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The concept of “biological ageing” or “premature senescence” in relation to psychiatric diseases originally arose from the evidence that severe mental diseases (such as Major Depressive Disorder, Schizophrenia, Bipolar Disorder, or Post-Traumatic Stress Disorder) are associated with early mortality and with increased risk of developing certain senescence-associated medical comorbidities. Over the last years the research on the field has been stimulated by studies exploring the role of molecular underpinnings of senescence, i.e. molecular pathways at the peripheral and central level which are thought to have a causal role in, or to reflect, the ageing processes, in mental diseases. In the present symposium recent developments on the topic emerging from clinical and preclinical data will be presented and critically discussed.
W0081 - Chronological and Biological Age: Why Relevant for Psychiatrists?
Introduction: Depression is the mental disorder with the largest disease burden impact. That is due to its high prevalence, chronicty, early onset but also due to its impact on various aging-related somatic morbidities and mortality. This talk will describes to what extent depression characteristics are related to chronologial and biological aging patterns.
Methods: Data will be shown from the Netherlands Study of Depression and Anxiety (NESDA, www.nesda.nl). In this study, a large cohort of over 3000 individuals (18-65 years), among which over 1200 with a DSM-based major depressive disorder (MDD), are now followed for 9 years. The association between depression characteristics and chronological and biological age will be described. Biological age was determined at various biological system-levels, including telomere length, epigenetics, transcriptomics, metabolomics and proteomics.
Results: Older persons with a current MDD do not differ in overall disease severity as compared to younger persons with a current MDD. However, older depressed persons do differ in the types of symptoms they experience (more neurovegetative, somatic symptoms and less mood symptoms) and in their chronic course (with twice more chronicity in the oldest depressed persons compare to the younges depressed persons). At all biological system-levels, there was evidence for more advaned biological aging among persons with depression. This was not differential across chronological age groups.
Discussion: Findings suggest that depression characteristics are linked to both chronological and biological age. It will be discussed what this could mean for clinical practice and intervention.
W0082 - The Opportunities and Obstacles of Studying Telomere Length as a Biological Aging Marker in Psychiatry
Aging can be described as the life-long accumulation of damage to the tissues, cells, and molecules of the body. One of the most widely used markers to study biological aging is telomere length. Telomeres are non-coding DNA structures located at the ends of chromosomes that become progressively shorter with age. Research in the past decade showed that persons with psychiatric disorders such as major depressive disorder, anxiety disorder or posttraumatic stress disorder on average have shorter telomeres, which might help explain the high levels of somatic morbidity in these patients. While telomere length is an elegant aging biomarker, reflecting a biological process in most living species, there are also some challenges. In human studies, the between-person variation is large and shortened telomeres showed not to be specific to psychiatric diagnosis but rather to a multitude of psychological and physiological stressors. Telomere length might therefore not be a diagnostic marker. It could, nonetheless, be an interesting target for pharmacological, psychological or exercise treatment. If persons with psychiatric disorders age biologically faster, to what extend can this be process be halted or even reversed with successful treatment? Other opportunities and obstacles of studying telomere length as a biological aging marker in psychiatry will be discussed in this session.
W0083 - Accelerated Epigenetic Aging in Depression and Post-traumatic Stress Disorder
Abstract BodyMajor depressive disorder (MDD) and post-traumatic stress disorder (PTSD) are two serious mental illnesses that are associated with excessive physical morbidity and with an earlier average age at death, even after accounting for lifestyle factors and suicide. The medical conditions with higher prevalence in these disorders are generally those that are more commonly seen in older individuals, such as cardiovascular disease and others. This raises the possibility that these disorders are not only “mental illnesses,” but that they may be accompanied by core somatic pathology. Indeed, these illnesses may be characterized by an accelerated biological aging process at the cellular level. Consistent with this, previous studies in these illnesses often found accelerated telomere shortening, one form of accelerated cell aging. A newer measure of biological aging, that provides superior correspondence with disease and mortality rates, is “epigenetic aging.” As individuals age, certain highly predictable locations (CpG sites) in the DNA become sequentially methylated, altering gene transcription and protein translation. The rate at which these site-specific epigenetic changes occur, is often characterized by “epigenetic clocks,” which are among the best current measures of biological aging. In our studies in PTSD and in MDD we found significantly accelerated epigenetic aging using two separate epigenetic clocks: accelerated “Horvath clock” aging in PTSD and accelerated “GrimAge clock” aging in MDD. These findings complement those with telomere length in supporting accelerated biological/ cellular aging in these two conditions. It remains unknown whether these cellular changes contribute to the increased somatic morbidity and mortality, or whether they are merely correlational. Nonetheless, these findings may add to our understanding of MDD and PTSD pathophysiology and may suggest novel treatments for the psychiatric symptoms as well as their somatic comorbidities.
W0084 - Treatment Implications of Cellular Aging-associated Biology for Psychiatric Conditions
W0085 - Brain Aging in Major Depressive Disorder
Depression and anxiety are common and often comorbid mental health disorders that represent risk factors for aging-related conditions. Brain aging has shown to be more advanced in patients with Major Depressive Disorder (MDD). Here, we extend prior work by investigating multivariate brain aging in patients with MDD and/or anxiety disorders and examine which factors contribute to older appearing brains. Adults aged 18-57 years from the Netherlands Study of Depression and Anxiety underwent structural MRI. A pre-trained brain age prediction model based on >2,000 samples from the ENIGMA consortium was applied to obtain brain-predicted age differences (brain-PAD, predicted brain age minus chronological age) in 65 controls and 220 patients with current MDD and/or anxiety. Brain-PAD estimates were associated with clinical, somatic, lifestyle, and biological factors. After correcting for antidepressant use, brain-PAD was significantly higher in MDD (+2.78 years, Cohen’s d=0.25, 95% CI -0.10-0.60) and anxiety patients (+2.91 years, Cohen’s d=0.27, 95% CI -0.08-0.61), compared to controls. There were no significant associations with lifestyle or biological stress systems. A multivariable model indicated unique contributions of higher severity of somatic depression symptoms (b=4.21 years per unit increase on average sum score) and antidepressant use (-2.53 years) to brain-PAD. Advanced brain aging in patients with MDD and anxiety was most strongly associated with somatic depressive symptomatology. We also present clinically relevant evidence for a potential neuroprotective antidepressant effect on the brain-PAD metric that requires follow-up in future research.
W0086 - Frailty Index as a Clinical Measure of Biological Age in Psychiatry
The concepts of “accelerated biological ageing” and “premature biological senescence” have been receiving increasing attention in relation to psychiatric diseases, with clinical, epidemiological and molecular observations suggesting that psychopathological processes can have significant relationships with aging-related phenomena. The deficit accumulation model postulates that the individual’s biological age and functional status is related to the amount of health deficits accumulated over time and that one’s biological age can be estimated by summarizing health deficits in a single continuous variable, the so-called “frailty index” (FI). In this presentation it will be discussed the possibility that the FI, which condenses information arising from multidimensional evaluations, represents a potential clinically-useful macroscopic indicator of biological age which can add relevant information to the measurements currently implemented in the study of accelerated biological age in psychiatric diseases.