#hippocampus — Public Fediverse posts

DATE: October 22, 2026 at 02:00PM
SOURCE: PSYPOST.ORG

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TITLE: Older adults with depression tend to have smaller volumes of a specific part of the hippocampus brain region

URL: https://www.psypost.org/older-adults-with-depression-tend-to-have-smaller-volumes-of-a-specific-part-of-the-hippocampus-brain-region/

An analysis of more than 2,000 cognitively healthy older adults found that those with depression tended to have a smaller volume in one part of the hippocampus, a brain region central to memory and one of the first affected by Alzheimer’s disease. The association did not appear to be explained by amyloid and tau, two proteins linked to Alzheimer’s disease. The paper was published in Translational Psychiatry.

Alzheimer’s disease is the most common form of dementia in older adults. It gradually disrupts memory, thinking, behavior, and everyday functioning. The disease is accompanied by characteristic changes in the brain, including abnormal clumps of amyloid protein, called plaques, and twisted strands of tau protein, called tangles, along with the loss of nerve cells.

Research suggests that depression may also play a role in the risk of Alzheimer’s disease. People who experience depression during their lifetime appear to have a higher risk of developing Alzheimer’s disease later on. One possible connection between the two conditions involves the hippocampus, which is central to memory and is among the first areas affected by Alzheimer’s disease.

Depression has likewise been associated with changes in the structure of the hippocampus, although previous studies have produced inconsistent findings. Part of the difficulty may be that the hippocampus is not a single uniform structure but consists of several smaller regions (called hippocampal subfields) that can be affected differently by depression and Alzheimer’s disease. Antidepressant medications may also play a role, as some evidence suggests that they could protect against hippocampal shrinkage, while other findings raise questions about their effects in older adults.

Study author Danielle Luu of the Stevens Neuroimaging and Informatics Institute at the University of Southern California and colleagues set out to examine how depression and antidepressant use relate to the volume of hippocampal subfields in older adults without cognitive problems. They also wanted to know whether Alzheimer’s-related factors, including amyloid and tau buildup and the APOE4 gene variant, which raises Alzheimer’s risk, play a role in these relationships.

The researchers considered two possibilities for antidepressants. The medications might be linked to larger subfield volumes by relieving depressive symptoms. Alternatively, they might be linked to smaller volumes, either because of unknown harmful effects on the brain or because doctors are more likely to prescribe them to people with more severe depression.

The researchers analyzed data from the Health and Aging Brain Study-Health Disparities, which recruited Hispanic, Black, and white older adults through the University of North Texas in Fort Worth. The analysis included 2,009 cognitively unimpaired adults between 50 and 90 years of age, with an average age of about 65.

Of these participants, 630 were classified as having depression, either because they scored 10 or higher on the Geriatric Depression Scale or because they reported having been diagnosed with depression by a health care provider. The remaining 1,379 participants were classified as not depressed.

Participants underwent high-resolution MRI scans of the hippocampus and reported whether they used antidepressant medications. The researchers used the scans to calculate volumes of three hippocampal subfields: the CA1, the subiculum, and a composite region that included the CA2, CA3, and the dentate gyrus (CA23DG). Subsets of participants also underwent PET scans measuring amyloid (684 people) and tau (386 people) in the brain.

Participants with depression tended to have a smaller CA23DG, but depression was not associated with the volume of the CA1 or the subiculum. The association was small and held after the researchers accounted for body mass index and physical activity, as well as tau levels and APOE4 status. When amyloid was added to the analysis, the association was no longer statistically significant, but its size was similar, which the authors attribute to the smaller number of participants with amyloid scans.

The severity of current depressive symptoms and the age at which depression began were not associated with the volume of any subfield. In exploratory analyses, the link between depression and smaller subfields appeared stronger in men than in women, but the authors interpret this cautiously because the formal test of a sex difference was not statistically significant.

Among participants with depression, those who used antidepressant medications tended to have smaller CA1 and CA23DG volumes than those who did not. These associations weakened to borderline levels after the researchers accounted for body mass index and physical activity. When antidepressant use and depression were included in the same analysis, the link between depression itself and a smaller CA23DG faded, while antidepressant use remained associated with a smaller CA23DG.

The authors suggest that the medication findings may reflect what is known as indication bias, meaning that people with more severe depression may be more likely to be prescribed medication in the first place. Antidepressant users reported fewer current depressive symptoms than non-users, suggesting the medications were relieving symptoms, but the researchers did not have information on how severe participants’ depression was before treatment or how long they had taken medication.

“It is important to study AD [Alzheimer’s disease] in the context of mental health, since rates of depression rise with age. Moreover, it is crucial to investigate how depression and antidepressant medication use affect the hippocampus, a region of the brain that is heavily impacted by AD. Understanding the relationship between depression and the development of AD is important for exploring preventative measures against brain atrophy and dementia,” study authors concluded.

The study contributes to the scientific understanding of the neural underpinnings of depression in older adults. However, it should be noted that the design of this study does not allow any causal inferences to be derived from the results. Depression diagnoses and medication use were self-reported rather than drawn from medical records, and the analyses involving amyloid and tau were based on smaller subsets of participants.

The researchers did not compare different types or doses of antidepressants. They note that the possibility that the medications themselves affect hippocampal structure should be tested in randomized controlled trials.

The paper, “Depression and hippocampal subfield volume in older adults,” was authored by Danielle Luu, Alicia M. Twisselmann, Victoria R. Tennant, Brandon J. Hall, Arjun Mahajan, Audrey Kim, Jamie Terner, Marylan L. Davison, Koral Wheeler, Christopher R. K. Ching, James Hall, Matthew T. Borzage, Leigh Johnson, Arthur W. Toga, Sid E. O’Bryant, Kristine Yaffe, and Meredith N. Braskie for the HABS-HD Study Team.

URL: https://www.psypost.org/older-adults-with-depression-tend-to-have-smaller-volumes-of-a-specific-part-of-the-hippocampus-brain-region/

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DATE: October 21, 2026 at 06:00AM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
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TITLE: Neuroscientists uncover brain clues to why some people with childhood trauma struggle to look forward to things

URL: https://www.psypost.org/neuroscientists-uncover-brain-clues-to-why-some-people-with-childhood-trauma-struggle-to-look-forward-to-things/

A new brain imaging study published in The Journal of Neuroscience indicates that the way a memory-related brain region communicates with the brain’s reward centers is linked to motivational difficulties in young adults with a history of childhood trauma. Among individuals who experienced higher levels of early life adversity, weaker activity and connectivity in the hippocampus were associated with a reduced ability to look forward to pleasurable experiences. These findings suggest that targeting memory and novelty-processing circuits could offer a new avenue for addressing motivational symptoms in trauma-exposed populations.

Anhedonia is a psychological condition defined by a reduced ability to experience pleasure or a lack of motivation to pursue rewarding activities. It is a common symptom across several mental health conditions, including major depression and schizophrenia. Psychologists typically divide anhedonia into two categories: consummatory anhedonia, the inability to feel pleasure in the moment while engaging in an enjoyable activity, and anticipatory anhedonia, a diminished capacity to feel excited about or motivated to pursue future rewards.

To understand the biological roots of anhedonia, neuroscientists often examine the mesolimbic dopamine system, a network of brain structures that release and respond to the chemical messenger dopamine to drive reward-seeking behavior. Two central hubs in this network are the ventral tegmental area, a cluster of dopamine-producing neurons in the midbrain near the top of the brainstem, and the nucleus accumbens, a deep forebrain structure within the ventral striatum that processes reward and motivation. For instance, a longitudinal study covered by PsyPost in 2015 found that adolescents who experienced emotional neglect in childhood showed a drop in ventral striatum activity when receiving rewards over a two-year period, which predicted an increase in depressive symptoms.

While human brain imaging studies of anhedonia have largely concentrated on the striatum, animal research points to the hippocampus as an upstream regulator of this reward network. The hippocampus is a seahorse-shaped structure tucked deep within the temporal lobe on each side of the brain. Although best known for forming and retrieving memories, it also acts as a novelty detector. When an organism encounters something unfamiliar, the hippocampus sends signals through a multi-step neural circuit to the ventral tegmental area and the nucleus accumbens, triggering dopamine release that encourages exploration and goal-directed action.

Because the hippocampus contains a dense concentration of receptors that bind to stress hormones like cortisol, exposure to childhood abuse or neglect can alter how this structure develops and functions. In humans, a 2026 brain-mapping preprint from members of the same research group, which has not yet been peer reviewed, reconstructed the physical nerve tracts connecting the hippocampus, ventral tegmental area, and nucleus accumbens, providing structural evidence that these regions form an integrated loop supporting adaptive behavior. A study covered by PsyPost in 2022 found that people with moderate to severe childhood trauma reported more social anhedonia, a reduced interest in social connection, alongside differences in brain structure.

The research team behind the new study, led by first author Kathleen J. O’Brien of Temple University and senior author Vishnu “Deepu” Murty of the University of Oregon’s Adaptive Memory Lab, wanted to test whether disruptions in hippocampal-reward communication interact with childhood trauma to explain why some people struggle with anhedonia.

“This study was motivated by a large animal literature that suggests that regions implicated in novelty processing, like the hippocampus, are critical for anhedonia, but characterization of this circuit had not been translated into the human literature,” Murty told PsyPost.

To investigate this question, the researchers recruited participants from the Philadelphia site of a broader project examining psychosis risk in young adults, ensuring the sample included a wide range of anhedonia severity. Out of 102 individuals who completed functional magnetic resonance imaging scans, the final sample included 92 participants with usable resting-state brain scans (37 males and 55 females) and 80 participants with usable task-based scans (34 males and 46 females). The participants ranged in age from 18 to 30 years old, with an average age of about 21.

Participants completed a modified version of the Childhood Trauma Questionnaire Short-Form, a self-report survey assessing experiences of emotional abuse, emotional neglect, and physical neglect before age 16. They also filled out the Temporal Experience of Pleasure Scale, which uses separate subscales to measure anticipatory pleasure and consummatory pleasure. Lower scores on these scales indicate higher levels of anhedonia.

Inside the magnetic resonance imaging scanner, which measures brain activity by detecting changes in blood flow, the researchers focused on the anterior hippocampus, the front third of the structure that connects most densely with reward circuits. First, participants underwent a 5.8-minute resting-state scan while looking at a cross on a screen. This allowed the scientists to measure baseline functional connectivity, meaning how closely activity in the anterior hippocampus synchronized with activity in the nucleus accumbens and ventral tegmental area while at rest.

Next, participants completed a target-detection task designed to measure how the brain responds to novelty and pursues goals. An hour before entering the scanner, participants had been familiarized with 80 outdoor scene photographs, viewing each one six times. Immediately prior to scanning and again inside the scanner, participants were shown a single specific target landscape. During the brain scan, participants watched a sequence of images flash on the screen for two seconds each and had to press a button every time the target landscape appeared.

Mixed in with the 40 target trials were the 80 familiar scenes and 80 completely new outdoor scenes the participants had never seen before. Using this setup, the researchers measured how strongly the anterior hippocampus activated in response to the novel images compared to the familiar ones. They also used a forward-prediction model to test whether heightened hippocampal activity during novel scenes predicted stronger activation in the ventral tegmental area when the target image appeared shortly afterward.

In their statistical analyses, the researchers controlled for participant age, as age was correlated with baseline connectivity between the hippocampus and the ventral tegmental area, and they verified in follow-up tests that accounting for psychosis-risk status did not change the outcomes. Across all four brain measures, the authors found no statistically significant links or trauma interactions related to consummatory anhedonia. In other words, hippocampal circuit function did not explain differences in the ability to enjoy pleasurable activities in the moment.

For anticipatory anhedonia, however, interactions emerged between childhood trauma and three of the four hippocampal circuit measures. Resting connectivity between the anterior hippocampus and the ventral tegmental area showed no such interaction. Among individuals with higher levels of childhood trauma (defined as one standard deviation above the sample average), weaker resting-state connectivity between the anterior hippocampus and the nucleus accumbens was associated with greater anticipatory anhedonia.

Similarly, in this high-trauma group, a blunted response in the anterior hippocampus when viewing novel scenes, as well as a weaker link between hippocampal responses to novel scenes and later activity in the ventral tegmental area during subsequent target detection, were both linked to worse anticipatory anhedonia. Among participants with lower levels of childhood trauma (one standard deviation below the average), these brain measures showed no statistically significant relationship with anticipatory pleasure.

To determine whether each of these neural measures contributed independently rather than reflecting the exact same underlying brain process, the scientists ran a machine-learning variable selection technique that removes redundant predictors and retains only the strongest ones. The resulting combined model accounted for 24 percent of the total variance in anticipatory anhedonia scores, or 20 percent after adjusting for the number of predictors in the model.

Even when evaluated simultaneously alongside overall trauma severity, both the interaction between trauma and resting hippocampus-accumbens connectivity and the interaction between trauma and task-based hippocampus-to-ventral-tegmental-area signaling remained independent predictors of anticipatory anhedonia. The interaction involving the hippocampus’s response to novel scenes was retained by the selection procedure but fell short of statistical significance in the final model, while higher trauma levels were themselves associated with greater anticipatory anhedonia.

The findings are in line with research covered by PsyPost in 2025, which found that chronic stress in mice weakened connections from the hippocampus to the nucleus accumbens and reduced reward-seeking, and that a single dose of ketamine restored both. That work examined stressed animals directly rather than brain scans and self-reported trauma in people. The authors suggest that when early life adversity coincides with weakened communication between the hippocampus and dopamine centers, the brain may struggle to use novel environmental cues to spark motivation and update expectations about future rewards.

“The average person should take away that early life stress may make you vulnerable to anhedonia, a lack of pleasure, but that engagement of circuits centered on novelty and exploration can minimize that risk,” Murty explained. “Sometimes there is a misinterpretation that these mesolimbic systems are just there for reward processing, but rather they are sensitive to motivation and behaviors like novelty, information seeking, and perhaps even curiosity.”

There are a few things to keep in mind when interpreting these results. Because the study is cross-sectional, meaning all data were collected at a single point in time, it cannot establish that childhood trauma or hippocampal alterations directly cause anhedonia. It is possible that preexisting differences in brain circuitry make certain individuals more sensitive to the emotional fallout of early stress, or that prolonged exposure to childhood stress gradually wears down hippocampal pathways over time. Longitudinal studies that track children and adolescents across development will be necessary to determine the exact sequence of events.

The study does have some other limitations. The researchers also did not test whether engaging these circuits, for instance through novel experiences, would actually lower anhedonia in people with a history of trauma. The trauma measure relied on young adults recalling their childhoods, and due to the online nature of the initial screening survey and ethical constraints regarding mandatory reporting without direct participant contact, the researchers excluded questions about physical and sexual abuse, meaning the findings specifically reflect emotional abuse and emotional or physical neglect.

In addition, the sample was drawn from a psychosis-risk study in which 22 participants met criteria for clinical high risk, so the results may differ in a general population of young adults, and replication in larger samples will be helpful given the modest statistical strength of the interaction findings.

The resting-state brain scans lasted just under six minutes, whereas recent neuroimaging standards suggest that longer scan times can yield more stable estimates of baseline brain connectivity. Future research could also expand beyond the hippocampus and midbrain to examine how other brain regions involved in emotion and decision-making, such as the amygdala and the prefrontal cortex, work together to influence motivation after early life stress.

Looking ahead, the research team plans to examine how these brain mechanisms connect to personal recall and everyday emotional life. “Our long-term goal is to try to understand how these findings relate to subjective experience of anhedonia, and how those might relate to memories of the past,” Murty noted.

The study, “Functional Integrity of Mesolimbic-Hippocampal Circuits Is Associated with Anhedonia in Individuals with Early Life Stress,” was authored by Kathleen J. O’Brien, Blake L. Elliott, Ian O’Shea, Jason Schiffman, Vijay A. Mittal, Lauren M. Ellman, and Vishnu P. Murty.

URL: https://www.psypost.org/neuroscientists-uncover-brain-clues-to-why-some-people-with-childhood-trauma-struggle-to-look-forward-to-things/

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