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Posterior cingulate cortex

The posterior cingulate cortex (PCC) is a paralimbic region of the medial parietal cortex in the human brain, located posterior to the corpus callosum and encompassing Brodmann areas 23 and 31, bounded by the cingulate sulcus, parieto-occipital sulcus, and corpus callosum.^[1] It features a transitional cytoarchitecture between isocortex and allocortex, with subdivisions into dorsal (areas d23 and anterior 31) and ventral (areas v23 and posterior 31) regions that exhibit distinct neuronal layering and density.^[1]^[2] The PCC is highly interconnected, forming reciprocal links with the medial temporal lobe (including the hippocampus), ventromedial and dorsolateral prefrontal cortex, thalamus, striatum, and other parietal areas, which facilitate integration across distributed brain networks.^[1] It serves as a central hub of the default mode network (DMN), a system active during rest and internally directed tasks, where it exhibits event-related deactivation during externally focused, attention-demanding activities.^[3]^[1] These connections enable the PCC to balance internal and external attentional demands, supporting adaptive cognitive processing.^[1] Functionally, the PCC contributes to diverse cognitive processes, including episodic memory retrieval and consolidation (particularly via ventral subregions linked to the medial temporal lobe), spatial navigation and visuospatial orientation (involving dorsal and retrosplenial portions), self-referential thinking, prospection, and narrative comprehension.^[3]^[2]^[1] It also plays a key role in decision-making, cognitive control, and behavioral adaptation to unexpected environmental changes by integrating sensory feedback with past experiences.^[3] The region's metabolic activity and category-selective responses (e.g., to people or places) underscore its position at the apex of cortical hierarchies for abstract representation.^[3] Clinically, PCC dysfunction is implicated in various neurological and psychiatric disorders, including Alzheimer's disease (with early amyloid deposition and hypometabolism), schizophrenia (reduced gray matter volume and connectivity disruptions), autism, depression, ADHD, and traumatic brain injury, often manifesting as deficits in memory, attention, and social cognition.^[1]^[2] These alterations highlight the PCC's vulnerability and its broader impact on adaptive behavior and internal mentation.^[1]

Anatomy

Location and boundaries

The posterior cingulate cortex (PCC) is defined as the caudal portion of the cingulate cortex, situated on the medial surface of the cerebral hemispheres immediately superior to the corpus callosum. It encompasses the region posterior to the mid-cingulate cortex and wraps around the splenium of the corpus callosum, forming part of the posteromedial cortex. This positioning places it within the medial parietal lobe, contributing to its role in integrating sensory and cognitive processes, though its exact extent can vary slightly across individuals.^[4]^[2] The PCC is delimited by several key sulci that define its anatomical boundaries. Anteriorly, it is bounded by the central portion of the cingulate gyrus at the level of the splenium of the corpus callosum, often marking the transition via the isthmus of the cingulate. Posteriorly, the parieto-occipital sulcus forms the caudal limit, separating it from more occipital regions. Superiorly, the cingulate sulcus (including its marginal ramus) provides the dorsal boundary, while inferiorly, the callosal sulcus (or splenial sulcus arc) separates it from the corpus callosum itself. These boundaries ensure the PCC's distinct enclosure within the medial brain wall, visible prominently on midsagittal magnetic resonance imaging (MRI) sections as a curved gyrus above the callosal midline.^[4]^[5]^[6] In relation to adjacent structures, the PCC borders the precuneus superiorly, facilitating interactions in visuospatial and attentional networks; it adjoins the retrosplenial cortex posteriorly, which includes regions involved in spatial navigation; and it connects anteriorly to the isthmus of the cingulate, a transitional zone linking to the parahippocampal gyrus. Grossly, the PCC corresponds to Brodmann areas 23 and 31, with area 23 occupying the ventral and dorsal portions and area 31 the dorsal extension into the parietal transition, while it adjoins the retrosplenial cortex (areas 29 and 30) posteriorly wrapping the splenium. These areas were originally delineated by Korbinian Brodmann in 1909 based on cytoarchitectural features, establishing the foundational parcellation still used in modern neuroanatomy.^[4]^[7]^[2]

Cytoarchitectural organization

The posterior cingulate cortex (PCC) exhibits a granular cytoarchitecture typical of homotypical isocortex, characterized by well-developed layers II and IV, with prominent pyramidal cell populations in layers III and V.^[7] This contrasts with the agranular organization of the anterior cingulate cortex, where layer IV is less distinct; in the PCC, layer III of area 23 contains a denser packing of medium-sized pyramidal cells, contributing to its thicker and more robust supragranular layer.^[8] Layer V across PCC subregions features large pyramidal neurons with dense packing, particularly in areas 23b and 31, while layer VI varies in width, being notably broad in area 23c.^[7] The PCC is parcellated into distinct subregions based on these laminar features: area 23 (dorsal PCC) includes subdivisions 23a (with a prominent layer IIIc populated by large pyramidal cells), 23b (dense layer V), and 23c (wide layer VI); area 31 encompasses dorsal and ventral portions with a narrow layer III and dense layer V; and bordering retrosplenial areas 29 and 30 exhibit periallocortical traits, such as thin layers III and IV in area 29 and a wide layer II with dense layer III in area 30.^[7] These subdivisions reflect variations in cellular density, with area 23 showing overall higher pyramidal cell counts in supragranular layers compared to transitional zones like area 31.^[9] Interneuron populations, including parvalbumin- and calbindin-positive cells, also vary across subregions, with denser distributions in granular layers of area 23 relative to the more heterogeneous layering in areas 29/30, influencing local circuit organization.^[9] Histochemical staining reveals high metabolic activity in the PCC, as indicated by intense cytochrome oxidase reactivity, particularly in layers III and V of area 23, underscoring its elevated energy demands compared to adjacent cortical regions.^[10] Subtle sexual dimorphisms have been observed in postmortem studies.^[11]^[12] Recent advances in high-resolution imaging, including 7T MRI multi-parametric mapping, have enabled finer in vivo parcellation of the PCC, confirming cytoarchitectonic boundaries such as 23a/b and 31a/b through correlations between quantitative metrics (e.g., R2* relaxation rates) and histological layer-specific cell densities.^[13] These updated maps build on classical delineations, providing probabilistic atlases that align microscopic features with macroscopic imaging for improved precision in human studies.^[14]

Structural connections in nonhumans

The posterior cingulate cortex (PCC) in nonhuman species, including rodents and primates, features a conserved architecture of structural connections that links limbic structures with cortical and subcortical regions, facilitating integration of spatial, memory, and sensory information. These connections, studied primarily through tract-tracing techniques, underscore evolutionary parallels across mammals while revealing species-specific emphases.^[15] Primary afferents to the PCC arise from the subiculum, presubiculum, and retrosplenial cortex, conveyed mainly through the cingulum bundle, a key white matter tract running along the cingulate gyrus. Additional inputs originate from thalamic nuclei, particularly the anterior thalamic nuclei, which provide relay from subcortical limbic pathways in both rodents and nonhuman primates. These afferent patterns have been delineated in rodents using anterograde and retrograde tracers like biotinylated dextran amine (BDA) and Fluoro-Gold, revealing dense projections from hippocampal-associated areas to PCC homologs.^[15] In primates such as macaques, similar thalamic and hippocampal afferents are observed, with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injections confirming robust inputs from the anterior medial and lateral dorsal thalamic nuclei.^[16] Efferent projections from the PCC extend to the CA1 field of the hippocampus, entorhinal cortex, and prefrontal cortical areas, establishing bidirectional loops essential for memory consolidation and executive function. Reciprocal connections with the parietal association cortex further integrate sensory-motor signals, as evidenced by tracer studies showing labeled terminals in areas like the posterior parietal lobule following PCC injections. In rodent models, viral tracers such as CAV2-Cre have highlighted efferents to prefrontal regions like the orbital medial prefrontal cortex (ORBm) and anterior cingulate area (ACA), supporting navigational integration.^[15] Primate studies using cholera toxin subunit B (CTb) and BDA in macaques demonstrate stronger efferent targeting of the dorsolateral prefrontal cortex (DLPFC) and entorhinal cortex, with dense hippocampal projections via the subiculum.^[17]^[16] Tract-tracing with horseradish peroxidase (HRP) and its conjugates in both rodents and primates has provided seminal evidence of these dense hippocampal-PCC pathways, with HRP injections into the PCC yielding extensive retrograde labeling in CA1 and subicular regions.^[18]^[19] Species-specific variations highlight adaptive specializations: in macaques, the PCC exhibits stronger visuo-spatial inputs from the posterior parietal lobe, including areas PG and PE, as mapped by retrograde tracers like Fast Blue, enabling enhanced processing of visual landmarks for navigation.^[16]^[20] In rodents, connections prioritize olfactory and spatial navigation circuits, with prominent reciprocal links to ORBm for odor-guided behavior and retrosplenial cortex for head-direction signaling, confirmed through BDA and fluorescent dextran tracing.^[15] Recent methodological advances, including diffusion tensor imaging (DTI) in rhesus macaques, have validated the cingulum bundle as the dominant pathway for PCC afferents and efferents, with high-resolution tractography reconstructing superior and perihippocampal subdivisions linking the PCC to precuneus and hippocampal regions. These DTI findings, based on multi-subject templates, achieve Dice similarity coefficients above 0.84 for cingulum segmentation, corroborating earlier tracer data through 2023.^[21]^[22]

Structural connections in humans

The posterior cingulate cortex (PCC) in humans receives strong afferent inputs from the medial temporal lobe, including the hippocampus and parahippocampal gyrus, which facilitate memory-related processing through the ventral subdivision of the PCC.^[1] These inputs are primarily routed via the cingulum bundle, a major white matter tract that also conveys projections from the medial prefrontal cortex to the PCC, supporting integration of cognitive and emotional signals.^[23] Additionally, thalamic relays from the lateral dorsal nucleus provide key subcortical afferents to the PCC, contributing to its role in spatial and limbic functions.^[24] Efferent projections from the PCC target several cortical regions, including the angular gyrus in the inferior parietal lobule, the superior frontal gyrus, and the insula, enabling coordination across association areas for attention and interoceptive awareness.^[25] The PCC maintains bidirectional connectivity with the adjacent precuneus, forming a posteromedial hub that underpins default mode network operations.^[26] The primary white matter pathway for PCC connectivity is the cingulum bundle, which arches over the corpus callosum and links the PCC to frontal and temporal regions; contributions from the superior longitudinal fasciculus further connect it to parietal and frontal cortices.^[27] Diffusion tensor imaging (DTI) studies report average fractional anisotropy values of 0.45-0.55 in the cingulum bundle, indicating robust microstructural integrity in healthy adults.^[28] Recent 7T MRI and tractography research has refined understanding of cingulum sub-bundles, revealing specialized pathways from the PCC: dorsal sub-bundles prioritize memory integration with temporal regions, while ventral ones emphasize emotional processing via prefrontal links.^[29] These high-resolution findings highlight subregional differentiation not fully resolved in lower-field imaging.^[30]

Development

Embryological origins

The posterior cingulate cortex (PCC) originates from the dorsal telencephalic plate, which emerges from the prosencephalon (forebrain) during weeks 5-7 of human gestation. This region forms as part of the medial wall of the developing telencephalon, differentiating into limbic structures alongside the adjacent hippocampal primordium.^[2] Neurons destined for the PCC arise through radial migration from the ventricular zone of the telencephalon, where progenitor cells proliferate and generate postmitotic neurons that ascend along radial glial scaffolds to form the cingulate primordium by approximately week 8 of gestation. This migratory process establishes the basic laminar organization of the PCC, with early-generated neurons settling in deeper layers.^[31] Key transcription factors, including Emx1 and Emx2, play essential roles in patterning the cingulate anlage by regulating cortical progenitor proliferation, arealization, and lamination in the dorsal telencephalon; their coordinated expression helps define the boundaries between neocortical and archicortical domains. Similarly, Lhx2 contributes to the development of the cortical hem and adjacent cingulate regions by modulating dorsal signaling centers and progenitor maintenance, with disruptions in Lhx2 function implicated in forebrain malformations such as holoprosencephaly.^[32]^[33]^[34] The developmental timeline progresses with the appearance of the cingulate sulcus around 19-22 weeks of gestation, marking the initial folding of the medial cortical surface, while PCC cytoarchitectural differentiation, including layer-specific maturation, is largely complete by mid-gestation (around week 20). In animal models, such as mice with Emx1/Emx2 mutations, knockouts lead to severe reduction of the cingulate cortex, including posterior regions, due to impaired progenitor expansion and areal specification, as demonstrated in studies through 2023.^[35]^[36]^[33]

Postnatal and functional maturation

The posterior cingulate cortex (PCC) undergoes significant volumetric changes during postnatal development, characterized by rapid gray matter expansion in early childhood followed by a peak and subsequent pruning. Longitudinal MRI studies indicate that gray matter volume in the PCC increases substantially from birth through age 5, with over 100% gain in the first year and an additional ~15% in the second year across cortical regions including the cingulate, reflecting proliferation of neurons and synapses. This growth peaks around ages 10-12 years, after which synaptic pruning leads to a gradual volume reduction, estimated at approximately 1.9% per year in the posterior cingulate gyrus from ages 8 to 20, optimizing neural efficiency.^[37]^[38]^[39] Myelination of the cingulum bundle, which provides key structural connections to the PCC, progresses rapidly in infancy and early childhood, supporting efficient neural signaling. Diffusion tensor imaging (DTI) reveals increasing fractional anisotropy (FA) in the cingulum from infancy onward, indicative of advancing myelination and axon organization, with significant maturation occurring by ages 2-4 years as associative fibers like the cingulum complete much of their myelin sheath formation. These changes enable faster transmission speeds and are part of broader white matter development, where FA values rise steadily through childhood, peaking in adolescence. Delays in this process are noted in preterm infants, where reduced FA in the cingulum correlates with altered microstructural integrity.^[40]^[41]^[42]^[43] Functional maturation of the PCC begins early, with intrinsic activity patterns detectable in the default mode network (DMN) by around 6 months of age, though connectivity remains immature. Resting-state fMRI studies show that DMN hubs including the PCC exhibit sparse, weak connections in young children (ages 7-9), with minimal integration between the posterior cingulate and medial prefrontal regions compared to adults. By adolescence, DMN connectivity strengthens linearly, particularly involving the PCC with midline structures like the dorsomedial prefrontal cortex, achieving adult-like spatial organization and efficiency around ages 12-18, as evidenced by longitudinal data from cohorts like the ABCD study tracking 9- to 11-year-olds into later years.^[44]^[45]^[46] Critical periods for PCC refinement occur around puberty, when gonadal hormones influence synaptic pruning, reducing redundant connections to enhance network specificity. This hormone-driven process, involving surges in estrogen and testosterone, modulates pruning in cortical regions including the cingulate, with disruptions potentially altering developmental trajectories. In preterm infants, these periods are vulnerable, showing protracted delays in PCC-related connectivity and volume normalization into childhood. Resting-state fMRI studies indicate that by age 7, the PCC shows strengthened functional links with hippocampal networks within the DMN, supporting emerging episodic memory capabilities.^[47]^[48]^[43]

Functions

Memory and cognition

The posterior cingulate cortex (PCC) contributes to episodic memory by integrating spatial and contextual details through the hippocampal-PCC loop, which facilitates the binding of event-specific information for later recall. This circuit supports the construction of coherent autobiographical narratives by linking hippocampal representations of experiences with broader contextual associations processed in the PCC. Lesion and deep brain stimulation studies in humans reveal that disruptions to the PCC impair encoding and retrieval of episodic memories, leading to reduced accuracy and detail in autobiographical recall, as seen in cases where stimulation during encoding predicts subsequent memory deficits via altered hippocampal gamma oscillations. Damage to the PCC as part of the default mode network further disrupts autobiographical memory, resulting in fragmented or generic recollections rather than vivid, personal episodes. In spatial navigation, the PCC interacts with the retrosplenial cortex via dedicated pathways to process head-direction signals and enable landmark-based orientation. Primate studies demonstrate that macaque PCC neurons exhibit robust responses to vestibular self-motion cues, integrating them with visual landmarks to update spatial representations during active exploration. These projections from the retrosplenial cortex to the PCC and onward to parietal areas form a ventral stream for translating egocentric motion into allocentric maps, essential for route planning and topographic orientation in complex environments. The PCC modulates cognitive control by facilitating attention switching and suppressing task-unrelated thoughts, allowing redirection toward goal-relevant stimuli. Functional MRI evidence shows that reduced PCC activity correlates with enhanced performance in attention-shifting tasks, where suppression of default mode interference in the PCC promotes efficient cognitive set reconfiguration. During periods of mind-wandering, PCC activation increases with task-unrelated thought, but targeted downregulation via neurofeedback or task demands enables better control over attentional focus, as observed in paradigms requiring rapid shifts between cognitive demands. Regarding memory stages, the PCC displays distinct patterns in encoding versus retrieval, with greater BOLD signal responses during retrieval than encoding, reflecting its role in reconstructing past experiences. This "encoding/retrieval flip" involves parametric modulation of PCC activity by the subjective vividness of retrieved memories, where more detailed recollections elicit stronger activations, consistent with fMRI findings across multiple experiments. Meta-analyses of neuroimaging data up to 2024 confirm this asymmetry, highlighting the PCC's preferential engagement in retrieval processes that demand integrative reconstruction over initial consolidation.

Emotion and self-referential processing

The posterior cingulate cortex (PCC) plays a key role in processing emotional salience, particularly in response to negative stimuli. Functional magnetic resonance imaging (fMRI) studies demonstrate bilateral PCC activation during valence decision tasks involving emotional words, with greater activity for both positively and negatively valenced words compared to neutral ones, suggesting involvement in detecting emotional arousal rather than valence specificity.^[49] In individuals with major depressive disorder, heightened PCC activation during the encoding of negative pictures (versus neutral) predicts subsequent symptom worsening over 18 months, indicating its role in the consolidation of emotionally aversive material.^[50] The PCC also contributes to fear conditioning through its connectivity with the amygdala, forming part of broader networks that integrate contextual threat signals; for instance, structural and functional links between the cingulate cortex and amygdala support adaptive aversive learning by propagating prediction errors during threat acquisition.^[51] In self-referential processing, the PCC serves as a core node, facilitating mind-wandering and the construction of personal narratives. It shows increased activity during introspective tasks, such as evaluating trait adjectives for the self versus another person (e.g., "me" versus "U.S. President"), with fMRI revealing greater PCC engagement for self-judgments, potentially reflecting the evaluation of personal relevance or "getting caught up" in one's experiences.^[52] Meta-analyses of neuroimaging studies confirm robust PCC activation in self-referential paradigms compared to other-referential ones, underscoring its integration of autobiographical memory and self-concept formation.^[53] This function extends to everyday introspection, where PCC hyperactivity during self-focused rumination links to heightened emotional distress. The PCC supports empathy and theory of mind (ToM) through connections with the medial prefrontal cortex (mPFC), enabling perspective-taking and inference of others' mental states. Coordinate-based meta-analyses identify consistent bilateral PCC (including precuneus) activation in both cognitive ToM (abstract mental state inference) and affective ToM (emotional state understanding), often overlapping with mPFC in social cognition networks.^[54] In clinical contexts, such as Alzheimer's disease, PCC dysfunction—manifesting as hypometabolism and reduced connectivity with the hippocampus—correlates with deficits in self-empathy and awareness, contributing to anosognosia without isolated lesion data.^[55] Lesion studies broadly implicate cingulate regions in empathy impairments, with PCC involvement inferred from network disruptions affecting social inference.^[56] Regarding pain processing, the PCC exhibits hyperactivation in chronic pain states, reflecting altered sensory-emotional integration. Resting-state fMRI meta-analyses reveal increased PCC activity (in slow-5 frequency bands) and abnormal default mode network connectivity in chronic pain patients versus healthy controls, with PCC/precuneus alterations predicting pain intensity via machine learning models.^[57] Structural changes, such as reduced gray matter volume in the right PCC, occur in conditions like temporomandibular disorder, correlating with heightened pain sensitivity.^[58] Functionally, enhanced connectivity between the PCC and mPFC associates with pain rumination, while reduced PCC links to dorsolateral PFC and anterior cingulate cortex in low back pain improve post-treatment, suggesting a modulatory role in descending pain inhibition pathways.^[58] In remitted depression, energy landscape analyses of fMRI data show altered dynamics in states involving the default mode network (including PCC) and limbic regions (including amygdala), with increased transition frequencies and appearance rates of coupled states correlating with rumination severity.^[59] These findings, from 2025 studies, indicate bidirectional effective connectivity changes that perpetuate affective loops in major depressive disorder.^[60]

Default mode network and intrinsic activity

The default mode network (DMN) is a large-scale brain network active during periods of rest and introspection, with the posterior cingulate cortex (PCC) serving as its principal hub due to its extensive connectivity and central role in integrating network components.^[61] Key DMN components include the medial prefrontal cortex, angular gyrus, and inferior parietal lobule, which collectively support spontaneous cognition when external demands are low.^[62] The PCC facilitates communication across these subsystems, exhibiting anticorrelations with task-positive networks such as the dorsal attention network, which reflects a dynamic opposition between internal and external focus.^[63] Intrinsic activity in the PCC is characterized by elevated baseline metabolism, approximately 20% higher than the average cortical level, underscoring its role as a metabolically demanding hub even in the absence of tasks.^[64] This high metabolic rate supports the DMN's spontaneous fluctuations, as measured by seed-based functional connectivity MRI (fcMRI), where PCC anticorrelations with the dorsal attention network typically range from r = -0.3 to -0.5, indicating robust negative coupling during rest.^[65] Such patterns highlight the PCC's contribution to the brain's intrinsic organization, maintaining network coherence without external stimuli.^[66] As a task-negative region, the PCC exhibits consistent deactivation during focused attention on external goals, allowing resources to shift toward task-positive networks while enabling internal mentation such as mind-wandering.^[67] This deactivation supports the DMN's role in unconstrained thought processes, with the PCC's suppression correlating with enhanced performance in attention-demanding tasks.^[68] DMN dynamics involving the PCC show state-dependent fluctuations linked to arousal levels, with reduced arousal promoting stronger within-network connectivity and heightened anticorrelations with attention networks.^[69] Graph theory analyses reveal the PCC's high centrality in the DMN, with nodal degree metrics often exceeding 50 connections, positioning it as a critical integrator for network efficiency and information flow.^[70] Recent research using large-scale fMRI datasets has elucidated the developmental trajectory of DMN-PCC integration, showing that adult-like patterns emerge by late childhood, with progressive strengthening of anterior-posterior connectivity from early infancy onward.^[71] These findings, drawn from longitudinal studies, indicate that PCC maturation refines DMN coherence, stabilizing intrinsic activity patterns by adolescence.^[72]

Meditation and mindfulness

The posterior cingulate cortex (PCC) exhibits distinct activation patterns during different meditative practices. In focused attention meditation, where practitioners concentrate on a single object such as the breath, PCC activity typically decreases, reflecting reduced mind-wandering and default mode network (DMN) engagement.^[73] Conversely, open monitoring meditation, involving non-reactive awareness of thoughts and sensations, is associated with relatively increased PCC involvement or less pronounced deactivation compared to focused attention, facilitating broader attentional monitoring.^[74] Neurofeedback applications targeting the PCC have emerged as a tool to enhance mindfulness training. Real-time functional magnetic resonance imaging (fMRI) neurofeedback-augmented mindfulness training (NAMT) enables participants to voluntarily downregulate PCC activity, often achieving significant reductions in blood-oxygen-level-dependent (BOLD) signals during sessions focused on breath awareness. In 2025 studies involving adolescents, this approach led to notable BOLD decreases in the PCC (p < 0.001), correlating with reduced perceived stress and negative affect, particularly in those with early life adversity exposure.^[71] Long-term meditation practice induces structural changes in the PCC among expert practitioners. Longitudinal MRI studies of mindfulness-based programs demonstrate gray matter thickening in the PCC, with increases in density observed after 8 weeks of training compared to controls, who showed decreases. Cross-sectional comparisons of long-term meditators reveal enhanced PCC volume, supporting sustained neuroplasticity from regular practice.^[75] These effects arise through mechanisms that diminish DMN dominance during mindfulness, promoting decoupling from self-referential networks. By reducing PCC-driven rumination, meditation enhances present-moment awareness and attentional flexibility. Electroencephalography (EEG) evidence further supports this, showing increased alpha power during meditation sessions that correlates with PCC deactivation, as indicated by elevated coherence metrics in posterior regions. Recent 2025 reviews highlight these alpha oscillations as markers of reduced DMN activity and improved mindfulness states.^[76]

Clinical significance

Neurodegenerative disorders

The posterior cingulate cortex (PCC) exhibits early and prominent changes in Alzheimer's disease (AD), including hypometabolism detectable via fluorodeoxyglucose positron emission tomography (FDG-PET), which serves as a sensitive biomarker for disease onset. Studies have shown marked reductions in glucose metabolism in the PCC, with decreases of approximately 20-22% observed in very early stages compared to healthy controls, often preceding widespread cortical involvement. This hypometabolism correlates with cognitive impairment and is considered a hallmark of AD progression, reflecting disrupted energy metabolism in this region.^[77]^[78] Tau pathology in AD prominently affects the PCC, with neurofibrillary tangles accumulating in cortical layers such as III and V, contributing to neuronal dysfunction and synaptic loss. This laminar distribution of tau aggregates disrupts local circuitry and is associated with the region's vulnerability within the default mode network (DMN). Annual atrophy rates in the PCC for AD patients range from 2-5%, accelerating with disease stage and correlating with memory decline.^[79]^[80]^[81] Amyloid-beta deposition in the PCC is also significant in AD, showing high binding on Pittsburgh compound B PET (PiB-PET) imaging, particularly in the precuneus and posterior cingulate regions. Elevated amyloid levels in the PCC predict faster cognitive decline, with hazard ratios for progression to dementia around 3-4 in amyloid-positive mild cognitive impairment cases.^[82]^[83] In other tauopathies, the PCC displays variable involvement. Progressive supranuclear palsy features gliosis and tau accumulation in the PCC alongside subcortical structures, contributing to motor and cognitive symptoms. In contrast, frontotemporal dementia variants, such as behavioral variant FTD, relatively spare the PCC compared to AD, with pathology more concentrated in frontal and temporal lobes.^[84]^[85] Parkinson's disease shows milder PCC involvement, primarily linked to non-motor symptoms like apathy and cognitive fluctuations, potentially mediated by dopamine denervation effects extending to cortical regions. FDG-PET reveals subtle hypometabolism in the PCC in advanced stages, associated with default mode network alterations.^[86]^[87] Recent research as of 2025 highlights anti-tau therapies targeting PCC pathology, with phase II trials of monoclonal antibodies like posdinemab investigating effects on tau-positive AD patients. These interventions aim to halt tau spread within DMN hubs like the PCC and show promise in stabilizing cognitive function.^[88]^[89]

Psychiatric disorders

In major depressive disorder (MDD), the posterior cingulate cortex (PCC) demonstrates hyperconnectivity with the subgenual anterior cingulate cortex (sgACC), as evidenced by resting-state functional magnetic resonance imaging (rs-fMRI) studies showing abnormally elevated connectivity between these regions in depressed patients compared to healthy controls.^[90] This hyperconnectivity is linked to rumination, a core symptom of depression, with electroencephalography (EEG) analyses revealing increased PCC-sgACC connectivity in the beta-3 frequency band (r = 0.54, p = 0.022) that persists even in remitted patients and correlates positively with rumination scores after controlling for residual symptoms.^[91] In schizophrenia, structural imaging studies indicate reduced PCC volume, with gray matter deficits in the posterior cingulate gyrus amounting to approximately 14% compared to controls, contributing to overall cingulate abnormalities observed across patient cohorts.^[92] These volumetric reductions are associated with fragmentation of the default mode network (DMN), where impaired interactions among DMN subsystems diminish the PCC's central role in coordinating self-referential processing and attention, thereby disrupting self-monitoring functions essential for reality testing.^[93] Anxiety disorders feature heightened functional coupling between the amygdala and PCC, as demonstrated in resting-state fMRI where increased amygdala-PCC connectivity correlates with elevated anxious/depressed symptoms (Rho = 0.38, p = 0.02) and reduced social competence, potentially amplifying threat vigilance and emotional dysregulation.^[94] Accompanying these connectivity changes are GABAergic deficits in the PCC, with lower GABA concentrations predicting higher trait anxiety levels and reflecting inhibitory imbalances that may exacerbate anxiety-related hyperactivity in self-referential circuits. Bipolar disorder involves volumetric fluctuations in the PCC tied to mood states, with manic episodes accelerating cortical gray matter loss, including in cingulate regions, as longitudinal MRI data reveal progressive thinning linked to episode frequency and severity. Lithium treatment modulates PCC metabolism, increasing fractional amplitude of low-frequency fluctuations (fALFF) in this region post-administration, which normalizes DMN activity and supports mood stabilization through enhanced intrinsic functional dynamics.^[95] Recent investigations as of 2025 highlight aberrant dynamic connectivity involving the PCC in MDD with suicidal ideation, where transcranial magnetic stimulation-electroencephalography (TMS-EEG) reveals heightened effective connectivity metrics in the PCC (F(2,224) = 4.35, p = 0.02) among suicidal patients compared to non-suicidal counterparts and controls, underscoring its role in ideation severity within fronto-cingulate circuits.^[96]

Neurodevelopmental disorders

In autism spectrum disorder (ASD), structural alterations in the posterior cingulate cortex (PCC) are evident from early childhood, with toddlers exhibiting enlarged cortical surface area in this region as part of broader cerebral overgrowth patterns. Longitudinal MRI studies indicate that this surface area expansion in ASD toddlers, including the PCC, contributes to approximately 10-15% larger total brain volume compared to typically developing peers by age 2-3 years, driven primarily by accelerated surface area rather than thickness changes.^[97]^[98] Mendelian randomization analyses further support a causal link between ASD and increased PCC surface area, potentially disrupting typical developmental trajectories and contributing to social and cognitive deficits.^[99] Functionally, reduced default mode network (DMN) integrity involving the PCC is a hallmark of ASD, characterized by hypoconnectivity between the PCC and other DMN nodes like the medial prefrontal cortex, which impairs self-referential thought and social cognition.^[100]^[101] These DMN disruptions are observed across age groups and correlate with symptom severity, highlighting the PCC's role in the core neurodevelopmental pathophysiology of ASD.^[102] In attention-deficit/hyperactivity disorder (ADHD), the PCC shows delayed postnatal maturation, aligning with broader cortical delays observed in the disorder. Diffusion tensor imaging (DTI) studies reveal lower fractional anisotropy (FA) in the cingulum bundle, which connects to the PCC, indicating microstructural white matter immaturity that persists into adolescence and reflects delayed myelination and fiber organization.^[103] This reduced FA in the cingulum is associated with attention deficits, as the pathway supports executive control and DMN regulation.^[104] During attention tasks, individuals with ADHD exhibit hypoactivation in the PCC, part of DMN dysregulation where failure to suppress default mode activity interferes with task-focused cognition.^[105] These findings suggest that PCC-related delays contribute to the core attentional impairments in ADHD, with structural immaturity preceding functional deficits.^[106] Intellectual disability, particularly in genetic syndromes like Down syndrome caused by trisomy 21, involves PCC hypoplasia linked to disrupted neuronal migration during early brain development. Trisomy 21 impairs radial and tangential migration of cortical progenitors, leading to reduced PCC volume and surface area in affected individuals, as evidenced by morphometric MRI analyses showing dissociations in cortical folding and gray matter density.^[107]^[108] These structural changes result in hypometabolism in the PCC, further compounding cognitive delays by affecting memory encoding and spatial processing networks.^[109] In Down syndrome, the PCC's reduced size correlates with intellectual outcomes, underscoring trisomy 21's impact on cingulate development and its role in syndromic intellectual disability.^[110] Early-onset epilepsy frequently involves the PCC as a seizure focus, resulting in gliosis that alters local circuitry and hinders memory development. Stereo-EEG studies identify PCC origins in pediatric cingulate epilepsies, where seizures propagate via limbic pathways, leading to reactive gliosis detectable on FLAIR imaging in the posterior cingulate and adjacent regions.^[111]^[112] This gliosis disrupts PCC connectivity within the DMN, contributing to memory impairments such as reduced autobiographical recall, which is more pronounced with younger onset age and frequent seizures.^[113] In children, these PCC-focused epilepsies manifest as altered awareness seizures with autonomic features, and the resulting gliotic changes impede the typical maturation of memory-related functions reliant on the PCC.^[114]

Acquired brain injuries and other conditions

The posterior cingulate cortex (PCC) is vulnerable to damage from traumatic brain injury (TBI), particularly through diffuse axonal injury affecting the cingulum bundle, a key white matter tract connecting the PCC to medial temporal and prefrontal regions. Diffusion tensor imaging (DTI) studies have revealed decreased fractional anisotropy in the cingulum bundles bilaterally following TBI, indicating disrupted microstructural integrity and axonal damage that contributes to cognitive impairments.^[115] Such injuries often manifest in post-traumatic amnesia, where abnormal functional connectivity between the parahippocampal gyrus and PCC disrupts memory encoding and retrieval processes.^[116] Ischemic strokes in the posterior cerebral artery (PCA) territory can directly impair the PCC due to its vascular supply from PCA branches, leading to posteromedial cortical damage and associated amnestic syndromes characterized by episodic memory deficits.^[1] Recovery from such PCC involvement often involves neuroplastic mechanisms, including perilesional reorganization and shifts in functional connectivity within the default mode network, which support gradual restoration of cognitive functions over time.^[117] In chronic pain syndromes like fibromyalgia, the PCC exhibits hyperactivity as part of central sensitization, where amplified neural responses to nociceptive input heighten pain perception. Functional MRI (fMRI) studies demonstrate increased PCC activation during pain processing, correlating with self-referential aspects of pain catastrophizing and contributing to widespread hypersensitivity.^[118] Substance use disorders induce structural and metabolic alterations in the PCC. Chronic alcohol consumption leads to gray matter volume reductions in posterior cortical regions, including the PCC, reflecting atrophy linked to prolonged neurotoxicity and oxidative stress.^[119] In cocaine use disorder, positron emission tomography imaging shows decreased metabolic activity in the cingulate cortex, including the PCC, during cue-exposure tasks, which may underlie impaired inhibitory control and heightened craving.^[120] Emerging therapeutic approaches, such as repetitive transcranial magnetic stimulation (rTMS) targeting default mode network nodes like the PCC, have shown promise in TBI recovery by enhancing connectivity and yielding modest improvements in memory outcomes in randomized controlled trials.^[121]

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