Frontal Cortex Function Research Articles

Event-related potentials study on the effects of high neuroticism on senile false memory.

To study the false memory among senile normal people with high neuroticism and low neuroticism using neuropsychological scales and event-related potentials (ERPs), and to explore the effects of high neuroticism on false memory and its neuroelectrophysiological mechanism. A cross-sectional study was conducted, in which the general situation questionnaire, adult version of Eysenck personality questionnaire (EPQ) and Montreal cognitive assessment (MoCA) scale were used to establish a multi-dimensional survey in senile normal people over 60 years old from communities in Zhengzhou, and the EPQ and general situation questionnaire were used to comprehensively screen and divide the study subjects into high neuroticism group and low neuroticism group from 206 senile people. The population was matched by 1:1 according to gender, age (±2 years), and years of education (±2 years), and 40 subjects were finally enrolled for detection of electroencephalograph (EEG) components using ERPs. The Deese-Roediger-McDermott (DRM) paradigm of false memory was designed using E-prime2.0 system, and the stimulus program was presented. The EEG signals of the study subjects were recorded in real time and acquired using 64-channel Neuroscan EEG signals acquisition system. High neuroticism group was evidently lower in the mean accuracy than low neuroticism group, and the difference in the mean accuracy was statistically significant (P = 0.013), but the difference in reaction time was not statistically significant. 2. The mean amplitude of EEG component N400: The difference in the main effect of N400 in the brain region was significantly different (P<0.001), and the mean amplitude of N400 was the largest in frontal region, followed by central region and parietal region successively (all P<0.05). There was no statistically significant difference in the neurotic main effect or the interaction effect of neuroticism and brain region. The latency of N400: There was no significant difference in the neurotic main effect, main effect of the brain region or the interaction effect of neuroticism and brain region. 3. The mean amplitude of EEG component LPC: The difference in the main effect of the brain region was significantly different (P<0.001), and the mean amplitude of LPC was the largest in frontal region, followed by central region and parietal region successively (all P<0.05). There was no significant difference in the neurotic main effect, neuroticism or the interaction effect of neuroticism and brain region. As to the latency of LPC, there was significant difference in the main effect of the brain region (P = 0.025), and the latency of LPC was shorter in frontal region than that in central region (P<0.05). The differences in the neurotic main effect, interaction effect of neuroticism and brain region were not statistically significant. High neuroticism can significantly increase the false memory of senile normal people. The EEG components N400 and LPC are potential early indicators of high neuroticism affecting false memory. High neuroticism may influence false memory by affecting the frontal cortex function.

Stimulating social interest: The translational value of basic investigations into frontal cortex function

Fan etal. use electrical stimulation during a novel social interaction paradigm to demonstrate a role for the orbitofrontal cortex in directing social attention. Their results shed new light on the basic functions of the orbitofrontal cortex and have translational value in understanding circuit modulation for psychiatric disorders.

Neurometabolic activity in the thalamic and frontal cortex and cognitive functions in adolescents with generalized epileptic syndromes

The study aimed to analyse the mutual correlations between the metabolic activity of the brain evaluated by the magnetic resonance spectroscopy method (MRS) and intelligence and cognitive functions in adolescents with idiopathic generalised epilepsies (IGE). The focus of the study was placed on the activity of the thalamus and frontal cortex.Twenty newly diagnosed patients with juvenile absence epilepsy (JAE) and juvenile myoclonic epilepsy (JME) were included in the study. Adolescents underwent primary structural neuroimaging (1.5T) and advanced evaluation of the frontal cortex and thalamus by MRS. Concentrations of N-acetyl aspartate (NAA), creatine plus phosphocreatine (Cr) and choline (Cho) were measured and were expressed as ratios of NAA/Cr, NAA/Ch and NAA/Cr+Ch. Patients also completed a panel of IQ and cognitive tests (e.g., FePsy Battery – classification test, verbal fluency test, RAVLT memory test). The correlation between the level of metabolites and the results of intellectual and cognitive tests was examined.Strong correlations were found between IQ and some cognitive functions and metabolic ratios in the IGEs group. Overall the patients whose NAA/Cr, NAA/Ch, NAA/Cr+Ch ratios were lower, obtained worse results in IQ and in some of the neuropsychological tests.The metabolite activity in the thalamus and frontal cortex impacts the results of neuropsychological tests in the group of patients with IGE.

What happens to the inhibitory control functions of the right inferior frontal cortex when this area is dominant for language?

A low number of individuals show an atypical brain control of language functions that differs from the typical lateralization in the left cerebral hemisphere. In these cases, the neural distribution of other cognitive functions is not fully understood. Although there is a bias towards a mirrored brain organization consistent with the Causal hypothesis, some individuals are found to be exceptions to this rule. However, no study has focused on what happens to the homologous language areas in the right frontal inferior cortex. Using an fMRI-adapted stop-signal task in a healthy non right-handed sample (50 typically lateralized and 36 atypically lateralized for language production), our results show that atypical lateralization is associated with a mirrored brain organization of the inhibitory control network in the left hemisphere: inferior frontal cortex, presupplementary motor area, and subthalamic nucleus. However, the individual analyses revealed a large number of cases with a noteworthy overlap in the inferior frontal gyrus, which shared both inhibitory and language functions. Further analyses showed that atypical lateralization was associated with stronger functional interhemispheric connectivity and larger corpus callosum. Importantly, we did not find task performance differences as a function of lateralization, but there was an association between atypical dominance in the inferior frontal cortex and higher scores on schizotypy and autistic spectrum traits, as well as worse performance on a reading accuracy test. Together, these results partially support the Causal hypothesis of hemispheric specialization and provide further evidence of the link between atypical hemispheric lateralization and increased interhemispheric transfer through the corpus callosum.

What happens to the inhibitory control functions of the right inferior frontal cortex when this area is dominant for language?

A low number of individuals show an atypical brain control of language functions that differs from the typical lateralization in the left cerebral hemisphere. In these cases, the neural distribution of other cognitive functions is not fully understood. Although there is a bias towards a mirrored brain organization consistent with the Causal hypothesis, some individuals are found to be exceptions to this rule. However, no study has focused on what happens to the homologous language areas in the right frontal inferior cortex. Using an fMRI-adapted stop-signal task in a healthy non right-handed sample (50 typically lateralized and 36 atypically lateralized for language production), our results show that atypical lateralization is associated with a mirrored brain organization of the inhibitory control network in the left hemisphere: inferior frontal cortex, presupplementary motor area, and subthalamic nucleus. However, the individual analyses revealed a large number of cases with a noteworthy overlap in the inferior frontal gyrus, which shared both inhibitory and language functions. Further analyses showed that atypical lateralization was associated with stronger functional interhemispheric connectivity and larger corpus callosum. Importantly, we did not find task performance differences as a function of lateralization, but there was an association between atypical dominance in the inferior frontal cortex and higher scores on schizotypy and autistic spectrum traits, as well as worse performance on a reading accuracy test. Together, these results partially support the Causal hypothesis of hemispheric specialization and provide further evidence of the link between atypical hemispheric lateralization and increased interhemispheric transfer through the corpus callosum.

Frontal cortex activity during the production of diverse social communication calls in marmoset monkeys

Vocal communication is essential for social behaviors in humans and non-human primates. While the frontal cortex is crucial to human speech production, its role in vocal production in non-human primates has long been questioned. It is unclear whether activities in the frontal cortex represent diverse vocal signals used in non-human primate communication. Here we studied single neuron activities and local field potentials (LFP) in the frontal cortex of male marmoset monkeys while the animal engaged in vocal exchanges with conspecifics in a social environment. We found that both single neuron activities and LFP were modulated by the production of each of the four major call types. Moreover, neural activities showed distinct patterns for different call types and theta-band LFP oscillations showed phase-locking to the phrases of twitter calls, suggesting a neural representation of vocalization features. Our results suggest important functions of the marmoset frontal cortex in supporting the production of diverse vocalizations in communication.

Neural association between cognitive function and anhedonia in adolescents with melancholic major depressive disorder: A fNIRS study

BackgroundCognitive dysfunction is common among adolescent patients with major depressive disorder (MDD). However, the pattern and magnitude of cognition impairment in patients during melancholic episodes remains unclear. The purpose of this study was to compare the neurocognitive performance and the underlying cerebral blood flow activation of adolescent patients with melancholic and non-melancholic features. MethodsFifty-seven and 44 adolescent patients with MDD with or without melancholic feature (MDD-MEL/nMEL) and 58 healthy controls (HCs) were recruited. We used the repeatable battery for the assessment of neuropsychological status (RBANS) measuring neurocognitive function, and used functional near infrared spectroscopy (fNIRS) monitoring cerebral hemodynamic changes, described by β value. The non-parametric test and post-hoc analysis were conducted in RBANS scores and β values among three groups. Spearman correlation and mediating analysis was performed for RBANS scores, β values, and clinical symptoms in the MDD-MEL group. ResultsThere were no significant difference in RBANS scores between MDD-MEL and MDD-nMEL group. Compared with patients in MDD-nMEL, patients in MDD-MEL have lower β values in eight channels (ch10, ch16, ch20, ch25, ch27, ch37, ch41, ch45). The cognitive function is significantly correlated with anhedonia, and the β values play a partial mediating role between anhedonia and cognitive function. LimitationIt's a cross-sectional study and monitoring longitudinal effects are needed to further elucidate the mechanism. ConclusionThe cognitive function in adolescents with MDD-MEL may not significantly differ from those with MDD-nMEL. However, the anhedonia may influenced the cognitive function by altering the function of medial frontal cortex.

A revised perspective on the evolution of the lateral frontal cortex in primates.

Detailed neuroscientific data from macaque monkeys have been essential in advancing understanding of human frontal cortex function, particularly for regions of frontal cortex without homologs in other model species. However, precise transfer of this knowledge for direct use in human applications requires an understanding of monkey to hominid homologies, particularly whether and how sulci and cytoarchitectonic regions in the frontal cortex of macaques relate to those in hominids. We combine sulcal pattern analysis with resting-state functional magnetic resonance imaging and cytoarchitectonic analysis to show that old-world monkey brains have the same principles of organization as hominid brains, with the notable exception of sulci in the frontopolar cortex. This essential comparative framework provides insights into primate brain evolution and a key tool to drive translation from invasive research in monkeys to human applications.

Region-selective control of the thalamic reticular nucleus via cortical layer 5 pyramidal cells

Corticothalamic pathways, responsible for the top-down control of the thalamus, have a canonical organization such that every cortical region sends output from both layer 6 (L6) and layer 5 (L5) to the thalamus. Here we demonstrate a qualitative, region-specific difference in the organization of mouse corticothalamic pathways. Specifically, L5 pyramidal cells of the frontal cortex, but not other cortical regions, establish monosynaptic connections with the inhibitory thalamic reticular nucleus (TRN). The frontal L5–TRN pathway parallels the L6–TRN projection but has distinct morphological and physiological features. The exact spike output of the L5-contacted TRN cells correlated with the level of cortical synchrony. Optogenetic perturbation of the L5–TRN connection disrupted the tight link between cortical and TRN activity. L5-driven TRN cells innervated thalamic nuclei involved in the control of frontal cortex activity. Our data show that frontal cortex functions require a highly specialized cortical control over intrathalamic inhibitory processes.

Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder

BackgroundImpaired response inhibition in individuals with cocaine use disorder (CUD) is hypothesized to depend on deficient noradrenergic signaling in corticostriatal networks. Remediation of noradrenergic neurotransmission with selective norepinephrine reuptake inhibitors such as atomoxetine may therefore have clinical utility to improve response inhibitory control in CUD. MethodsWe carried out a randomized, double-blind, placebo-controlled, crossover study with 26 participants with CUD and 28 control volunteers investigating the neural substrates of stop-signal inhibitory control. The effects of a single dose of atomoxetine (40 mg) were compared with placebo on stop-signal reaction time performance and functional network connectivity using dynamic causal modeling. ResultsWe found that atomoxetine speeded Go response times in both control participants and those with CUD. Improvements in stopping efficiency on atomoxetine were conditional on baseline (placebo) stopping performance and were directly associated with increased inferior frontal gyrus activation. Further, stopping performance, task-based brain activation, and effective connectivity were similar in the 2 groups. Dynamic causal modeling of effective connectivity of multiple prefrontal and basal ganglia regions replicated and extended previous models of network function underlying inhibitory control to CUD and control volunteers and showed subtle effects of atomoxetine on prefrontal-basal ganglia interactions. ConclusionsThese findings demonstrate that atomoxetine improves response inhibition in a baseline-dependent manner in control participants and in those with CUD. Our results emphasize inferior frontal cortex function as a future treatment target owing to its key role in improving response inhibition in CUD.

The neural basis of compound word processing revealed by varying semantic transparency and morphemic neighborhood size

This study investigated the neural basis of compound word processing by using fMRI and Chinese two-character compounds for lexical decision. Semantic transparency and morphemic neighborhood size were manipulated to augment the processing profile for measurement. The behavioral results disclosed a semantic transparency effect and its interaction with the neighborhood size, which supported existence of a mechanism for compound processing. The fMRI results located a neural substrate in the left inferior prefrontal cortex (BA 45) which reacted in an interactive manner to the two variables. While its activities were lower when their neighborhood size was larger for processing transparent compounds, its activities became higher when their neighborhood size was larger for processing opaque compounds. When scaling to a larger scope, the function of this mechanism fitted well with the theoretical account of unification function of the left inferior frontal cortex for language processing.

Call for a more balanced approach to understanding orbital frontal cortex function.

Orbital frontal cortex (OFC) research has historically emphasized the function of this associative cortical area within top-down theoretical frameworks. This approach has largely focused on mapping OFC activity onto human-defined psychological or cognitive constructs and has often led to OFC circuitry bearing the weight of entire theoretical frameworks. New techniques and tools developed in the last decade have made it possible to revisit long-standing basic science questions in neuroscience and answer them with increasing sophistication. We can now study and specify the genetic, molecular, cellular, and circuit architecture of a brain region in much greater detail, which allows us to piece together how they contribute to emergent circuit functions. For instance, adopting such systematic and unbiased bottom-up approaches to elucidating the function of the visual system has paved the way to building a greater understanding of the spectrum of its computational capabilities. In the same vein, we argue that OFC research would benefit from a more balanced approach that also places focus on novel bottom-up investigations into OFC's computational capabilities. Furthermore, we believe that the knowledge gained by employing a more bottom-up approach to investigating OFC function will ultimately allow us to look at OFC's dysfunction in disease through a more nuanced biological lens. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

The Therapeutic Targets of Fingolimod (FTY720) Are Involved in Pathological Processes in the Frontal Cortex of Alzheimer's Disease Patients: A Network Pharmacology Study.

Background: The sphingosine-1-phosphate receptor (S1PR) modulator fingolimod (FTY720), which is commonly used as an immunomodulator in multiple sclerosis treatment, has recently been found to reduce pathological changes in the brain tissue of Alzheimer's disease (AD) animal models, but this has yet to be verified in human brain tissue. In this study, network pharmacology methods were applied to determine the potential pharmacological mechanisms of fingolimod in the frontal cortex of AD patients.Methods: The pharmacological macromolecular targets of fingolimod and fingolimod phosphate were downloaded from SwissTarget and DrugBank. Systematic intersection analysis of the expression profiles of brain frontal cortex tissues (423 AD tissues and 266 control tissues) was performed to obtain AD-associated fingolimod targets (F-ADGs). Immune cell infiltration analysis and a primary mouse cortical culture RNA-seq drug screen database were used to identify immune-related F-ADGs and cortex-related F-ADGs. Then, the expression values of F-ADGs were correlated with the disease severity score (MMSE score) of AD patients to identify severity-related F-ADGs. We also analyzed miRNA expression microarray data in the frontal cortex of AD patients associated with disease severity to obtain severity-related F-ADG-miRNAs.Results: A total of 188 F-ADGs were detected in the frontal cortices of AD patients and were enriched in biological processes such as synaptic signaling, inflammatory response, and response to oxygen-containing compounds. Eleven immune-related F-ADGs (like FPR1, BLNK.) and 17 cortex-related F-ADGs (like ALDH1L1, DUSP1.) were detected. Other F-ADGs, such as S1PR1 and GABBR2, although not classified into the above two categories, were still predicted by bioinformatics methods to play an important role in the development of AD. Two F-ADGs (GNAQ and MMP14) and 28 miRNAs (like miR- 323a-3p, miR-181a-5p.) were found to be associated with AD severity (MMSE 0-27 group). Fifteen F-ADGs (like ALDH1L1, FPR1, and IL6.) and 46 miRNAs (like miR-212-5p, miR-93-5p.) were found to be associated with mild or moderate dementia AD patients' severity (MMSE11-22 subgroup).Conclusions: Fingolimod may affect the brain frontal cortex function of AD patients in many different ways, such as affecting immune cell infiltration, nerve cell, or glial cell function, and synaptic function. miRNAs may also be involved. ALDH1L1, FPR1, S1PR1, and GABBR2 may be core drug targets.

From affective to cognitive processing: Functional organization of the medial frontal cortex.

The medial wall of the primate frontal lobe encompasses multiple anatomical subregions. Based on distinct neurophysiological correlates and effects of lesions, individual areas are thought to play unique roles in behavior. Further, evidence suggests that dysfunction localized to specific subregions is commonly found in different neuropsychiatric disorders. The neurobiological underpinnings of these disorders, however, remain far from clear. Here, to better understand the functions of medial frontal cortex (MFC) and its role in psychiatric disease, we focus on its functional organization. We describe the emerging pattern in which more dorsal regions subserve temporally extended cognitive functions and more ventral regions predominantly subserve affective functions. We focus on two specific domains, decision-making and social cognition, that require integration across emotion and cognition. In each case, we discuss the current understanding of the functions believed to depend on subregions of MFC as a stepping-stone to speculate on how they might work in unison. We conclude with an overview of how symptoms of certain psychiatric disorders relate to our understanding of MFC functional organization and how further discovery could fuel advances in circuit-based therapies.

Social processing by the primate medial frontal cortex.

The primate medial frontal cortex is comprised of several brain regions that are consistently implicated in regulating complex social behaviors. The medial frontal cortex is also critically involved in many non-social behaviors, such as those involved in reward, affective, and decision-making processes, broadly implicating the fundamental role of the medial frontal cortex in internally guided cognition. An essential question therefore is what unique contributions, if any, does the medial frontal cortex make to social behaviors? In this chapter, we outline several neural algorithms necessary for mediating adaptive social interactions and discuss selected evidence from behavioral neurophysiology experiments supporting the role of the medial frontal cortex in implementing these algorithms. By doing so, we primarily focus on research in nonhuman primates and examine several key attributes of the medial frontal cortex. Specifically, we review neuronal substrates in the medial frontal cortex uniquely suitable for enabling social monitoring, observational and vicarious learning, as well as predicting the behaviors of social partners. Moreover, by utilizing the three levels of organization in information processing systems proposed by Marr (1982) and recently adapted by Lockwood, Apps, and Chang (2020) for social information processing, we survey selected social functions of the medial frontal cortex through the lens of socially relevant algorithms and implementations. Overall, this chapter provides a broad overview of the behavioral neurophysiology literature endorsing the importance of socially relevant neural algorithms implemented by the primate medial frontal cortex for regulating social interactions.

Shared Neural Representations of Cognitive Conflict and Negative Affect in the Medial Frontal Cortex

Influential theories of Medial Frontal Cortex (MFC) function suggest that the MFC registers cognitive conflict as an aversive signal, but no study directly tested this idea. Instead, recent studies suggested that nonoverlapping regions in the MFC process conflict and affect. In this preregistered human fMRI study (male and female), we used MVPAs to identify which regions respond similarly to conflict and aversive signals. The results reveal that, of all conflict- and value-related regions, only the ventral pre-supplementary motor area (or dorsal anterior cingulate cortex) showed a shared neural pattern response to different conflict and affect tasks. These findings challenge recent conclusions that conflict and affect are processed independently, and provide support for integrative views of MFC function.SIGNIFICANCE STATEMENT Multiple theories propose that the MFC, and the dorsal ACC in particular, integrates information related to suboptimal outcomes from different psychological domains (e.g., cognitive control and negative affect) with the aim of adaptively steering behavior. In contrast to recent studies in the field, we provide evidence for the idea that cognitive control and negative affect are integrated in the MFC by showing that a classification algorithm trained on discerning cognitive control (conflict vs no conflict) can predict affect (negative vs positive) in the voxel pattern response of the dorsal ACC/pre-SMA.

BDNF mRNA Expression in Leukocytes and Frontal Cortex Function in Drug Use Disorder.

The brain-derived neurotrophic factor (BDNF) is a neurotrophin recognized to play a major role in neuroplastic modifications associated to drug abuse, being involved in various behavioral changes found in drug use disorders, such as drug sensitization, craving and relapses. These neuroplastic changes were shown to affect the prefrontal cortex functions, which can be briefly measured through cognitive tests such as the Frontal Assessment Battery (FAB). In this study we investigated the BDNF mRNA expression in peripheral blood lymphocytes of crack-cocaine use disorder (CUD) and alcohol use disorder (AUD) patients, after drug detoxification treatment, using a real-time PCR approach and examining its association to FAB performance. BDNF mRNA expression was found to be higher by 2.25-fold in CUD patients and by 2-fold in the AUD patients when normalized to controls, and these values were found to be associated with FAB scores. This preliminary study evaluates, for the first time, BDNF mRNA expression in leukocytes and its relationship to FAB scores in crack-cocaine and alcohol use disorder patients.

Global cortical hypoexcitability of the dominant hemisphere in major depressive disorder: A transcranial magnetic stimulation study

Accumulating evidence suggests that major depressive disorders (MDD) are associated with an imbalance of excitation-inhibition within the prefrontal cortex (PFC), generated by a deficit of inhibitory synaptic transmission onto glutamatergic principal neurons. Transcranial magnetic stimulation (TMS) protocols can be used to measure neuronal excitability and GABAergic inhibition and thus provide additional evidence to evaluate this theory. In the present study, TMS protocols were used to compare GABAergic function and cortical excitability of dominant hemisphere in unmedicated patients with MDD versus a control group of healthy individuals. The study included 43 MDD patients according to DSM-V and 20 age- and sex- matched healthy volunteers. Psychological evaluation was conducted using the Beck Depression Inventory (BDI). Resting and active motor thresholds (rMT and aMT) together with contralateral and ipsilateral cortical silent periods (cSP, and iSP) were measured for each participant. rMT and aMT were higher in MDD patients compared with the control group, while cSP and iSP were significantly shorter in duration. There were significant positive correlations between the BDI score and rMT, aMT (P=0.001 and 0.002 respectively), and a negative correlation with cSP duration (P=0.001). Global hypoexcitability of both pyramidal cortical neurons (elevated MTs) and GABAergic controls (shortened SPs) was evidenced within the left/dominant motor cortex in MDD. These results are consistent with previous reports of abnormal glutamate and GABA function in frontal cortex.

Mindfulness-based therapy modulates default-mode network connectivity in patients with opioid dependence

Recently, mindfulness-based programs have shown promising clinical effects in the treatment of substance-use disorders (SUD). While several studies linked mindfulness to decreased default mode network (DMN) connectivity in meditators, only a few studies investigated its effects in patients with SUD. This study aimed to detect changes in DMN connectivity in opiate dependent patients receiving mindfulness based therapy (MBT) during their first month of treatment. Data from 32 patients that were assigned to MBT or treatment as usual (TAU) groups was investigated using resting-state functional MRI at 1.5 T before and after four weeks of treatment. Independent Component Analysis was used to investigate distinct (anterior vs. posterior) DMN subsystems. Connectivity changes after treatment were related to measures of impulsivity, distress tolerance and mindfulness. Increased mindfulness scores after treatment were found in patients receiving MBT compared to TAU. Within the anterior DMN, decreased right inferior frontal cortical connectivity was detected in patients who received MBT compared to TAU. In addition, within the MBT-group decreased right superior frontal cortex connectivity was detected after treatment. Inferior frontal cortex function was significantly associated with mindfulness measures. The data suggest that MBT can be useful during abstinence from opiates. In opiate-dependent patients distinct functional connectivity changes within the DMN are associated with MBT.

High serum high-density lipoprotein-cholesterol is associated with memory function and gyrification of insular and frontal opercular cortex in an elderly memory-clinic population.

The issue of whether serum lipid marker values are cognitively and neurologically significant for elderly individuals attending a memory clinic has been controversial. We investigated the associations of serum lipid markers with the memory function and cortical structure in 52 patients aged ≥75 years who had attended our memory clinic based on their subjective memory complaints. None had a history of medication for hyperlipidemia. The Wechsler Memory Scale-Revised (WMS-R) was administered to all patients for the assessment of their memory function. Serum low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDLC), and triglyceride (TG) were measured for each patient. Surface-based morphometry (SBM) was performed for the calculation of each patient's cortical thickness and gyrification index based on structural MRI data. Our analyses revealed that the serum HDLC level was positively and significantly correlated with the WMS-R subtests of visual paired associates I/II and logical memory I (p < 0.05). The serum TG level was negatively correlated with the logical memory I subtest. The SBM results showed positive correlations between the serum HDLC level and the gyrification indices of the bilateral insular and frontal opercular cortices, and those two gyrification indices were positively correlated with the logical memory I and visual paired associates I/II. These results suggest that in these elderly patients, a high serum HDLC level was associated with not only preserved memory function but also gyrification of the insular and frontal opercular cortex. We conclude that elderly individuals' serum lipid markers should be carefully assessed in memory clinic settings, because serum HDLC may be a biomarker for memory function and cortical structure.