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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.

Scientists Uncover Alzheimer’s Disease in the Novels of Agatha Christie and Iris Murdoch

As Garrard explains, a patient’s vocabulary becomes restricted, and they use fewer words that are specific labels and more words that are general labels. For example, it’s not incorrect to call a golden retriever an “animal,” though it is less accurate than calling it a retriever or even a dog. Alzheimer’s patients would be far more likely to call a retriever a “dog” or an “animal” than “retriever” or “Fred.” In addition, Garrard adds, the words Alzheimer’s patients lose tend to appear less frequently in everyday English than words they keep—an abstract noun like “metamorphosis” might be replaced by “change” or “go.”

destroying life's narrative

Alzheimer's disease ... unfortunately literally erases a very important part of our sense of self, which is the narrative that we have in our heads about who we are. This narrative is something that the brain constructs and we're not even aware that it's actually a constructed thing. When we just think of ourselves, we have this expansive narrative inside us about who we are and what Alzheimer's unfortunately does is it puts a stop to the narrative forming. So because short-term memory formation is impaired, it becomes harder and harder for a person with Alzheimer's to start having new memories, and once you stop having or forming new memories, these memories don't get incorporated into your narrative. So, in some sense, your narrative stops forming. As the disease progresses it starts eating away at the existing narrative. It starts basically destroying a whole range of memories that go toward constituting the person that you are. ...