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Adium brain enhancer5/26/2023 Sleep difficulties defined by a score of greater than 5 on the Pittsburgh Sleep Quality Index (PSQI), and the presence of mild-to-moderate anxiety, with scores ≥12 and ≤ 28 on the Hamilton Anxiety Questionnaire sub-score A (HAM-A), were required for inclusion in the study. Subjects had a Mini-Mental State Examination score (MMSE) equal to or greater than 24. Subjects were men or women between 50 and 70 years of age with self-reported complaints of cognition (memory and concentration), and with anxiety and sleep disorder. Our efficacy evaluation included determination of body magnesium status, tests of cognition in four domains (executive function, working memory, attention, and episodic memory), and measurements of sleep quality and emotional state. Recent studies show sleep disorder is strongly correlated with cognitive impairment, and even the chance of getting AD. 47% of MCI patients have anxiety symptoms, and 83% of those with MCI and anxiety develop AD compared to only 41% of those with MCI without anxiety. The common core non-cognitive symptoms in MCI patients are anxiety and sleep disorder. It is common that patients with brain atrophy not only have MCI but also have neuropsychiatric symptoms. There is only a 30% chance that someone with SMC has MCI. Many people who think they have memory issues actually have a normal cognitive profile when tested with objective memory tests. This was necessary because previous studies show that SMC is not a good sole indicator of mild cognitive impairment (MCI). Their cognitive impairment was later confirmed by an object cognitive test (Trail Making Test - Part B).Sleep and anxiety disorder were used as inclusion criteria to increase the chance of recruiting subjects who had cognitive impairment with an underlyingneurodegenerative condition. We used three inclusion criteria, including subjective memory complaints (SMC), sleep disorder, and anxiety, to select subjects who had cognitive impairment. Here, we conducted a randomized, double-blind, placebo-controlled trial to evaluate the efficacy and safety of a treatment regimen consisting of 12 weeks of oral intake of MMFS-01, a compound containing L-TAMS, in older adults with cognitive impairment. L-TAMS treatment also enhances fear memory extinction and prevents fear memory over-generalization, leading to a reduction of anxiety in rats. The increase of synapse density in aging rats is linearly correlated with memory improvement. At a functional level, L-TAMS treatment reverses cognitive impairment in aging rats and AD model mice. Furthermore, L-TAMS treatment increases the number of NR2B containing NMDA receptors, resulting in an enhancement of synaptic plasticity in aging rats and Alzheimer’s disease (AD) model mice. L-TAMS treatment increases synapse density in brain regions critical for executive function and memory, such as the prefrontal cortex and hippocampus. To overcome this problem, we developed L-Threonic acid Magnesium salt (L-TAMS, formerly MgT), a compound that can effectively enhance CSF magnesium concentration via oral intake. In human, increasing blood magnesium by up to 300% only changes CSF magnesium by less than 19%. This is because active transport systems tightly control the amount of magnesium that crosses first from digestive tract into blood, and then from blood to cerebrospinal fluid (CSF). In an intact rodent, treatment with conventional magnesium salts is ineffective at elevating brain magnesium and improving memory function. Mechanistically, we found that intracellular magnesium in neurons serves as a critical second messenger controlling neuronal energy supply and functional synapse density. Elevating neuronal intracellular magnesium can increase functional synapse density and plasticity in cultured hippocampal neurons. In our pre-clinical studies, we found that the level of brain magnesium is a critical factor controlling synapse density and plasticity. Therapeutic strategies that prevent net synapse loss and increase synapse density may have great potential for cognitive impairment. Since synapses are the elemental units of neural communication, synapse loss and reduction of synaptic plasticity should have a major impact on neural signaling, resulting in impaired cognition. So far, the best structural predictor of cognitive decline is the degree of synaptic loss. Brain atrophy is associated with neuronal, axonal, and synaptic loss. Although the neuropathological process underlying cognitive impairment remains elusive, the best correlate to cognitive impairment is brain atrophy. Cognitive impairment in elderly is a major problem that can affect activities of daily living (ADL) and qualityof life.
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