Intergenerational transmission of maternal and adolescent depressive symptoms: cross-sectional and cross-lagged panel network analysis

Abstract

Background

Maternal depressive symptoms are a well-documented risk factor for adolescent depression, yet the symptom-level mechanisms of intergenerational transmission remain insufficiently understood.

Methods

A total of 1140 mother–adolescent dyads completed the PHQ-9 at baseline (T1), with 921 dyads reassessed 6 months later (T2). Cross-lagged panel network analysis was applied to examine symptom-level stability, cross-symptom predictions, and intergenerational associations across time.

Results

The analysis revealed strong autoregressive effects for maternal sleep disturbance and adolescent suicidal ideation, indicating that these symptoms were particularly persistent over time. Within-group cross-symptom effects were also observed: adolescent suicidal ideation predicted later sad mood, anhedonia, and sleep problems, while maternal fatigue and guilt predicted subsequent anhedonia and appetite problems, and maternal psychomotor changes predicted later suicidal ideation. Intergenerational pathways were identified whereby maternal psychomotor symptoms at T1 predicted adolescent psychomotor symptoms at T2 (β = 0.11), and maternal depressed mood predicted adolescent sleep problems (β = 0.10), with a reverse pathway from adolescent guilt to maternal guilt (β = 0.08).

Conclusions

Depressive symptoms in mothers and adolescents are maintained through temporally stable and cross-activating symptoms within individuals, and transmitted across generations through specific symptom-to-symptom pathways. These findings refine theoretical understanding of how depressive symptoms persists and spreads in families and highlight key symptoms as promising targets for future research and preventive efforts.

Supplementary Information

The online version contains supplementary material available at 10.1186/s13034-026-01034-3.

Introduction

The high prevalence and substantial impact of depressive symptoms among adolescents have raised widespread concern worldwide [35]. The intergenerational transmission of depression model [18] posits that maternal depressive symptoms significantly increase offspring’s vulnerability to depressive symptoms through both genetic and environmental mechanisms. Although prior studies have provided some evidence for such intergenerational effects, most have examined depression at a broad syndrome level [12, 31], overlooking the heterogeneous symptoms and the dynamic ways in which symptoms are transmitted across generations. This gap limits our understanding of the specific symptom-to-symptom pathways through which maternal depressive symptoms may shape adolescent depressive outcomes, thereby underscoring the need for a symptom-level analytic approach. Guided by the intergenerational transmission of depression model [18], the present study employs cross-sectional and cross-lagged panel network analyses to identify core symptoms, assess their persistence and cross-symptom influences within each generation, and uncover intergenerational symptom-to-symptom pathways between mothers and adolescents.

The intergenerational transmission of depression

According to the model of intergenerational transmission of depression [18], maternal depressive symptoms significantly increase the risk of developing similar symptoms in the offspring [17, 53]. As the primary caregiver, a mother’s emotional state and mental health have a profound impact on her child’s emotional and psychological development [54]. Therefore, studying the intergenerational transmission of mother and adolescent depressive symptoms not only helps to understand this process but also provides theoretical support for developing more effective intervention strategies [18]. Moreover, the theory of emotional contagion offers a framework for understanding the intergenerational transmission of mother and adolescent depressive symptoms [1, 23]. From the perspective of emotional contagion theory, similar emotional states can be induced in a majority of people through their close social contacts [1, 23]. Hence, emotional contagion is more likely to take place among the frequently communicating and emotionally bonded family members and intimate friends [44]. Within Chinese families, mothers tend to take the main responsibility and contribute more time and energy to household caring [55]. Considering the extended duration of time spent with adolescents [51], mother’s emotional state can directly or indirectly influence her child’s emotional experiences and mental health through emotional communication and behavioral patterns [55]. Growing up in such a negative emotional environment, a child may imitate the mother’s emotional responses, leading to emotional instability or depressive symptoms [46]. Depressed mothers may exhibit inconsistent parenting behaviors, such as lack of support, or excessive criticism, all of which affect the child’s emotional regulation and depressive symptoms [41, 51]. Prolonged exposure to a negative family environment significantly heightens children’s vulnerability to developing negative self-evaluations and a pessimistic outlook on the future, both of which serve as key risk factors for the onset of depressive symptoms [14].

While numerous studies have demonstrated the intergenerational transmission of depressive symptoms from parents to offspring during infancy and childhood [20, 43], far less is known about whether these effects persist into adolescence—a developmental stage marked by heightened vulnerability to depressive symptoms. Challenging the sensitive window hypothesis, which designates infancy as the critical period, Dittmann et al. [9] showed that the intergenerational risk of maternal depressive symptoms is not confined to the postpartum years but intensifies when depressive symptoms persists into the preschool period, predicting children’s emotional and behavioral difficulties as well as elevated maternal abuse potential. These findings indicate that the impact of maternal depressive symptoms accumulates and becomes more pronounced over time [9], underscoring the need for research that extends beyond infancy and childhood. Building on this evidence, the present study investigates whether maternal depressive symptoms continue to shape adolescent depressive symptoms during this particularly vulnerable developmental stage.

Indeed, accumulating evidence indicates that parental depression contributes to the intergenerational transmission of depression risk in adolescence [12, 49]. For instance, maternal depressive symptoms has been linked to disrupted developmental trajectories of offspring reward processing, a key endophenotype of depressive symptoms, thereby conferring heightened vulnerability to depressive disorders [12]. Another study demonstrated bidirectional associations between parental and adolescent depressive symptoms [31], such that higher parental depressive symptoms predicted subsequent increases in adolescent depressive symptoms, and vice versa. These reciprocal effects were consistent across both parent- and youth-reports, suggesting robust intergenerational transmission [31]. Although parental rejection and low warmth were associated with youth depressive symptoms, they did not mediate these associations, indicating that the link primarily reflects direct reciprocal influences rather than indirect effects through parenting behaviors [31]. Therefore, examining the intergenerational transmission of depressive symptoms between parents and adolescents remains an important yet understudied issue.

Intergenerational symptom dynamics between mothers and adolescents

While some research has explored the impact of maternal depressive symptoms on adolescent depressive symptoms [31, 49], most studies have focused on traditional linear associations at the mean level, which overlook the specific pathways through which symptoms are transmitted between mothers and children. From a dynamic symptom network perspective [4], depressive symptoms are not isolated entities but are connected nodes that can mutually influence one another through reinforcing feedback mechanisms. Traditional variable-centered research paradigms thus fail to capture these complex symptom-to-symptom associations, limiting our understanding of the intergenerational transmission process and constraining the identification of effective intervention targets [19, 54].

Psychopathological network theory provides a new perspective for understanding maternal and adolescent depressive symptoms [5, 39]. In this framework, depressive symptoms are conceptualized as a complex network in which each node (symptom) is connected to others through edges (relationships), forming an interconnected system [4]. In contrast to traditional variable-centered approaches that primarily examine linear associations at the level of overall scores or symptom dimensions, network theory emphasizes that psychopathology emerges from dynamic symptom-to-symptom interactions, which can be direct, reciprocal, and embedded in broader feedback mechanisms [7, 26, 57].

Most previous research on depressive symptom networks, including studies using the PHQ-9, has primarily focused on the individual level. Only a few studies have adopted an intergenerational perspective to examine direct associations between maternal and adolescent symptoms over time. In terms of depressive symptom network among adolescents, one research [7] using network analysis found that “sad mood”, “irritability”, “worry too much”, and “guilty” were central symptoms in the network model of adolescents. In addition, the node of “guilty”, “sad mood”, and “suicide ideation” were bridge symptoms linking anxiety and depressive symptoms. A study using network analysis revealed that “sad mood” was the core symptoms within the depressive symptoms network and the edge between “anhedonia” and “sad mood” was the strongest positive edge in the anxiety and depressive symptoms community [35]. Another study using network analysis found that “lack of energy” was the most central depressive symptoms in the network during school time, while “guilty” was the most central depressive symptoms in the network during summer vacation [32]. Besides, one study [30], using symptom network approach found that the node strength of “motor” was differently between rural and urban adolescents, while there was no notable disparity in the global strength and structure of the network between the two groups. The network models in one recent study [57] revealed several core symptoms with high centrality indices among Chinese adolescents. Within the depressive symptom network, feeling down or hopeless (PHQ2), psychomotor retardation/restlessness (PHQ8), and suicidal ideation (PHQ9) consistently demonstrated the highest strength and closeness, indicating their central roles in the depressive structure. These findings suggest that suicidal ideation, hopelessness, and psychomotor symptoms represent core features of adolescent depressive symptoms, with their prominence varying by developmental stage and gender.

To date, only a few studies [26, 57] have explored the intercorrelated associations of depressive symptoms in PHQ-9 among mothers and adolescents. One recent study [26] employed a large-scale cross-sectional network analysis of depressive and anxiety symptoms in 8032 Chinese adolescent–parent dyads using PHQ-9 and GAD-7. The analysis revealed that nervousness was the most central symptom among adolescents, whereas fatigue was the most central symptom among parents and in the overall network. Importantly, parental fatigue and adolescents’ suicidal ideation emerged as critical bridge symptoms, linking parental and adolescent psychopathology. Another study [64], adopted the an 8-item version of the Center for Epidemiology Studies Depression Scale (CESD-8) to assess their depressive symptoms and utilized the longitudinal cross-lagged panel network (CLPN) analyses to explore the dynamic pathways through which depressive symptoms circulate within nuclear families. Drawing on three consecutive follow-up datasets, Zhang et al. [64]. found that mothers’ felt depressed symptoms consistently held the highest in-expected influence, indicating greater susceptibility to activation by other family members’ symptoms. Conversely, fathers’ felt depressed symptoms exhibited the highest and most stable out-expected influence, reflecting a sustained role in initiating symptom spread across the network. In addition, fathers’ everything an effort and mothers’ felt sad and everything an effort symptoms showed high levels of both in- and out-expected influence, suggesting they function as bidirectional conduits for depressive symptom transmission. These findings underscore the pivotal role of specific parental symptoms in shaping the longitudinal transmission of depressive symptoms within family systems.

The present study

Guided by the intergenerational transmission of depression model [18], this study applied dynamic network analysis to examine how maternal and adolescent depressive symptoms co-occur, persist, and are transmitted across time and generations. Cross-sectional network analysis was used to identify core and bridging symptoms, while cross-lagged panel networks revealed predictive symptom-to-symptom pathways. The aim was not merely methodological innovation, but to elucidate the mechanisms through which depressive symptoms are sustained within individuals and transmitted intergenerationally. This study contributes by adopting a dyadic, intergenerational framework, integrating both contemporaneous and longitudinal analyses, and grounding findings within a Chinese cultural context. Collectively, these features provide a culturally informed understanding of intergenerational depressive symptom transmission and highlight actionable targets for prevention and intervention.

Methods

Participants

The inclusion criteria for families in this study were: adolescents aged 10–18, attending grades 4–12, and mothers aged 30–60, consistent with China’s legal marriage age. Families were excluded if they were single-parent, divorced, or non-traditional in structure, including cases where one or both biological parents were absent, prolonged parental separation occurred due to divorce or abandonment, or adolescents lived apart from parents for extended periods. To ensure data completeness, the “Questionnaire Star” survey platform was configured to prevent the submission of incomplete responses, thereby eliminating missing data in recorded questionnaires. Partially completed or unsubmitted surveys were not recorded or included in the analysis. Each family was assigned an 8-digit ID, derived from the last four digits of each parent’s phone number, to link responses across measures. Invalid responses were excluded based on: (1) response times shorter than 600 s [52], (2) incorrect answers to quality-control items (e.g., selecting “4” when instructed otherwise), and (3) errors in the 8-digit ID (e.g., incorrect length or patterns like “00000000”). The final sample consisted of 921 mother–adolescent dyads, defined as those with valid data from mothers and adolescents at Time 1 (December 2023), along with repeated measures of adolescent data from mothers and adolescents collected at Time 2 (June 2024). Demographic details are presented in Table 1.

Table 1.

Demographic information of participants

Variables	Mothers		Adolescents
	N/M	%/SD	N/M	%/SD
Age	40.06	4.509	13.03	2.103
Gender
Male			414	45.0%
Female			507	55.0%
The only-child status
The only one child			439	47.7%
More than one child			482	52.3%
Educational level
Primary school	15	1.6%
Lower general secondary education	176	19.1%
Higher general secondary education	221	24.0%
Vocational education	253	27.5%
University education	256	27.8%

Procedure

Participants were recruited through a nationwide online initiative involving schools, counseling centers, and educational institutions. Teachers and school staff distributed the study invitation and online informed consent forms using platforms such as WeChat. The materials provided a clear explanation of the study’s purpose, procedures, and estimated time commitment. After obtaining informed consent, adolescents and their parents independently completed the online survey through Questionnaire Star, a secure online survey platform.

Ethical approval for the study was granted by the Ethics Committee of the first author’s institution. The informed consent forms emphasized data confidentiality, anonymity, and participants’ right to withdraw from the study at any time. No personally identifying information was collected. Participants were reminded of their rights, and families were invited to contact the research team if they had any questions or needed support.

The first wave of data collection took place in December 2023, during which valid responses were obtained from 1140 mother-adolescent dyads. A second wave was conducted in June 2024 and included mothers and adolescents from the original sample. A total of 921 mother-adolescent dyads completed the follow-up assessment, resulting in a follow-up rate of 80.8%.

Measures

Depressive symptoms

The Chinese version of the Patient Health Questionnaire-9 (PHQ-9) was utilized to evaluate the frequency of depressive symptoms over the past 2 weeks. Each item is rated on a four-point scale (0 = not at all, 3 = nearly every day). In the current study, we used the Chinese version of the PHQ-9, which has been well validated in Chinese populations, including adolescents [26, 34]. The Cronbach’s α for the PHQ-9 of mothers and adolescent at Time 1 were 0.903 and 0.880 in the current study. The Cronbach’s α for the PHQ-9 of mothers and adolescent at Time 1 were 0.913 and 0.950 in the current study.

Data analysis

The statistical analyses were conducted using R Studio. The preliminary analyses included an examination of the correlation between the key variables and testing for their normality of distribution. A series of network analyses were then performed, which entailed estimating contemporaneous networks for T1 and T2, and a temporal network from T1 to T2.

First, the R package bootnet was applied to construct the Gaussian Graphical Models (GGM) which examined the contemporaneous associations between different depressive symptoms among mothers and adolescents [10], . Network estimation was done using a penalty method that aims to minimize false-positive findings by eliminating potentially spurious associations, while producing a sparse network structure, namely, the least absolute shrinkage and selection operator (LASSO) regularization. With this method, the degree of the penalty is determined by the tuning parameter γ, which was chosen utilizing the Extended Bayesian Information Criterion (EBIC). The tuning parameter γ in this study was set to default (i.e., 0.5) to ensure a balance between sensitivity and specificity in the network estimation. Then the R package qgraph was used to visualize the network structures by drawing nodes (i.e., different depressive symptoms) and edges (i.e., the unique connection between two nodes, reflecting partial correlations between nodes after controlling for all other nodes [38]. To explicitly determine the core pathway linking maternal and adolescent depressive symptoms, we focused on bridge edge. To elucidate which symptom has the greatest association with nodes attaching to other symptoms, we estimated the bridge strength (i.e., the sum of the absolute weights of edges that cross symptoms).

Second, to explore the prospective and dynamic associations between maternal and adolescent depressive symptoms, a cross-lagged panel network from T1 to T2 was built using the R package glmnet. The cross-lagged panel network could test the effects of nodes at T1 on all other nodes at T2, adjusting for auto-regressive effects (i.e., regressing each node at T2 on itself at T1). The least absolute shrinkage and selection operator regularization with tenfold cross-validation approach was adopted to estimate a sparse network. Cross-lagged out-strength (i.e., the sum of the absolute weights of outgoing edges connected to a node) and in-strength (i.e., the sum of the absolute weights of incoming edges connected to a node) were calculated. Higher cross-lagged in-strength scores indicated that a specific node at T2 was affected to a greater degree by other nodes at T1. In contrast, lower cross-lagged out-strength scores suggested that a specific node at T1 had a more significant effect on other nodes at T2. Next, the R package qgraph was also used to plot the temporal network structure [11], . Finally, non-parametric and case-dropping bootstrapping methods implemented in the R package bootnet were used to assess the accuracy and stability of the parameter estimates of the network (i.e., edge weight, strength, bridge strength, out-strength, in-strength. The full code and data materials are available at: https://github.com/KongHN/Cross-sectional_and_cross-lagged_network_analysis. Narrow 95% confidence intervals (CIs) of edge weights indicated an accurate network; correlation stability coefficients (CS-coefficients) ≥ 0.25 represented an acceptable degree of stability, and ≥ 0.50 suggested a strong stability [10].

Results

Contemporaneous networks

Figure 1 illustrates the contemporaneous networks at two time points. Blue lines denote positive associations, whereas red lines indicate negative associations. Line thickness indicates the strength of connections. The number of non-zero edges in the T1 and T2 networks was 82 and 79 of all possible 153 edges. The mean edge weight was 0.051 and 0.055, and the density of the network structure was 0.54 and 0.52, respectively. As is shown in tables S1 and S2, within the adolescent depressive symptoms cluster, the strongest non-zero edges were sad mood–guilty (r = 0.32), anhedonia–energy (r = 0.32), and anhedonia–sad mood (r = 0.29) at T1, and concentration–motor (r = 0.42), anhedonia–sad mood (r = 0.34), and sad mood–energy (r = 0.29) at T2. Within the mother depressive symptoms cluster, the strongest non-zero edges were concentration–motor (r = 0.34), anhedonia–sad mood (r = 0.31), anhedonia–energy (r = 0.23) at T1, and motor–suicide ideation (r = 0.36), anhedonia–sad mood (r = 0.32), and anhedonia–energy (r = 0.30) at T2. Across mother and child clusters, the strongest non-zero edges were mother sad mood–sad mood (r = 0.07), mother concentration–child concentration (r = 0.06), mother energy–child energy (r = 0.05) at T1, and mother motor–child motor (r = 0.04), child anhedonia–mother sad mood (r = 0.03), and child appetite–mother anhedonia (r = 0.02) at T2. Sad Mood in adolescent depressive symptoms (EI = 1.16) had the largest node EI centrality at T1 and motor in maternal depressive symptoms (EI = 1.10) had the largest node EI centrality at T2 (see online Supplementary Table S3 for more details). Contemporaneous network metrics were high for edge weight (CS-coefficient_t1/t2 = 0.75) and EI (CS-coefficient_t1/t2 = 0.75), indicating a strong degree of stability and precision.

Fig. 1.

Contemporaneous networks at T1 and T2. MDS1–MDS9 denote maternal responses to the nine items of the PHQ-9 at the given time point. CMD1–CMD9 (or CDS1–CDS9, depending on the table) represent child responses to the corresponding PHQ-9 items. PHQ-9 items assess the following depressive symptoms: (1) Little interest or pleasure in doing things (anhedonia; loss of interest; lack of interest); (2) Feeling down, depressed, or hopeless (sad mood; depressed mood; feeling down; hopelessness); (3) Trouble falling or staying asleep, or sleeping too much (sleep disturbance; sleep problems; insomnia); (4) Feeling tired or having little energy (low energy; fatigue; tiredness); (5) Poor appetite or overeating (appetite problems; loss of appetite; eating problems); (6) Feeling bad about yourself—or that you are a failure or have let yourself or your family down (guilt; self-blame; worthlessness); (7) Trouble concentrating on things, such as reading or watching television (concentration problems; poor concentration; attention difficulties); (8) Moving or speaking slowly, or being unusually fidgety or restless (psychomotor symptoms; psychomotor retardation; motor symptoms; motor changes); (9) Thoughts that you would be better off dead, or thoughts of self-harm (suicidal ideation; suicide ideation; suicide thoughts; self-harm thoughts). For example, MDS1 reflects the mother’s report on Item 1 (anhedonia), while CDS9 reflects the child’s response to Item 9 (suicidal ideation)

Cross-lagged panel network results

Figure 2 displays the cross-lagged panel network results, with arrows indicating the temporal relationships between the nodes within and across constructs. Mother sleep (β = 0.35) and child suicide ideation (β = 0.35) were the nodes with the largest auto-regression coefficients (see online Supplementary Table S4 for more details). As is shown in Table S4, within the adolescent depressive symptoms cluster, the greatest edges were suicide ideation → sad mood (β = 0.23), suicide ideation → anhedonia (β = 0.21), and suicide ideation → sleep (β = 0.20). Within the maternal depressive symptoms cluster, the greatest edges were energy → anhedonia (β = 0.13), guilty → appetite (β = 0.12), and motor → suicide ideation (β = 0.11). The strongest cross-lagged bridge edges connecting maternal symptoms and adolescent symptoms were mother motor → child motor (β = 0.11), mother sad mood → child sleep (β = 0.10), and child guilty → mother guilty (β = 0.08). Furthermore, temporal network metric coefficients showed high stability and accuracy for edge weight (CS-coefficient = 0.283), in-EI (CS-coefficient = 0.283), and out-EI (CS-coefficient = 0.283).

Fig. 2.

Cross-lagged panel network from T1 to T2. For visualization, a beta threshold of 0.05 for the regression weights was chosen. Abbreviations in the figure are the same as those in Fig. 1

Discussion

This study employed cross-sectional and cross-lagged panel network analyses to examine the intergenerational transmission of depressive symptoms between mothers and adolescents. The findings indicate that maternal and adolescent symptoms are closely interconnected, supporting the notion of symptom-level transmission within families. By identifying core symptoms in both generations and mapping potential pathways of symptom progression, our results provide a more nuanced understanding of how depressive symptoms may be transmitted across time and generations.

The present study provides empirical support for the intergenerational transmission of depressive symptoms between parents and adolescents. Specifically, our findings demonstrate that maternal depressive symptoms continue to affect offspring well into adolescence, thereby challenging the “sensitive window” hypothesis that designates infancy as the primary period of vulnerability [9]. These converging findings underscore the cumulative nature of maternal depressive symptoms and the need to expand research beyond early childhood. Grounded in these findings, we underscore the need to consider adolescence—a period of heightened emotional vulnerability—as a critical window for understanding the ongoing influence of maternal depressive symptoms on offspring outcomes.

Some studies that employed methods other than network analysis [2, 29] have also provided evidence for the intergenerational transmission of depressive symptoms between parents and adolescents. For example, Ip et al. [29] showed that maternal depressive symptoms predicted children’s internalizing problems through mothers’ limited emotion regulation strategies, suggesting a pathway that may also underlie the intergenerational transmission of depressive symptoms into adolescence. Moreover, the intergenerational transmission of depressive symptoms may be understood through the lens of reward processing concordance [12]. As adolescence involves significant remodeling of reward-related neural circuits—such as the striatum and prefrontal cortex—maternal depressive symptoms may disrupt normative developmental trajectories, thereby altering adolescents’ reward responsiveness and contributing to the neurodevelopmental transmission of depression risk [12]. Another study [2] found that maternal early-onset depression (< 20 years) was associated with blunted reward processing in both mothers and their adolescent daughters (10–19 years), suggesting a potential neural mechanism underlying the intergenerational transmission of depressive symptoms during adolescence.

From the perspective of emotional contagion theory [47], previous studies have indicated a significant reciprocal contagion of emotional and psychological symptoms between mothers and children, particularly in the expression of depressive symptoms. According to emotional contagion theory [23, 47], emotional experiences within close relationships are easily transmitted between individuals. Maternal depressive symptoms may influence children through daily interactions, leading to emotional resonance and behavioral imitation [44, 49]. The mother’s sadness and lack of interest in activities may directly affect her child’s mood, causing the child to exhibit similar emotional withdrawal and sad mood [49]. Overall, our findings highlight the value of network approaches for uncovering symptom-to-symptom pathways across time and generations, and underscore the need for future studies to target parental depressive symptoms as a means of preventing and alleviating adolescent depression [19].

Core influential symptoms within mothers and adolescents

In contrast, maternal depressive symptoms in our study clustered around somatic dimensions, particularly sleep disturbances, low energy, and psychomotor problems. To some extent, this is similar to the previous finding [26] in a large-scale cross-sectional network analysis of depressive and anxiety symptoms in 8032 Chinese adolescent–parent dyads using PHQ-9 and GAD-7. In this study, fatigue was the most central symptom among parents and in the overall network [26]. These symptoms may reflect the multiple pressures mothers face from social expectations, work demands, and caregiving responsibilities [13, 48]. Somatic manifestations such as poor sleep, fatigue, and motor impairments not only reinforce one another—further intensifying mood deterioration and loss of motivation—but also create significant difficulties in emotion regulation and daily coping. In particular, sleep disturbances may play a pivotal role, as inadequate rest undermines physical health and weakens emotional regulation, compounding the psychological and physiological burden borne by mothers.

In the previous large-scale cross-sectional network [26], parental fatigue and adolescents’ suicidal ideation emerged as critical bridge symptoms linking parental and adolescent psychopathology. In our study, by contrast, the cross-generational links were relatively weak and primarily reflected concordance in specific symptoms, such as sadness, concentration, energy, and psychomotor problems, with additional child-to-mother associations (e.g., adolescent anhedonia with maternal sad mood). The cross-lagged panel network analysis, however, revealed significant autoregressive effects of maternal sleep disturbances and adolescent suicidal ideation within their respective networks. From the perspective of symptom maintenance mechanisms, these two core symptom nodes exhibit distinct self-reinforcing characteristics, suggesting that they may maintain and exacerbate the persistence of symptoms through a positive feedback loop [6]. Specifically, mother’s sleep disturbances may form a vicious cycle through mechanisms such as circadian rhythm dysregulation and impaired emotion regulation [21, 27]. Meanwhile, adolescent suicidal ideation may be self-reinforced through psychological processes like cognitive rumination and the accumulation of hopelessness [58]. Moreover, these two highly autoregressive symptom nodes may play a role as “central driving factors” within the broader psychopathological network, and their persistence could influence the stability of the entire network through symptom-symptom interactions [61]. This finding aligns with previous research discussing the central role of sleep disturbances in psychiatric networks and the transdiagnostic nature of suicidal ideation [3, 40], further emphasizing the importance of early identification and targeted treatment of these core symptom nodes in clinical interventions.

Our findings highlight adolescent suicidal ideation as both a temporally stable and dynamically influential symptom within the adolescent depressive symptom network. Specifically, suicidal ideation exhibited the strongest autoregressive pathway across the 6-month interval, underscoring its persistence and resistance to change over time. Beyond this stability, suicidal ideation also demonstrated robust cross-symptom predictive pathways, prospectively increasing the likelihood of subsequent sad mood, anhedonia, and sleep disturbance. Our findings aligned with prior evidence reported among Chinese adolescents [26, 57]. One recent study [57] revealed several core symptoms with high centrality indices among adolescents using cross-sectional network analysis. Within the depressive symptom network, feeling down or hopeless (PHQ-item 2), psychomotor retardation/restlessness (PHQ-item 8), and suicidal ideation (PHQ-item 9) consistently showed the highest strength and closeness, indicating their central roles in the depressive structure. Moreover, results from the cross-sectional network analysis of depressive symptoms in 8,032 Chinese adolescent–parent dyads revealed that parental fatigue and adolescent suicidal ideation served as key bridge symptoms [57], with the strongest link observed between parental and adolescent suicidal ideation. These results suggest that suicidal ideation functions as a central driver of symptom proliferation in adolescence, reinforcing not only its own chronicity but also catalyzing the activation of other core depressive symptoms. The emergence of suicidal ideation in adolescents is typically accompanied by severe cognitive distortions, such as self-denial and extreme pessimism about the future, which exacerbate emotional deterioration and may create a vicious cycle of symptoms [45]. Moreover, suicidal ideation in adolescents may not only represent an extreme manifestation of emotional distress but also reflect the immaturity of their emotion regulation mechanisms [42, 66]. From a clinical perspective, these findings emphasize the critical need for early detection and targeted intervention on suicidal thoughts in adolescents, as addressing this symptom may disrupt self-reinforcing cycles and mitigate the spread of depressive symptomatology across the broader network.

The depressive symptoms among mothers and adolescents may be closely tied to the Confucian cultures. Within Confucian, interdependence-oriented cultures such as China, emotional autonomy is often subordinated to relational harmony and filial obligations [16]. Traditional Chinese parenting values have been shown to prioritize parental authority and behavioral regulation over children’s internal needs and autonomy [28, 37, 60], a pattern that may implicitly discourage overt emotional autonomy and instead favor affective restraint. Within Chinese culture, some characteristics of parenting practices like “管”, such as parental strictness that Western children interpret as oppression and hostility, may be seen as attention and care [37, 57, 60]. For example, a recent study [57] revealed that Chinese parents commonly use psychological punishment, which, within the cultural context, is often interpreted not as hostility but as a form of responsibility and love expressed through strictness. For adolescents, such parenting may not immediately result in generalized depressive symptoms (like persistent low mood), but rather manifests as suicidal ideation [57], reflecting accumulated emotional suppression that erupts in more extreme expressions.

In Chinese familial contexts, emotional independence is often culturally discouraged, and adolescents are expected to suppress personal emotions and conform to family norms [16]. Within this cultural framework, expressing authentic feelings may be viewed not as healthy individuation but as disobedience or filial impiety [37]. As a result, adolescents tend to conceal rather than openly express distress, suppressing their emotions to maintain harmony and “save face” [60]. Over time, this suppression may not manifest through overt emotional expression but instead accumulate and erupt in more severe forms, most notably suicidal ideation [57].

Core intergenerational pathways linking maternal and adolescent symptoms

In the complex mechanisms of intergenerational transmission of mother and child depressive symptoms, we observed a cross-lagged connection between maternal and adolescent depressive symptoms, which was particularly prominent in domains such as motor impairments, mood and sleep disturbances, and feelings of guilt. Specifically, motor impairments in mothers not only affect the her own health but may also lead to a decrease in adolescents’ physical activity through reduced parent-adolescent interactions and modeling effects [15, 22]. Additionally, maternal sadness, under the influence of emotional contagion, may permeate adolescents’ daily life [51], disrupting their sleep quality [56]. According to emotional contagion theory, mirror neurons in the human brain are capable of mimicking and reproducing actions and emotional states performed by others [24]. When a mother exhibits sadness, the adolescent, through observation and imitation, activates the mirror neurons in their own brain, thereby “replicating” the mother’s sadness to some extent [33, 63]. It is important to note that this emotional transmission is not one-way: the adolescent’s expression of guilt may trigger the mother’s self-reflection and emotional resonance, leading her to experience similar feelings of self-blame or guilt [25]. This intertwined path of depressive symptom transmission offers new insights into the underlying mechanisms of emotional interactions between mothers and adolescents.

In interpreting the present findings, it is important to consider the role of cultural context in the intergenerational transmission of depressive symptoms within Chinese families. Chinese families are often guided by Confucian values, which emphasize hierarchy, obedience, and emotional restraint to promote social harmony [8, 37, 62]. In the Chinese cultural context, parenting is profoundly shaped by Confucian ideology, in which guan (管)—the act of governing and disciplining children—is regarded as a primary expression of parental love and responsibility [8, 37, 59, 60]. While culturally framed as care and responsibility, such parenting practices of “guan” (管) may implicitly promote obedience and emotional restraint over individual expression [37, 59]. These parenting practices are embedded within a broader face culture (mianzi wenhua, 面子文化), wherein children’s successes or failures are intimately tied to parental social standing [8]. Under this culture, Chinese families often emphasize behavioral regulation and emotional restraint as part of interpersonal discipline and socialization [37, 59]. As such, parents often resort to shame-based disciplinary strategies, such as social comparison [8] and psychological control [37], to motivate conformity to social expectations. For example, psychological control—often perceived negatively in Western contexts—may be interpreted as care or moral guidance in the Chinese setting [16], thereby diminishing the social value of emotional self-expression [60].

In Chinese families, parenting practices often emphasize modesty, compliance, and emotional restraint, fostering culturally shaped patterns of behavioral inhibition in adolescents [60]. Rooted in Confucian values, such restraint reflects broader norms of harmony, obedience, and social conformity [60]. Adolescents gradually internalize these expectations, leading to emotional suppression as a culturally embedded practice shaped by family dynamics and social norms [37, 59]. When combined with maternal emotional dysregulation, this suppression may heighten adolescents’ sensitivity to affective cues while limiting opportunities for emotional expression [60]. Consequently, youth may internalize maternal distress not through explicit communication but via attuned observation and psychological containment. This cultural dynamic can obscure early affective distress and facilitate intergenerational symptom transmission, often through somatization or behavioral substitution—for example, maternal sadness manifesting as adolescent sleep disturbance, or maternal psychomotor retardation mirrored in adolescents through similar somaticized symptoms.

In the Chinese cultural context, caregiving roles are traditionally gendered: mothers are primarily responsible for daily parenting and emotional management [50, 60], while fathers typically act as authority figures and behavioral regulators. As a result, mothers tend to engage in more frequent and emotionally intensive interactions with their children, making them more likely to employ psychologically controlling strategies to maintain closeness and compliance [16]. For instance, Chinese mothers may show concern or emotional involvement through behavioral control [36] or academic pressure [65], rather than verbal affirmation, which could differentially impact how adolescents internalize stress. In contrast to Western parenting that encourages emotional expression and autonomy, Chinese parent–child interactions may render certain symptoms—such as somatic complaints or sleep problems—more salient transmission pathways. In Chinese families, where direct emotional expression is often culturally discouraged, mothers and adolescents may resort to somatization to communicate psychological distress. These cultural considerations highlight the importance of examining symptom-level mechanisms within a sociocultural framework.

Implication

This study provides symptom-level insights into the intergenerational transmission of depressive symptoms between mothers and adolescents. By combining contemporaneous and cross-lagged panel network models, we were able to differentiate two complementary processes. First, regarding symptom persistence within individuals, maternal sleep disturbance and adolescent suicidal ideation displayed the strongest autoregressive effects across 6 months. These findings suggest that some symptoms function as particularly stable nodes in depressive networks, reinforcing themselves over time and contributing to the longitudinal maintenance of depressive symptoms within mothers and adolescents, respectively. From a clinical perspective, this highlights the value of early screening for persistent sleep problems in mothers and suicidal thoughts in adolescents, as stabilizing these symptoms may help to reduce the entrenchment of depressive patterns.

Second, regarding cross-generational transmission, specific directional pathways were identified linking maternal and adolescent symptoms. Maternal psychomotor disturbance predicted adolescent psychomotor disturbance, while maternal sad mood predicted adolescent sleep problems. These associations highlight that intergenerational transmission may operate through symptom-specific conduits rather than a generalized process of emotional contagion. This suggests that addressing maternal mood and behavioral symptoms may also yield indirect benefits for adolescents’ emotional and sleep regulation.

By clearly distinguishing symptom-level autoregressive effects from intergenerational cross-lagged associations, the present study advances theoretical understanding of how depressive symptoms is maintained and transmitted within families. The results indicate that depressive symptoms is sustained through temporally stable symptoms in individuals and simultaneously transmitted across generations through identifiable symptom bridges. Future prevention efforts may therefore consider targeting both persistent within-person symptoms and intergenerationally linked symptom pairs, while tailoring strategies to developmental and cultural contexts.

Limitations and future directions

Several limitations of the present study should be acknowledged. First, the reliance on self-report questionnaires (e.g., PHQ-9) may introduce measurement bias. Future investigations are encouraged to incorporate multi-informant approaches, behavioral observations, or physiological indicators to enhance the validity of assessment. Second, the sample was drawn exclusively from a single cultural context (China), which may constrain the generalizability of the findings. Cross-cultural replication efforts are therefore warranted. Third, although the 6-month follow-up enabled longitudinal modeling, the limited number of assessment time points restricted the capacity to capture more nuanced temporal dynamics. Future research employing intensive longitudinal designs, such as ecological momentary assessment, could offer more granular insights into within-person symptom fluctuations.

Fourth, while the application of cross-lagged panel network models allows for the exploration of temporal symptom-to-symptom associations, these models do not permit causal inference. Integrating experimental, genetically informed, or intervention-based methodologies would provide a more robust basis for causal conclusions. Fifth, the study did not control for several important potential confounding variables, including family income, parental psychiatric history, exposure to trauma, and neurodevelopmental or psychiatric comorbidities—factors known to influence the emergence and course of adolescent depressive symptoms. Accounting for such covariates in future research would improve the precision of model estimates and help delineate the unique contributions of intergenerational and symptom-level processes.

Finally, families characterized by single motherhood or paternal absence were excluded in order to maintain structural consistency across participants. While this approach enabled a more focused analysis of intact two-parent households, it limits the generalizability of the findings to diverse family configurations. The omission of non-traditional family structures precludes examination of how paternal absence or variation in paternal involvement may influence adolescent mental health outcomes. Future studies should explicitly incorporate diverse family constellations to better reflect contemporary societal realities and to capture a broader range of developmental contexts.

Despite these limitations, the present findings underscore the utility of network-based methodologies in advancing our understanding of symptom-level mechanisms underlying intergenerational transmission of depression. They also highlight the value of future research integrating diverse samples, comprehensive covariates, and multimethod designs to advance the field.

Conclusion

This study revealed longitudinal processes underlying the intergenerational transmission of depressive symptoms. Cross-lagged panel network analysis showed strong autoregressive effects for maternal sleep disturbance and adolescent suicidal ideation, indicating that these symptoms are particularly persistent over time. Within-group cross-symptom predictions were also observed, such that adolescent suicidal ideation predicted subsequent increases in sad mood, anhedonia, and sleep problems, while maternal fatigue predicted later anhedonia, maternal guilt predicted appetite problems, and maternal psychomotor changes predicted later suicidal ideation. Importantly, intergenerational pathways were identified whereby maternal psychomotor symptoms predicted adolescent psychomotor symptoms and maternal sad mood predicted adolescent sleep problems, with a reverse pathway also evident from adolescent guilt to maternal guilt. Together, these findings highlight that depressive symptoms are maintained through both symptom persistence and cross-symptom activation within individuals, and transmitted across generations through specific symptom-to-symptom pathways.

Supplementary Information

Below is the link to the electronic supplementary material.

Author contributions

All authors contributed to the conception and design of the study. Yizhen Ren prepared the study materials and collected the data. Haonan Kong conducted the data curation and analysis. Yizhen Ren and Zheng Zhang drafted the initial manuscript. Yangang Nie and Kaisheng Xie critically reviewed and revised the manuscript. All authors read and approved the final version.

Funding

This study was funded by the research projects of Humanities and Social Sciences Youth Foundation of Ministry of Education of China (25YJC190019).

Data availability

No datasets were generated or analysed during the current study. The work described is original research that has not been published previously and is not under consideration for publication elsewhere, in whole or in part.

Declarations

Ethics approval and consent to participate

Approval was obtained from the ethics committee of Ethics Review Committee of Education School, Guangzhou University (No. GUANGZHUSE2024045). The procedures used in this study adhere to the tenets of the Declaration of Helsinki.

Competing interests

The authors declare no competing interests.