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Cognitive enhancers are often taken for the long-term when little data on adverse effects is available. One of the barriers to the clinical trials that need to be done to assess the full and long-term effects of cognitive enhancers are the illegality of their use for enhancement purposes, and the hesitancy of Institutional Review Boards IRBs to approve studies of drugs for enhancement rather therapeutic purposes. In academia, modafinil has been used to increase productivity, although its long-term effects have not been assessed in healthy individuals.

Stimulants such as methylphenidate and atomoxetine are being used on college campuses, and by an increasingly younger group. Dopaminergics are substances that affect the neurotransmitter dopamine or the components of the nervous system that use dopamine. Attributable effects of dopamine are enhancement of attention, alertness, and antioxidant activity. Dopamine is the primary activity of stimulants like ritalin or amphetamine.


The protocol for this study is detailed at ClinicalTrials. All of the above screening events necessitated several visits to the nearby Byrd Institute or facilities. A third day entailed an office visit at the Byrd Institute during which a comprehensive battery of cognitive tasks was administered to establish baseline cognitive performance. This D2 visit was to confirm the caregivers were using proper TEMT procedures and to collect a blood sample. Cognitive assessment in the battery of cognitive tasks was done during clinical visits on 14, 30, and 60 days into treatment, as well as 2 weeks post-treatment.

After completion of the 2-month treatment period, a clinical visit occurred at 2 weeks post-treatment at which time the full cognitive battery was administered and a blood sample taken. The primary safety measure was an Adverse Event Assessment performed during every clinical visit at the Byrd Institute beginning with baseline. Secondary safety measures also collected at the same clinical visit time points were vitals e.

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The secondary safety measure of suicide tendencies was assessed at baseline, halfway through the 2-month treatment period, and at the completion of treatment. One ml volumes of the top plasma layer were aliquoted into 1. Also, 0. The two ml samples of CSF collected at baseline and on Day 60 were each aliquoted into 1. Standard, Streptavidin-HRP, and wash buffer solutions were prepared according to the menu.

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Instructions were followed according to those provided Standard, detection antibody, anti-rabbit IgG HRP, and wash buffer were all prepared according to the menu. The MRI images were then spatially normalized to standard space. This normalization transformation was then combined with transformation co-registration of pre-treatment PET images to MRI, which was then applied to the pre-treatment PET images to bring them into standard space. Normalization transformation from the earlier spatial normalization of MRI to standard space was then combined with transformations from pre- and post-treatment PET images that had been co-registered to MRI and pre-treatment PET images, respectively.

Finally, atlas volumes of interest VOIs were applied and quantitative data extracted. For each brain analyzed, quantitative data was obtained from brain areas, which included a total of 40 sub-areas from all four lobes of both the left and right cortices 20 areas on each side. DTI is a variant of fMRI that measures the diffusion of water molecules in brain tissue and is particularly sensitive to changes in white matter integrity [ 39, 40 ].

Briefly, data was motion corrected and eddy-current de-warped. Non-linear registration was carried out to align an FA white matter skeleton to atlas for each individual FA map. Subtraction of baseline from post-treatment FA maps were computed in a voxel-by-voxel manner and thresholded to a minimum change of 0. The skeletonized FA was used for analysis instead of the voxel-based FA maps. Region of Interest ROI analysis was performed in 12 predetermined structures identified from atlases provided within the fsl package.

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Wherever a significant ES was present, the associated p -value was also reported. Over the 2-month TEMT period, subjects received two 1-h daily treatments a total of approximately in-home treatments as administered by their caregiver. As well, subjects did not complain of headaches, brain sensations, or any other side effects of TEMT during or following treatment.

Caregiver recordings of blood pressure and temperature before, during, and min following every treatment also did not show consistent changes in these physiologic parameters associated with TEMT administration. The aforementioned safety endpoints collectively indicate that global brain TEMT administration at currently used parameters should be a safe therapeutic for AD subjects when given daily and long-term.

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Seven of the 8 subjects improved their performance, with a single subject displaying the typical decrease in ADAS-cog performance reported in numerous clinical trials for untreated control AD subjects over a similar time period [ 43 ]. Thus, removal of this one non-responder in a relatively small group of subjects revealed a considerably stronger ES.

Why Cognitive Enhancement Is in Your Future (and Your Past) - The Atlantic

Negative scores indicate improved performance. Increase in number of words recalled at Day60 end of treatment and 14D Post versus Baseline for A all eight subjects or B with omission of the one non-responder whose overall ADAS-cog performance is indicated by the green line in Fig. Effects of TEMT on other cognitive measures evaluated after 2 months of treatment D60 and 14 days following completion of treatment 14D Post compared to baseline performance. TEMT resulted in a reduction in forgetting at both Day60 and 14D Post versus Baseline improved memory is indicated by a decrease in percentage.

Daily TEMT administration for 2 months resulted in an increase in digits remembered at both Day60 and 14 days thereafter. For p-tau, levels were always higher in CSF because p-tau levels were essentially zero in plasma. Subjects exhibited no clear concentration difference for t-tau, with half of them having higher levels in CSF and the other half having higher levels in plasma. Progressive decreases in glucose utilization, often referred to as Cerebral Metabolic Rate for Glucose CMRgl , are consistently seen in AD subjects in longitudinal scans separated by 12 months [ 44, 45 ].

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  7. With stability in CMRgl thus assumed to be the case in AD subjects over any given 2-month period, we anticipated a priori that only a decrease or increase in CMRgl not simply stabilization observed over the 2-month TEMT period would indicate a treatment effect. Analysis of BL versus Day 60 end of treatment CMRgl involving all brain areas collectively and for all subjects combined indicated essentially no treatment-induced change in CMRgl average percent change of —0.

    Similarly, there was no treatment-induced change in CMRgl when only the 40 bilateral cortical regions frontal, parietal, temporal, and occipital were included average percent change of —1. Visual comparison of pre- versus post-treatment FDG-PET horizontal sections for individual subjects revealed that most subjects exhibited no clear pre- versus post-treatment visual differences in CMRgl. Horizontal sections from one such subject are shown in Fig.

    The upper scans were taken at baseline, with corresponding lower scans taken at the same level following 2 months of daily TEMT. Track-based statistical analysis for group differences between BL and Day60 end of treatment FA values indicated FA stability during the treatment period. Co-registration of DTI-derived fractional anisotropy FA images via tract-based spatial statistics TBSS resulted in a skeleton containing all major FA tracts common to all eight subjects, as shown in mid-sagittal, coronal, and horizontal sections.

    FA values were then compared in a voxel-by-voxel analysis for group differences between Baseline and Day60 end of treatment. In contrast to the above FA analysis involving combined pre- versus post-treatment FA comparisons from all eight subjects, clear differences in FA were revealed when subjects were evaluated individually.

    In view of the inability thus far of drugs to stabilize or reverse the memory impairment of AD, investigating non-pharmacologic interventions against the disease are now clearly warranted. Results indicate no deleterious side effects during the 2-month treatment period and reversal of cognitive impairment in key tasks e.

    This is the first study to administer TEMT to the entire human brain over an extended period of time.

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    As such, a primary goal of this open-label clinical trial was to determine the safety of daily, long-term, and global TEMT—specifically in AD subjects. Therefore, TEMT appears to be a safe therapeutic intervention for chronic treatment of AD, at least for the parameters and treatment regime utilized in this study. A battery of established AD cognitive tasks was utilized to evaluate the effects of 2-month daily TEMT administration on cognitive function in the eight AD subjects of this study at both completion of treatment and two weeks thereafter.

    Since a typical decline in ADAS-cog expected for AD subjects is around 4 points over a to month period [ 48 ], 2 months of TEMT appears to have reversed cognitive decline as measured by the ADAS-cog of responding AD subjects as a group, perhaps back to the cognitive level subjects had 12 to 15 months earlier. These improvements in Rey AVLT 5-trial recall and Retroactive Interference but not Proactive Interference were predicted from our prior AD transgenic mouse studies, wherein the same results were seen in the same three measures of an analogous cognitive interference task utilizing essentially the same TEMT parameters and testing regime [ 23 ].

    A third task wherein improvement was seen following TEMT was in repeating digits. It is important to indicate that cognitive testing was not done immediately after morning treatments at home, but rather starting around 2 hours thereafter and in the clinic. This extended beneficial period for hours following TEMT is consistent with our multiple studies in AD transgenic mice utilizing essentially the same TEMT treatment regime in which we demonstrated cognitive protection and impairment reversal with testing done 2—8 hours after morning treatment [ 23, 24, 27 ].

    Underscoring an even more protracted cognitive benefit of TEMT in the present study, cognitive performance of AD subjects at 14 days following completion of TEMT often resulted in a similarly enhanced level of performance as immediately following TEMT completion. Thus, a general maintenance of cognitive improvement for weeks, even without continued daily treatment, may be resulting from the TEMT regime presently utilized. The cognitive enhancements seen with TEMT administration are not likely due to repeated testing for a number of reasons.

    The Rey AVLT task, which targets episodic memory—an area particularly vulnerable to AD-related deficits—is likely to be especially resistant to practice effects, yet showed clear treatment benefits for the AD subjects of this study Third, repeated testing effects should have manifest themselves at the first repeat [ 53—55 ], but that was not the case for ADAS-cog repeated testing in this study. And fourthly, the tasks most likely to show a repeated testing-induced improvement clock draw, Trails A and B did not do so.

    Instead, stability in cognitive performance versus baseline was observed in those tasks, and in all other cognitive measures that did not exhibit cognitive improvement.

    Why Cognitive Enhancement Is in Your Future (and Your Past)

    Thus, either stability or cognitive improvement was observed for all cognitive tasks administered in this study. It is noteworthy that two academic groups in Italy have published uncontrolled clinical studies reporting that electromagnetic treatment quite different from the present study, nonetheless provided significant cognitive improvement to AD subjects in multiple standard tests [ 57, 58 ].

    From a similar pre-clinical perspective, the cognitive benefits of TEMT that we initially reported in AD transgenic mice have since been confirmed by three international laboratories utilizing similar or different EMF parameters [ 59—61 ]. Such concentration differences have called into question the accuracy of conventional ELISAs that are routinely used, in part due to the x greater concentration of proteins in plasma versus CSF that can interfere with ELISA-based assays and cause decreased assay sensitivity [ 64, 75, 76 ].