Depressive Symptoms In Dementia Research Articles

Ayurvedic Management of Alzheimer’s Dementia with Depressive Symptoms - A Case Study

Dementia is a syndrome due to degeneration of the cerebral cortex, usually of a chronic or progressive nature, in which there is disturbance of multiple higher cortical functions, including memory, thinking, orientation, calculation, comprehension, capacity to learn, language skills and judgment. Alzheimer’s dementia, Frontotemporal dementia, dementia with lewy bodies, vascular dementia, Huntington’s dementia and Parkinson dementia are the types of dementia. Alzheimer’s dementia is the most common one among the category. The prevalence of depressive symptoms in dementia is 30% and is presented with symptoms such as poor appetite, sleep perversions and social withdrawal. Features of Smrti vibhrama and characteristics of Pranavrta vyana are being observed Alzheimer’s dementia. There is still no effective cure for dementia in contemporary medicine. So, developing an Ayurvedic protocol to treat dementia is a necessity. This is the case of a 72-year-old male presented with loss of interest in daily activities, fatigue, reduced appetite and increased sleep for duration of 7 months and underwent treatment for 1 month. Diagnosis was done based on the criteria in DSM 5 and the severity was assessed by Mini- mental status Examination and Hamilton’s Depression Scale. The management was a combination of modalities including Deepana, Pacana, Virecana, Nasya and follow-up of 1 month. The treatment modalities were found to be effective in the cognitive and depressive symptoms as well as improving the social behaviour in dementia patient.

Characterization of Depressive Symptoms in Dementia and Examination of Possible Risk Factors.

Depression in individuals with Alzheimer's disease (AD) is common, distressing, difficult to treat, and inadequately understood. It occurs more frequently in AD than in older adults without dementia. The reasons why some patients develop depression during AD and others do not remain obscure. We aimed to characterize depression in AD and to identify risk factors. We used data from three large dementia focused cohorts: ADNI (n = 665 with AD, 669 normal cognition), NACC (n = 698 with AD, 711 normal cognition), and BDR (n = 757 with AD). Depression ratings were available using the GDS and NPI and in addition for BDR the Cornell. A cut-off of≥8 was used for the GDS and the Cornell Scale for Depression in Dementia,≥6 for the NPI depression sub-scale, and≥2 for the NPI-Q depression sub-scale. We used logistic regression to examine potential risk factors and random effects meta-analysis and an interaction term to look for interactions between each risk factor and the presence of cognitive impairment. In individual studies there was no evidence of a difference in risk factors for depressive symptoms in AD. In the meta-analysis the only risk factor which increased the risk of depressive symptoms in AD was previous depression, but information on this was only available from one study (OR 7.78 95% CI 4.03-15.03). Risk factors for depression in AD appear to differ to those for depression per se supporting suggestions of a different pathological process, although a past history of depression was the strongest individual risk factor.

A data-driven examination of apathy and depressive symptoms in dementia with independent replication.

We found four classes: no symptoms, apathy, depression and apathy/depression.Apathy conferred a higher probability for agitation.Apathy diagnostic criteria should include accompanying neuropsychiatric symptoms.

Non‐medication treatments effective for depressive symptoms in dementia

Non‐medication treatments effective for depressive symptoms in dementia

Nonpharmacological or Pharmacological Treatments for Depressive Symptoms in Dementia

Nonpharmacological and pharmacological strategies can be used to manage depressive symptoms in people with dementia, though few studies have compared

Sulforaphane Reverses the Amyloid-β Oligomers Induced Depressive-Like Behavior.

Depression is one of the most common behavioral and psychological symptoms in people with Alzheimer's disease (AD). To date, however, the molecular mechanisms underlying the clinical association between depression and AD remained elusive. Here, we study the relationship between memory impairment and depressive-like behavior in AD animal model, and investigate the potential mechanisms. Male SD rats were administered amyloid-β oligomers (AβOs) by intracerebroventricular injection, and then the depressive-like behavior, neuroinflammation, oxidative stress, and the serotonergic system were measured in the brain. Sulforaphane (SF), a compound with dual capacities of anti-inflammation and anti-oxidative stress, was injected intraperitoneally to evaluate the therapeutic effect. The results showed that AβOs induced both memory impairment and depressive-like behavior in rats, through the mechanisms of inducing neuroinflammation and oxidative stress, and impairing the serotonergic axis. SF could reduce both inflammatory factors and oxidative stress parameters to protect the serotonergic system and alleviate memory impairment and depressive-like behavior in rats. These results provided insights into the biological mechanisms underlying the clinical link between depressive disorder and AD, and offered new drug options for the treatment of depressive symptoms in dementia.

Management of Late-Life Depression in the Context of Cognitive Impairment: a Review of the Recent Literature.

Evidence regarding the treatment of late-life depression is not necessarily generalizable to persons with a neurocognitive disorder and comorbid depression. Thus, this article reviews recent evidence that pertains to the treatment of depression in older adults with neurocognitive disorders, and synthesizes and critically analyzes this literature to identify methodological issues and gaps for the purpose of future research. Controlled trials and meta-analyses examining depression treatment in neurocognitive disorders, published between 2015 and 2019 (N = 16 reports), can be divided into those addressing pharmacotherapy, psychological and behavioral therapy, and somatic therapy. The evidence generally does not support benefit of antidepressant medication over placebo in treating depressive disorders in dementia. No pharmacological studies since 2015 have examined antidepressant medication in participants with mild cognitive impairment (MCI). Problem adaptation therapy demonstrates efficacy for depression in MCI and mild dementia. Other psychological and behavioral interventions for depressive symptoms in dementia demonstrate mixed findings. The only somatic treatment trials published since 2015 have assessed bright light therapy, with positive findings but methodological limitations. Psychological, behavioral, and somatic treatments represent promising treatment options for depression in neurocognitive disorders, but further studies are needed, particularly in participants with depressive disorders rather than subclinical depressive symptoms. Little is known about the treatment of depression in patients with MCI, and rigorous identification of MCI in late-life depression treatment trials will help to advance knowledge in this area. Addressing methodological issues, particularly the diagnosis and measurement of clinically significant depression in dementia, will help to move the field forward.

Assessing depression in Greek dementia patients: Which scale to use?

Depression in dementia is known to deteriorate patients' cognitive function and Quality of Life and to increase the burden of care. Although detecting depression in dementia is crucial, there is no gold standard for its screening and diagnosis. We examined the psychometric properties of 3 different scales in detecting depression in dementia. Results will be useful as community services for dementia in the country are developing and the need for reliable detection of depression in dementia patients is urgent. Our sample consisted of 136 Greek dementia patients who consulted a memory clinic. For the diagnosis of depression, DSM-IV criteria for major depression and 3 different depression measures were used: a self-assessment scale (Geriatric Depression Scale; GDS), a caregiver assessment scale (Neuropsychiatric Inventory-Depression; NPI-D) and a clinician rated scale (Cornell Scale for Depression in Dementia; CSDD). For the evaluation of the screening performance of the three depression scales receiver operating characteristic curve (ROC) analysis was applied. The DSMIV criteria served as the gold standard method for the diagnosis of major depression. CSDD showed the best psychometric properties for the diagnosis of depression in dementia. The ROC curve analysis revealed that among the three measures, the CSDD had the wider AUC (0.919), second in the width of the AUC was the GDS (0.871), and last was the NPI-D (0.812). The prevalence of depression ranged from 18.4% according to DSM-IV criteria to 42.6% using the NPI-D. Using the GDS (cut off point: 7/8) and the CSDD (cut off point: 6/7), depression was present in 26.9% and 33.1% of the patients, respectively. Correlations between scales used were significant (r from 0.432 to 0.660; p<0.001). Caregivers tend to report more depressive symptoms in dementia compared to patients' and clinicians' ratings. CSDD should be used in specialized centers, but GDS may be an alternative in patients able to complete the assessment. The need to establish valid criteria for the diagnosis of depression in dementia is urgent.

Management of Depression in Patients with Dementia: Is Pharmacological Treatment Justified?

Depression in the context of dementia is common and contributes to poorer outcomes in individuals and those who care for them. Non-pharmacological treatments are the preferred initial approach to managing these symptoms but data in support of these are scarce. There are a number of pharmacological treatment options available to clinicians but efficacy is uncertain and concern about potential side effects in an aging and vulnerable population needs to be taken into consideration. This review aims to provide a concise overview of pharmacological treatments for depression in dementia. Antidepressants are the mainstay of pharmacological treatment for clinically significant depression in the general population but evidence to support their use in dementia is mixed. Trials of antidepressants should generally be reserved for individuals with depression where the symptoms are distressing and surpass the threshold for major depression. Acetylcholinesterase inhibitors and memantine are effective in the symptomatic treatment of Alzheimer's disease but current evidence does not support their use to treat depressive symptoms in dementia. Similarly, antipsychotics and mood stabilizers have no proven efficacy for depression and the risk of adverse effects seems to outweigh any potential benefit. Pain can be a frequent problem in dementia and may have significant effects on behavior and mood. Preliminary evidence supports a role of adequate analgesia in improving mood in people with dementia.

Treating Depression in Older Adults with Dementia

Treating Depression in Older Adults with Dementia

Galantamine in the Treatment of Minor Depression With Mild to Moderate Alzheimer’s Dementia in an Elderly Woman

To the Editor: Depression is present in about 20%–40% of dementia patients; 15%–50% of Alzheimer's dementia patients have depression.1,2 Depression is common in the early stages of the disease and remains fairly constant through most stages of Alzheimer's dementia.3 Depression exacerbates the cognitive deficits of the preexisting dementia. In Alzheimer's dementia, mild to moderate depression may also manifest as new onset of agitation, wandering, apathy, insomnia, or change in functional status. Depressive symptoms in dementia should be viewed as a cause of significant and treatable “excess disability.”4 Case report. Ms A, an 80-year-old woman, presented with a 2-year history of cognitive decline and an 8-month history of minor depression. Depression features included low mood with decreased interest in social activities, being less energetic, psychomotor slowing, and being more withdrawn and lonely. Sleep and appetite were good. She met only 3 of the 9 features of the DSM-IV criteria for major depressive disorder. Her Geriatric Depression Scale (GDS)5 score was 11/30. Her Cornell Scale for Depression in Dementia6 score for depression in dementia was 13. Her Mini-Mental State Examination (MMSE)7 score was 22/30, and she met the DSM-IV criteria for Alzheimer's dementia. Computed tomography scan of the brain revealed generalized atrophy. Ms A was started on galantamine 8 mg orally twice a day, which was subsequently increased to 16 mg orally twice a day after 4 weeks. Her minor depression features responded very well with galantamine monotherapy after 2 months. At that time, her MMSE score was 23/30, her GDS score was 4/30, and her Cornell Scale for Depression in Dementia score was 6. Depression is associated with defects of multiple neurotransmitters, including serotonin, dopamine, catecholamine, and acetylcholine. Depression in Alzheimer's dementia is linked to catecholaminergic deficit or degeneration of serotonergic neurons, and this process is also known to occur early in Alzheimer's dementia.8 Galantamine is an acetylcholinesterase inhibitor and an allosteric modulator of nicotinic acetylcholine receptor (nAChR) and is used in the treatment of dementia. Nicotinic acetylcholine receptors exist not only on neuronal cell bodies and dendrites but also on those located on axon terminals and are involved in the modulation of multiple neurotransmitter releases. Neuronal nAChR is a family of ligand-gated ion channels that are widely distributed in the brain and are controlled by acetylcholine and nicotine receptor agonists. In the genetically depressive rats, nicotine showed antidepressant-like effects through the involvement of α4β2 nicotinic acetylcholine receptor subtype. The α4 subunit in combination with the β2 subunit mediates dopaminergic and nonadrenergic release.9 Modulation of nAChR facilitates the release of a number of neurotransmitters, including acetylcholine, dopamine, norepinephrine, serotonin, γ-aminobutyric acid (GABA), and glutamate.10 Striatal nicotinic acetylcholine receptors with high affinity for nicotinic agonists are involved with the release of a number of neurotransmitters, including dopamine.11 Dopamine deficiency is associated with anhedonia, lack of interest, and psychomotor slowing (bradyphrenia), and it may arise as a consequence of cholinergic defects involving nAChR. Studies suggest galantamine in addition to mediating cholinergic neurotransmission also through nicotinic acetylcholine receptors may influence several other neurotransmitter systems, possibly modulating the activity of serotonin, dopamine, glutamate, and GABA in certain nerve tracts.12,13 So, it is possible that galantamine, a cholinesterase inhibitor used in the treatment of dementia, may also have some antidepressant effect. If large studies prove this effect, we may not need to use an antidepressant in addition to a cholinesterase inhibitor in patients who have depression with dementia. This means less medication usage and potentially less adverse effect to these patients.

Relation between neuritic plaques and depressive state in Alzheimer's disease.

Meynen G, Van Stralen H, Smit JH, Kamphorst W, Swaab DF, Hoogendijk WJG. Relation between neuritic plaques and depressive state in Alzheimer's disease. To investigate for the first time in a prospective study the relationship between depressive state and the neuropathological hallmarks of Alzheimer's disease, using a scale for depressive symptoms in dementia, while controlling for clinical severity of dementia. Within the framework of a prospective longitudinal study of depression in Alzheimer's disease, patients with dementia underwent a clinical evaluation every six months during the last years of their lives, using the Cornell scale for depression in dementia to assess depressive symptoms and using the Functional Assessment Staging scale to control for clinical severity of dementia. The brains of 43 Alzheimer patients were obtained. The last clinical evaluations prior to death together with post-mortem neuropathology measures were analysed. We found a correlation between the Cornell scores and the sum score for the density of neuritic plaques in the entire cortex (p = 0.027), and even stronger in the temporal cortex (p = 0.012). The observed correlations were independent of sex, age of death, clinical dementia severity and duration of Alzheimer's disease. This study shows a positive relationship between depressive state at time of death and the presence of neuritic plaques in Alzheimer's disease, which is independent of the clinical severity of dementia.

Is the geriatric depression scale a reliable screening tool for depressive symptoms in elderly patients with cognitive impairment?

To determine the reliability of the 30-item Geriatric Depression Scale (GDS-30) for the screening of depressive symptoms in dementia and mild cognitive impairment (MCI) using the Cornell Scale for Depression in Dementia (CSDD) as the 'gold standard'. Diagnosed according to strictly applied clinical diagnostic criteria, patients with MCI (n = 156) and probable Alzheimer's disease (AD) (n = 247) were included. GDS-30, CSDD, Mini Mental State Examination (MMSE) and Global Deterioration Scale were assessed in all patients at inclusion. The AD group was divided in three subgroups: mild AD (MMSE>or=18) (n = 117), moderate AD (MMSE< 18 and >or=10) (n = 89) and severe AD (MMSE<10) (n = 38). In MCI patients, moderate but highly significant correlations were found between GDS-30 and CSDD scores (Pearson: r = 0.565; p < 0.001). In mildly (r = 0.294; p = 0.001), moderately (r = 0.273; p = 0.010) and severely (r = 0.348; p = 0.032) affected AD patients, only weak correlations between GDS-30 and CSDD scores were calculated. ROC curve analysis showed that sensitivity and specificity values of respectively 95% and 67% were achieved when a GDS-30 cut-off score of 8 was applied in MCI patients. In AD patients, too low sensitivity and specificity values did not allow selecting an optimal cut-off score by means of ROC curve analysis. Using the CSDD as 'gold standard', we demonstrated that the GDS-30 is a reliable screening tool for depressive symptoms in MCI but not in AD patients.

O2-07-02: Is the geriatric depression scale a reliable screening tool for depressive symptoms in elderly patients with cognitive impairment?

SUMMARY Objective To determine the reliability of the 30-item Geriatric Depression Scale (GDS-30) for the screening of depressive symptoms in dementia and mild cognitive impairment (MCI) using the Cornell Scale for Depression in Dementia (CSDD) as the ‘gold standard’. Methods Diagnosed according to strictly applied clinical diagnostic criteria, patients with MCI (n ¼ 156) and probable Alzheimer’s disease (AD) (n ¼ 247) were included. GDS-30, CSDD, Mini Mental State Examination (MMSE) and Global Deterioration Scale were assessed in all patients at inclusion. The AD group was divided in three subgroups: mild AD (MMSE� 18) (n ¼ 117), moderate AD (MMSE< 18 and � 10) (n ¼ 89) and severe AD (MMSE<10) (n ¼ 38). Results In MCI patients, moderate but highly significant correlations were found between GDS-30 and CSDD scores (Pearson: r ¼ 0.565; p < 0.001). In mildly (r ¼ 0.294; p ¼ 0.001), moderately (r ¼ 0.273; p ¼ 0.010) and severely (r ¼ 0.348; p ¼ 0.032) affected AD patients, only weak correlations between GDS-30 and CSDD scores were calculated. ROC curve analysis showed that sensitivity and specificity values of respectively 95% and 67% were achieved when a GDS-30 cut-off score of 8 was applied in MCI patients. In AD patients, too low sensitivity and specificity values did not allow selecting an optimal cut-off score by means of ROC curve analysis. Conclusion Using the CSDD as ‘gold standard’, we demonstrated that the GDS-30 is a reliable screening tool for depressive symptoms in MCI but not in AD patients. Copyright # 2009 John Wiley & Sons, Ltd.

Post‐stroke dementia and depression: frontosubcortical dysfunction as missing link?

Testing the hypothesis that depressive symptoms in dementia reflect dysfunction in fronto-subcortical pathways. Both depression and dementia can be the result of vascular damage of the brain. The nature of the depressive symptomatology seems to be related to concommittant cognitive disturbances in that subjects show more so-called motivational symptoms of depression. These symptoms can be the result of frontal-subcortical dysfunction. It could be very helpful for clinical practice if these subjects could be identified by simple diagnostic procedures. Associations were computed between measures of depressive symptoms and a set of neuropsychological tests in a sample of 54 subjects with a post-stroke dementia. Although we used an extensive set of neuropsychological tests, most subjects were able to participate only in a small part of them, because of disease severity. Our hypothesis was supported by a negative correlation between scores on the verbal semantic fluency task and the total numbers of motivational depressive symptoms. None of the neuropsychological tests was significantly related to the number of mood symptoms neither did they correlate with the total number of depressive symptoms. This study gives further evidence for the assumption that motivational-based depressive symptoms partially originate from fronto-subcortical dysfunction.

Depressive symptoms and white matter changes in patients with dementia

The aim of the present study was to investigate if depressive symptoms in demented patients are associated with white matter changes (WMCs) in the brain. WMCs are frequently found in patients with dementia, as well as among elderly nondemented patients with depressive symptoms. However, it is less established whether or not WMCs are related to depressive symptoms in demented patients. 67 (26 men, 41 women) patients with primary degenerative dementia (Alzheimer's disease, frontotemporal dementia), vascular dementia (VaD), or mixed Alzheimer/VaD dementia were included in the study. The patients were young-old (mean 68.1, SD 7.3). All patients underwent a standardized examination procedure and MRI of the brain. The degree of WMCs was visually rated, blindly. Depressive symptoms were rated according to the Gottfries-Bråne-Steen scale (anxiety, fear-panic, depressed mood). No significant relationship was found between WMCs and depressive symptoms in the demented patients. The possible involvement of WMCs in the pathogenesis of depressive symptoms in dementia is unclear. A link between disruptions of frontal-subcortical pathways, due to WMCs, and depressive symptomatology in dementia has been hypothesised from earlier findings, which would imply common elements of pathogenesis for depressive symptomatology and cognitive impairment in dementia. However, the results of the present study do not add further support to this hypothesis.

High cholesterol level and depressive symptoms in dementia

High cholesterol level and depressive symptoms in dementia

Depression and Alzheimer's disease

Depressive symptoms, due either major depression or clinically significant, subsyndromal depression, occur commonly in the course of Alzheimer's disease. For a variety of clinical and methodological reasons, this remains an area that begs for new investigation. At the very least, these depressive symptoms should be viewed as a cause of significant and treatable "excess disability" (Kramer and Reifler, 1992). Demented patients with clinically significant depression (e.g., depressed mood, significant loss of appetite, insomnia, fatigue, irritability, and agitation) should be considered for a trial of antidepressant therapy, even when they fail to meet full diagnostic criteria for major depression. These symptoms will, in most instances, respond to antidepressant therapy. The "rules" for treatment of depression in dementia are slightly different than for cognitively intact patients: (a) start low, go slower, (b) pay attention to cognitive toxicity of all medication combinations, and (c) depressive symptoms do not persist as long as in cognitively intact patients. Current treatments, especially those SSRI's like fluoxetine and sertraline that have cognitive enhancing effects, should be considered the "first line" antidepressants. We need to emphasize early detection and treatment of depressive symptoms in dementia in all arenas.

Life Events and Senile Dementia Affective Symptoms

Previous research in the elderly has linked threatening life events with depression. Dementia sufferers are known to be sensitive to stressful changes in their daily life such as relocation. This study investigates whether threatening life events are associated with depressive symptoms in dementia sufferers. Using the Life Events and Difficulties Schedule, this study examined life events before admission in a group of 70 dementia patients compared with two control groups: dementia sufferers in the community and mentally fit elderly people matched for age and sex. Life events with severe threat were not significantly more frequent in the dementia patients than in two control groups. However, depressive symptoms in the dementia sufferers were significantly associated with independent severe life events. This strong association was maintained when a multivariate analysis was used to control for the effects of other social factors and severity of cognitive impairment. This association appears to be specific to the threat aspect of life events since there was no association between depressive symptoms and events relating to change in the social environment. In dementia sufferers, threatening life events are associated with depressive symptoms. This means that dementia sufferers are responsive to stress in the same way as cognitively intact individuals, and clinicians need to be more aware of the social influences on them.

Dementia, awareness and depression

AbstractWe examined 170 outpatients, 103 with Alzheimer's disease, 43 with vascular dementia and 24 with various other causes, in order to investigate whether or not depressive symptoms were more likely to occur in dementia patients who had some degree of awareness of their cognitive deterioration. Awareness was rated on a four‐point scale that assessed discrepancies between the patient's and the caregiver's history. The level of awareness was significantly related to the severity of dementia but not to depression or to the score on Hamilton's depression scale. However, the score from the item “psychic anxiety” showed a weak but significant correlation with the level of awareness of one's deficits. It is concluded that intact awareness of deterioration was not clearly related to the development of depression or depressive symptoms in dementia.