Does the risk of developing dementia increase with the number of episodes in patients with depressive disorder and in patients with bipolar disorder? J Neurol Neurosurg Psychiatry

Department of Psychiatry, Aarhus University, Aarhus, Central Jutland, Denmark
Journal of Neurology Neurosurgery & Psychiatry (Impact Factor: 6.81). 01/2005; 75(12):1662-6. DOI: 10.1136/jnnp.2003.031773
Source: PubMed


Several findings suggest that some patients with depressive or bipolar disorder may be at increased risk of developing dementia. The present study aimed to investigate whether the risk of developing dementia increases with the number of affective episodes in patients with depressive disorder and in patients with bipolar disorder.
This was a case register study including all hospital admissions with primary affective disorder in Denmark during 1970-99. The effect of the number of prior episodes leading to admission on the rate of readmission with a diagnosis of dementia following the first discharge after 1985 was estimated. A total of 18,726 patients with depressive disorder and 4248 patients with bipolar disorder were included in the study.
The rate of a diagnosis of dementia on readmission was significantly related to the number of prior affective episodes leading to admission. On average, the rate of dementia tended to increase 13% with every episode leading to admission for patients with depressive disorder and 6% with every episode leading to admission for patients with bipolar disorder, when adjusted for differences in age and sex.
On average, the risk of dementia seems to increase with the number of episodes in depressive and bipolar affective disorders.

Download full-text


Available from: Per K Andersen, Feb 28, 2014
  • Source
    • "Increases in recurrent episodes associate with decreases or loss of treatment response [62]. Given that a 2-3% decrement in some cognitive measures is associated with each depressive episode, accumulating detrimental effects are likely to occur in recurrent depression, with increased frequency of depressive episodes enhancing the risk of Alzheimer's disease [70]. Consequently, recurrent depression associates with a number of structural brain changes, including volume reductions in the hippocampus and basal ganglia, as well as in the orbitofrontal and subgenual prefrontal cortices [71]. "

    Full-text · Dataset · Aug 2015
  • Source
    • "According to the World Health Organization, major depression is the leading cause of disability worldwide and a major contributor to the global burden of disease [1]. A very harmful aspect of recurrent depression, both from an individual and a socioeconomic perspective , is that the cumulative exposure to depression is associated with the development of cognitive dysfunction in the euthymic state [2] [3], and an increased risk for out-right dementia [4] [5]. The cognitive deterioration occuring with each depressive episode may render the individual more susceptible to new episodes [6] [7]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Neuronal genotoxic insults from oxidative stress constitute a putative molecular link between stress and depression on the one hand, and cognitive dysfunction and dementia risk on the other. Oxidative modifications to DNA are repaired by specific enzymes; a process that plays a critical role for maintaining genomic integrity. The aim of the present study was to characterize the pattern of cerebral DNA repair enzyme regulation after stress through the quantification of a targeted range of gene products involved in different types of DNA repair. 72 male Sprague-Dawley rats were subjected to either restraint stress (6h/day) or daily handling (controls), and sacrificed after 1, 7 or 21 stress sessions. The mRNA expression of seven genes (Ogg1, Ape1, Ung1, Neil1, Xrcc1, Ercc1, Nudt1) involved in the repair of oxidatively damaged DNA was determined by quantitative real time polymerase chain reaction in the prefrontal cortex (PFC) and hippocampus (HC). DNA repair gene expression in PFC exhibited a general trend towards an induction after acute stress and a decrease after subchronic exposure compared to control animals. After chronic stress, a normalization towards control levels was observed. A similar pattern was seen in HC, but with overall smaller effects and without the induction after acute stress. Nuclear DNA damage from oxidation as measured by the comet assay was unaffected by stress in both regions. We conclude that psychological stress have a dynamic influence on brain DNA repair gene expression; however, since we were unable to identify concurrent changes in DNA damage from oxidation, the down-stream consequences of this regulation, if any, remains unclear. Copyright © 2014 Elsevier B.V. All rights reserved.
    Full-text · Article · Jan 2015 · Mutation Research/Genetic Toxicology and Environmental Mutagenesis
  • Source
    • "Interestingly, the risk for mild cognitive impairment (MCI) and dementia seems to be higher in bipolar patients (the same is true for MDD patients ) (Reischies and Neu 2000; Jorm 2001; Kessing and Nilsson 2003) and it continues to rise with the number of the disease? s past episodes (Kessing and Andersen 2004). Regarding the basis of cognitive functioning, evidence has been forthcoming in recent years of differences in brain structure between bipolar patients and healthy individuals, as well as changes over time in patients . "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cognitive impairment in patients with bipolar disorder (BD) is not restricted to symptomatic phases. It is also present in euthymia. There is evidence of differences in the brain's structure between bipolar patients and healthy individuals, as well as changes over time in patients. Lithium constitutes the gold standard in long-term prophylactic treatment. Appropriate therapy that prevents new episodes improves the disease's course and reduces the frequency of harmful outcomes. Interestingly, preclinical data suggest that lithium has a (additional) neuroprotective effect. There is limited data on its related effects in humans and even less on its long-term application. In this multi-center cross-sectional study from the International Group for the Study of Lithium-treated Patients (IGSLi), we compared three groups: bipolar patients without long-term lithium treatment (non-Li group; <3 months cumulative lithium exposure, ≥24 months ago), bipolar patients with long-term lithium treatment (Li group, ongoing treatment ≥24 months), and healthy subjects (controls). Strict inclusion and exclusion criteria were defined; the inclusion criteria for patients were diagnosis of BD types I or II, duration of illness ≥10 years, ≥5 episodes in patient's history and a euthymic mood state. Neurocognitive functioning was assessed using the Wechsler Adult Intelligence Scale-Revised (WAIS-R), the California Verbal Learning Test (CVLT), and a visual backward masking (VBM) task. A total of 142 subjects were included, 31 in the non-Li and 58 in the Li group, as well as 53 healthy controls. Treated patients with long-standing BD and controls did not differ significantly in overall cognitive functioning and verbal learning, recall, and recognition; regardless of whether lithium had been part of the treatment. Patients, however, demonstrated poorer early visual information processing than healthy controls, with the lithium-treated patients performing worse than those without. Our data suggest that bipolar patients with a long illness history and effective prophylactic treatment do not reveal significantly impaired general cognitive functioning or verbal learning and memory. However, they are worse at processing early visual information. Accompanying volumetric and spectroscopic data suggest cell loss in patients not treated with lithium that may be counterbalanced by long-term lithium treatment.
    Full-text · Article · Dec 2014
Show more