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The BDNF Val66Met gene polymorphism is a relevant factor explaining inter-individual differences to TMS responses in studies of the motor system. However, whether this variant also contributes to TMS-induced memory effects, as well as their underlying brain mechanisms, remains unexplored. In this investigation, we applied rTMS during encoding of a visual memory task either over the left frontal cortex (LFC; experimental condition) or the cranial vertex (control condition). Subsequently, individuals underwent a recognition memory phase during a functional MRI acquisition. We included 43 young volunteers and classified them as 19 Met allele carriers and 24 as Val/Val individuals. The results revealed that rTMS delivered over LFC compared to vertex stimulation resulted in reduced memory performance only amongst Val/Val allele carriers. This genetic group also exhibited greater fMRI brain activity during memory recognition, mainly over frontal regions, which was positively associated with cognitive performance. We concluded that BDNF Val66Met gene polymorphism, known to exert a significant effect on neuroplasticity, modulates the impact of rTMS both at the cognitive as well as at the associated brain networks expression levels. This data provides new insights on the brain mechanisms explaining cognitive inter-individual differences to TMS, and may inform future, more individually-tailored rTMS interventions.

Previous studies have shown abnormal power and functional connectivity of resting state electroencephalographic (EEG) rhythms in groups of Alzheimer's disease (AD) compared to healthy elderly (Nold) subjects. Here we tested the best classification rate of 120 AD patients and 100 matched Nold subjects using EEG markers based on cortical sources of power and functional connectivity of these rhythms. EEG data were recorded during resting state eyes-closed condition. Exact low-resolution brain electromagnetic tomography (eLORETA) estimated the power and functional connectivity of cortical sources in frontal, central, parietal, occipital, temporal, and limbic regions. Delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), beta 2 (20-30 Hz), and gamma (30-40 Hz) were the frequency bands of interest. The classification rates of interest were those with an area under the receiver operating characteristic curve (AUROC) higher than 0.7 as a threshold for a moderate classification rate (i.e., 70%). Results showed that the following EEG markers overcame this threshold: (i) central, parietal, occipital, temporal, and limbic delta/alpha 1 current density; (ii) central, parietal, occipital temporal, and limbic delta/alpha 2 current density; (iii) frontal theta/alpha 1 current density; (iv) occipital delta/alpha 1 inter-hemispherical connectivity; (v) occipital-temporal theta/alpha 1 right and left intra-hemispherical connectivity; and (vi) parietal-limbic alpha 1 right intra-hemispherical connectivity. Occipital delta/alpha 1 current density showed the best classification rate (sensitivity of 73.3%, specificity of 78%, accuracy of 75.5%, and AUROC of 82%). These results suggest that EEG source markers can classify Nold and AD individuals with a moderate classification rate higher than 80%.

Graph theory models a network by its nodes (the fundamental unit by which graphs are formed) and connections. 'Degree' hubs reflect node centrality (the connection rate), while 'connector' hubs are those linked to several clusters of nodes (mainly long-range connections). Here, we compared hubs modeled from measures of interdependencies of between-electrode resting-state eyes-closed electroencephalography (rsEEG) rhythms in normal elderly (Nold) and Alzheimer's disease dementia (ADD) participants. At least 5 min of rsEEG was recorded and analyzed. As ADD is considered a 'network disease' and is typically associated with abnormal rsEEG delta (<4 Hz) and alpha rhythms (8-12 Hz) over associative posterior areas, we tested the hypothesis of abnormal posterior hubs from measures of interdependencies of rsEEG rhythms from delta to gamma bands (2-40 Hz) using eLORETA bivariate and multivariate-directional techniques in ADD participants versus Nold participants. Three different definitions of 'connector' hub were used. Convergent results showed that in both the Nold and ADD groups there were significant parietal 'degree' and 'connector' hubs derived from alpha rhythms. These hubs had a prominent outward 'directionality' in the two groups, but that 'directionality' was lower in ADD participants than in Nold participants. In conclusion, independent methodologies and hub definitions suggest that ADD patients may be characterized by low outward 'directionality' of partially preserved parietal 'degree' and 'connector' hubs derived from rsEEG alpha rhythms.

The present study tested the two following hypotheses: (i) compared to non-athletes, elite athletes are characterized by a reduced cortical activation during the judgment of sporting observed actions; (ii) in elite athletes, a good judgment of observed sporting actions is related to a low cortical activation. To address these issues, electroencephalographic (EEG) data were recorded in 15 elite rhythmic gymnasts and 13 non-gymnasts. They observed a series of 120 rhythmic gymnastic videos. At the end of each video, the subjects had to judge the artistic/athletic level of the exercise by a scale from 0 to 10. The mismatch between their judgment and that of the coach indexed the degree of action judgment. The EEG cortical sources were estimated by sLORETA. With reference to a pre-stimulus period, the power decrease of alpha (8–12 Hz) rhythms during the videos indexed the cortical activation (event related desynchronization, ERD). Regarding the hypothesis (i), low- and high-frequency alpha ERD was lower in amplitude in the elite rhythmic gymnasts compared to the non-gymnasts in occipital and temporal areas (ventral pathway) and in dorsal pathway. Regarding the hypothesis (ii), in the elite rhythmic gymnasts high-frequency alpha ERD was higher in amplitude with the videos characterized by a high judgment error than those characterized by a low judgment error; this was true in inferior posterior parietal and ventral premotor areas (“mirror” pathway). These results globally suggest that the judgment of observed sporting actions is related to low amplitude of alpha ERD, as a possible index of spatially selective cortical activation (“neural efficiency”).

INTRODUCTION We evaluated whether the brain glymphatic drainage function estimated by the diffusion tensor imaging along the perivascular space (DTI‐ALPS) index relates to white matter (WM) integrity, Alzheimer's disease (AD) neuropathology, resting‐state electroencephalogram (rsEEG) alpha rhythms underpinning quiet vigilance, and cognitive decline in mild cognitive impairment (MCI). METHODS Clinical, neuroimaging, and rsEEG data were analyzed in matched mild cognitive impairment due to AD (ADMCI) and MCI not due to AD (noADMCI) participants. DTI‐ALPS index and aperiodic and periodic components of the rsEEG power spectra were calculated following standard pipelines. RESULTS Lower DTI‐ALPS index was associated with higher AD neuropathology and WM lesions, lower periodic rsEEG alpha rhythms, and worse cognition in patients with ADMCI and noADMCI as a whole population, with the ADMCI (over noADMCI) group showing lower DTI‐ALPS index, greater AD neuropathology, and lower periodic rsEEG alpha rhythms. CONCLUSIONS The DTI‐ALPS index may capture glymphatic system impairment linked to AD neuropathology, vigilance dysfunction, and cognitive decline in MCI. Highlights Prodromal patients with Alzheimer's disease (AD) showed low brain glymphatic drainage. Low glymphatic drainage was associated with AD neuropathology, white matter lesions, and worse cognition. Low glymphatic drainage may impact the neurophysiological alpha oscillating processes in quiet vigilance.

Objective. In this exploratory study, we tested whether electroencephalographic (EEG) rhythms may reflect the effects of a chronic administration (4 weeks) of an anti-amyloid β-site amyloid precursor protein (APP) cleaving enzyme 1 inhibitor (BACE-1; ER-901356; Eisai Co., Ltd., Tokyo, Japan) in TASTPM (double mutation in APP KM670/671NL and PSEN1 M146V) producing Alzheimer’s disease (AD) amyloid neuropathology as compared to wild type (WT) mice. Methods. Ongoing EEG rhythms were recorded from a bipolar frontoparietal and two monopolar frontomedial (prelimbic) and hippocampal channels in 11 WT Vehicle, 10 WT BACE-1, 10 TASTPM Vehicle, and 11 TASTPM BACE-1 mice (males; aged 8/9 months old at the beginning of treatment). Normalized EEG power (density) was compared between the first day (Day 0) and after 4 weeks (Week 4) of the BACE-1 inhibitor (10 mg/Kg) or vehicle administration in the 4 mouse groups. Frequency and magnitude of individual EEG delta and theta frequency peaks (IDF and ITF) were considered during animal conditions of behaviorally passive and active wakefulness. Cognitive status was not tested. Results. Compared with the WT group, the TASTPM group generally showed a significantly lower reactivity in frontoparietal ITF power during the active over the passive condition (p < 0.05). Notably, there was no other statistically significant effect (e.g., additional electrodes, recording time, and BACE-1 inhibitor). Conclusions. The above EEG biomarkers reflected differences between the WT and TASTPM groups, but no BACE-1 inhibitor effect. The results suggest an enhanced experimental design with the use of younger mice, longer drug administrations, an effective control drug, and neuropathological amyloid markers.

Background Alzheimer’s Disease (AD) and Sleep disturbances are closely linked in a bidirectional relationship. Indeed, sleep alterations represent a precipitating factor in early pathogenesis of neurodegeneration. Conversely, the accumulation of Aβ and tau proteins directly disrupts sleep‐wake cycles. Sleep disturbances are extremely prevalent in AD and the relationship between these disorders has been thoroughly investigated. Our study is the first to investigate the electroencephalographic cortical sources during the transitional stages between quiet wakefulness and light sleep in AD patients with MCI. Methods We analysed data from an international database (www.pdwaves.org) comprising clinical, neuropsychological, EEG morning recordings (45 minutes), cerebrospinal fluid (CSF), structural and functional MRI data in n=36 ADMCI, n=20 showing transition to light sleep (t‐ADMCI) and n=16 without transition to sleep (nt‐ADMCI)(Table 1). The database also included clinical, neuropsychological, and EEG data of n=11 matched healthy elderly (Nold) persons transitioning to light sleep. The EEG traces were reviewed by researchers blinded to the diagnosis, divided in 4” epochs and categorised in four different vigilance conditions: Eyes Open, Wakefulness, Flattening of alpha (drowinsess), Ripples (light sleep), according to the sleep classification by Hori et al (1994). Individual alpha frequency (IAF) was used to determine the EEG delta, theta, and alpha bands. Regional EEG cortical sources were estimated using the eLORETA freeware. Results Compared to Nold subjects, the ADMCI subjects showed greater Frontal Delta Cortical source activity in all vigilance conditions (p<0,001) (Figure 1). Furthermore, when compared to nt‐ADMCI, t‐ADMCI showed an increased diffuse delta cortical source activity (p<0.0001) during the wakefulness period (Figure 2). No differences between these two last groups emerged in CSF neurodegeneration biomarkers, neuropsychological testing nor structural or functional MRI measures. Conclusion The higher Frontal Delta Cortical Source activity across all vigilance conditions in t‐ADMCI subjects as compared to Nold, and the persistence of this result when compared to matched nt‐ADMCI patients, likely reflects the presence of dominant local delta rhythms, normally found during N3 and REM sleep, due to a low dopaminergic and cholinergic tone. Our findings might reflect a “disconnection” of frontal regions due to the loss of projections from monoaminergic subcortical nuclei, affected by early neuronal loss from AD neuropathology.

Background Huntington's disease (HD) differs from Alzheimer's disease (AD) in its clinical presentation, particularly regarding vigilance, with notable motor, functional, and cognitive impairments that may be mirrored in resting‐state electroencephalographic (rsEEG) rhythms. Method To evaluate this hypothesis, clinical and rsEEG data were gathered from age‐, sex‐, and education‐matched groups, including HD patients (N = 29), AD patients (N = 24), and healthy older participants (Nold, N = 29). EEG sources were computed using eLORETA software. Result The findings are as follows: (1) Compared to the Nold participants, both AD and HD patients exhibited higher widespread delta source activities (with HD > AD); (2) HD patients with the most pronounced motor deficits showed very high delta and theta source activities across widespread cortical regions; (3) HD patients with the most severe cognitive deficits exhibited lower alpha and higher delta source activities in widespread cortical regions; and (4) HD patients with the most significant functional deficits displayed very high delta source activities in widespread cortical regions. Conclusion These findings indicate that in HD patients during quiet wakefulness, disruptions in cortical neural synchronization at delta and alpha frequencies are distinctly linked to cognitive, motor, and functional impairments. This underscores a unique interaction between the cholinergic and dopaminergic systems, which likely modulates the generation of alpha and delta source activities.

Background Patients with mild cognitive impairment (MCI) typically show abnormal high delta (<4 Hz) and low alpha (8–12 Hz) rhythms measured from resting‐state eyes‐closed electroencephalographic (rsEEG) source activities as well as white matter lesions (WMLs) measured from magnetic resonance imaging (MRI). Here we tested the hypothesis that rsEEG rhythms may not deteriorate with the increase of WLMs in patients with MCI due and not due to Alzheimer's disease (ADMCI and noADMCI). Method An international database provided demographic, clinical, and rsEEG datasets for cognitively unimpaired older (Healthy; N = 30), ADMCI (N = 64), and noADMCI (N = 36) participants. The rsEEG rhythms spanned individual delta, theta, and alpha frequency bands. The eLORETA freeware estimated cortical rsEEG sources. The international database also provided MRI datasets for the ADMCI and noADMCI participants. T2 and Fluid Attenuated Inversion Recovery (FLAIR) images estimated the WMLs. Result The posterior rsEEG alpha source activities were lower in the groups of the ADMCI with a less increase of WMLs (ADMCI‐WML‐), ADMCI with a high increase of WMLs (ADMCI‐WML+), and noADMCI with a very high increase of WMLs (noADMCI‐WL++) compared to the Healthy group (p < 0.001; Figure 1). This effect was dramatic in the ADMCI‐WML‐ group, marked in the ADMCI‐WML+ group, and moderate in the noADMCI‐WML++. Furthermore, a positive association between the increase of WMLs and the worsening of executive function test scores (i.e., Trail making test part B‐A) was observed in the noADMCI group (t = 3.25, p < 0.005; Figure 2). Conclusion These results suggest that neurophysiological brain neural oscillatory synchronization mechanisms regulating cortical arousal and vigilance through alpha rsEEG rhythms are not affected by white matter tissue damage in MCI patients.