politicians and presidents. "Only a generation ago, our political leaders — like the rest of us — were likely to die of heart disease or cancer in their 60s and 70s, what we now think of as late middle age."
Substance present in ayahuasca brew stimulates generation of human neural cells: Harmine increases the number of neural progenitors, cells that give rise to neurons, study suggests -- ScienceDaily
In order to elucidate these effects, researchers from the D'Or Institute for Research and Education (IDOR) and the Institute of Biomedical Sciences at the Federal University of Rio de Janeiro (ICB-UFRJ) exposed human neural progenitors to this beta-carboline. After four days, harmine led to a 70% increase in proliferation of human neural progenitor cells.
Researchers were also able to identify how the human neural cells respond to harmine. The described effect involves the inhibition of DYRK1A, which is located on chromosome 21 and is over activated in patients with Down syndrome and Alzheimer's Disease.
"Our results demonstrate that harmine is able to generate new human neural cells, similarly to the effects of classical antidepressant drugs, which frequently are followed by diverse side effects. Moreover, the observation that harmine inhibits DYRK1A in neural cells allows us to speculate about future studies to test its potential therapeutic role over cognitive deficits observed in Down syndrome and neurodegenerative diseases," suggests Stevens Rehen, researcher from IDOR and ICB-UFRJ.
