Explore the vast range of titles available.

Interdisciplinary approaches are needed to understand the relationship between genetic factors and brain structure and function. Here we describe a database that includes genetic data on apolipoprotein E ( APOE ) and phosphatidylinositol binding clathrin assembly protein ( PICALM ) genes, both of which are known to increase the risk of late-onset Alzheimer's disease, paired with psychometric (memory, intelligence, mood, personality, stress coping strategies), basic demographic and health data on a cohort of 192 healthy middle-aged (50–63) individuals. Part of the database (~79 participants) also includes blood tests (blood counts, lipid profile, HSV virus) and functional neuroimaging data (EEG/fMRI) recorded with a resting-state protocol (eyes open and eyes closed) and two cognitive tasks (multi-source interference task, MSIT; and Sternberg's memory task). The data were validated and showed overall good quality. This open-science dataset is well suited not only for research relating to susceptibility to Alzheimer's disease but also for more general questions on brain aging or can be used as part of meta-analytical multi-disciplinary projects.

AD probability decreases in carriers of the e2 variant of the APOE gene (APOE-e2), whereas APOE-e4 is believed to be a strong risk factor (Strittmatter et al., 1993) and is associated with overall cognitive impairment and synapse loss (see review by Selkoe, 2002). The study revealed the synaptic paradox of the APOE-related risk of AD: surprisingly, it was APOE-e4, the gene variant that is linked to the highest risk of AD, that was most efficient in stimulating MAP signaling and in enhancing synaptogenesis. [...]a reported APOE-e4-related increase in synapse formation contradicted numerous findings indicating the highest loss of synapses and severity of cognitive decline in APOE-e4 carriers (Terry et al., 1991; Selkoe, 2002; Scheff et al., 2006; Purro et al., 2012; Chen et al., 2018). The direct effect of APOE-e4 on neurons can be modulated by the interplay of many factors, including the activity of glial cells (mainly astrocytes and microglia) and other risk-genes. [...]it was shown that neurons need astrocytes and microglia to eliminate redundant synapses (Lee and Chung, 2019).

The ability to identify and resolve conflicts between standard, well‐trained behaviors and behaviors required by the current context is an essential feature of cognitive control. To date, no consensus has been reached on the brain mechanisms involved in exerting such control: while some studies identified diverse patterns of activity across different conflicts, other studies reported common resources across conflict tasks or even across simple tasks devoid of the conflict component. The latter reports attributed the entire activity observed in the presence of conflict to longer time spent on the task (i.e., to the so‐called time‐on‐task effects). Here, we used an extended Multi‐Source Interference Task (MSIT) which combines Simon and flanker types of interference to determine shared and conflict‐specific mechanisms of conflict resolution in fMRI and their separability from the time‐on‐task effects. Large portions of the activity in the dorsal attention network and decreases of activity in the default mode network were shared across the tasks and scaled in parallel with increasing reaction times. Importantly, the activity in the sensory and sensorimotor cortices, as well as in the posterior medial frontal cortex (pMFC) – a key region implicated in conflict processing – could not be exhaustively explained by the time‐on‐task effects. Cognitive effort related to selecting appropriate behaviors in a context of interfering (conflicting) information activates common cognitive brain mechanisms (activation of the attention network and deactivation of the default mode network) mostly in a time‐on‐task manner. However, there is also a specific, conflict‐related activation (in pMFC), the intensity of which exceeds estimations based on the time‐on‐task model.

The symptoms of Alzheimer's disease (AD) are caused by neurodegeneration and atrophy in particular brain regions, especially in the temporal cortex. However, the influence of genetic risk on cortical thickness in non-demented individuals prior to disease onset remains unclear. This study aimed to explore the relationship between two AD risk genes (APOE/PICALM) and cortical thickness in selected regions of interest (ROIs) in non-demented, middle-aged individuals. Sixty-nine (N = 69) participants (34 females, 35 males; age: 55.45±3.19) underwent magnetic resonance imaging (MRI). They were divided into three groups based on their AD risk. Cortical thickness was analyzed using CAT12 software (surface-based morphometry with the Destrieux atlas) based on T1-weighted MR images in five ROIs referred as \"the cortical signature of AD\" in previous studies. APOE-e4 with PICALM-AA/AG carriers (A+P-) are characterized by a thinner cortex in the right temporal pole compared to non-carriers, controlling for sex. No other differences in cortical thickness were found in the selected ROIs. The direction of the findings aligns with existing literature reporting cortical thinning in amyloid-positive individuals, as well as in patients with mild cognitive impairment and Alzheimer's disease when compared to control groups.Competing Interest StatementThe authors have declared no competing interest.

The symptoms of Alzheimer’s disease (AD) are caused by neurodegeneration and atrophy in particular brain regions, especially in the temporal cortex. However, the influence of genetic risk on cortical thickness in non-demented individuals prior to disease onset remains unclear. This study aimed to explore the relationship between two AD risk genes (APOE/PICALM) and cortical thickness in selected regions of interest (ROIs) in non-demented, middle-aged individuals. Sixty-nine (N = 69) participants (34 females, 35 males; age: 55.45±3.19) underwent magnetic resonance imaging (MRI). They were divided into three groups based on their AD risk. Cortical thickness was analyzed using CAT12 software (surface-based morphometry with the Destrieux atlas) based on T1-weighted MR images in five ROIs referred as “the cortical signature of AD” in previous studies. APOE-ε4 with PICALM-AA/AG carriers (A+P-) are characterized by a thinner cortex in the right temporal pole compared to non-carriers, controlling for sex. No other differences in cortical thickness were found in the selected ROIs. The direction of the findings aligns with existing literature reporting cortical thinning in amyloid-positive individuals, as well as in patients with mild cognitive impairment and Alzheimer’s disease when compared to control groups.

Genetic susceptibility is a primary factor contributing to etiology of late-onset Alzheimer’s disease (LOAD). The exact mechanisms and timeline through which APOE/PICALM influence brain functions and contribute to LOAD remain unidentified. This includes their effects on individuals prior to the development of the disease. APOE/PICALM alleles were assessed to determine the genetic risk of LOAD in 79 healthy, middle-aged participants who underwent EEG and fMRI recordings. The resting-state signal was analyzed to estimate relative spectral power, complexity (Higuchi’s algorithm), and connectivity (coherence in EEG and ICA-based connectivity in fMRI). The main findings indicated that individuals at risk for LOAD exhibited reduced signal complexity and the so-called “slowing of EEG” which are well-known EEG markers of AD. Additionally, these individuals showed altered functional connectivity in fMRI (within attention related areas). Risk alleles of APOE/PICALM may affect brain integrity and function prior to the onset of the disease

Flexible behavior often requires processing of complex, interfering information. Research has investigated conflict-related brain processes mostly using single tasks which hindered direct comparison of different interference types. Thus, the question if they are resolved by a common mechanism or by a set of different, task-specific mechanisms remains open. In this study, we used event-related potentials (ERPs) to examine the spatio-temporal dynamics of cognitive control across Simon, flanker, multi-source and no-conflict conditions. Our findings reveal that all trial types engaged the same sequence of processing stages, as indicated by common ERP waveforms and consistent number and order of microstates across conditions. However, the intensity and duration of these common stages scaled with difficulty of the conflict task (as measured by RTs and accuracy) from Simon to flanker to multi-source interference. Flanker conflict uniquely influenced early ERP components strongly engaging the dorsal attentional system and visual areas, likely due to demands posed by the presence of flanker distractors. Later ERP components (with sources including ventral attention and somatomotor network areas) were affected by both conflicts. Accordingly, when flanker and Simon conflicts were presented together, early processes lineary summed up, but there was an interaction at the later stage of processing paralleling nonlinear drop of accuracy in a multi-conflict condition. Our study provides novel insights into the neural dynamics underlying cognitive control engaged across different conflict types and their interaction. The use of source analysis allowed us to ground ERP-based findings in the wider context of studies, including those using neuroimaging techniques.Competing Interest StatementThe authors have declared no competing interest.Footnotes* https://openneuro.org/datasets/ds004621/versions/1.0.1

The ability to identify and resolve conflicts between standard, well trained behaviors, and behaviors required by the current context is an essential feature of cognitive control. To date, no consensus has been reached on the brain mechanisms involved in exerting such control: while some studies identified diverse patterns of activity across different conflicts, other studies reported common resources across conflict tasks or even across simple tasks devoid of conflict component. The latter reports attributed the entire activity observed in the presence of conflict to longer time spent on the task (i.e. to the so-called time-on-task effects). Here we used an extended Multi-Source Interference Task (MSIT) which combines Simon and flanker types of interference to determine shared and conflict-specific mechanisms of conflict resolution in fMRI, and their separability from the time-on-task effects. Large portions of the activity in the dorsal attention network and decreases of activity in the default mode network were shared across the tasks and scaled in parallel with increasing reaction times. Importantly, activity in the sensory and sensorimotor cortices, as well as in the posterior medial frontal cortex (pMFC)–a key region implicated in conflict processing–could not be exhaustively explained by the time-on-task effects.