Depression in Mild Cognitive Impairment is associated with Progression to Alzheimer's Disease: A Longitudinal Study

Mussele, Stefan Van der; Fransén, Erik; Struyfs, Hanne; Luyckx, Jill; Mariën, Peter; Saerens, J.; Somers, Nore; Goeman, Johan; Deyn, Peter Paul De; Engelborghs, Sebastiaan

doi:10.3233/jad-140405

Cited by 113 publications

(86 citation statements)

References 66 publications

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“…6 Current literature suggests that depression in MCI is a strong risk factor for AD. 7,8 A lifetime history of depression (LMD) confers an increased risk of developing AD, and a single episode of late-life depression increases the risk of developing AD by 4- to 5-fold. 9 Studies have shown that patients with MCI having depressive symptoms are more likely to develop AD than those without depression.…”

Section: Introductionmentioning

confidence: 99%

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment

Chung

Plitman

Nakajima

et al. 2015

J Geriatr Psychiatry Neurol

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Depressive symptoms are frequently seen in patients with dementia and mild cognitive impairment (MCI). Evidence suggests that there may be a link between current depressive symptoms and Alzheimer disease (AD)-associated pathological changes, such as an increase in cortical amyloid-β (Aβ). However, limited in vivo studies have explored the relationship between current depressive symptoms and cortical Aβ in patients with MCI and AD. Our study, using a large sample of 455 patients with MCI and 153 patients with AD from the Alzheimer’s disease Neuroimaging Initiatives, investigated whether current depressive symptoms are related to cortical Aβ deposition. Depressive symptoms were assessed using the Geriatric Depression Scale and Neuropsychiatric Inventory-depression/dysphoria. Cortical Aβ was quantified using positron emission tomography with the Aβ probe 18F-florbetapir (AV-45). 18F-florbetapir standardized uptake value ratio (AV-45 SUVR) from the frontal, cingulate, parietal, and temporal regions was estimated. A global AV-45 SUVR, defined as the average of frontal, cingulate, precuneus, and parietal cortex, was also used. We observed that current depressive symptoms were not related to cortical Aβ, after controlling for potential confounds, including history of major depression. We also observed that there was no difference in cortical Aβ between matched participants with high and low depressive symptoms, as well as no difference between matched participants with the presence and absence of depressive symptoms. The association between depression and cortical Aβ deposition does not exist, but the relationship is highly influenced by stressful events in the past, such as previous depressive episodes, and complex interactions of different pathways underlying both depression and dementia.

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Section: Introductionmentioning

confidence: 99%

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment

Chung

Plitman

Nakajima

et al. 2015

J Geriatr Psychiatry Neurol

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“…The neuropsychological and functional scales were chosen based on their ability to characterise cognitive functioning in previous LLD and aMCI studies 31 32. GDS was chosen because of its reliability in assessing depressive symptoms in LLD and aMCI participants 33 34. Clinical assessment findings were reviewed during the weekly consensus conferences attended by neurologists, neuropsychologists and a geriatric psychiatrist (see online supplementary materials for detailed inclusion criteria of individual groups).…”

Section: Methodsmentioning

confidence: 99%

Disrupted small world topology and modular organisation of functional networks in late-life depression with and without amnestic mild cognitive impairment

Ward

Liu

et al. 2014

J Neurol Neurosurg Psychiatry

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Background The topological architecture of the whole-brain functional networks in those with and without late-life depression (LLD) and amnestic mild cognitive impairment (aMCI) are unknown. Aims To investigate the differences in the small-world measures and the modular community structure of the functional networks between patients with LLD and aMCI when occurring alone or in combination and cognitively healthy nondepressed controls. Methods Seventy-nine elderly participants [LLD (n = 23), aMCI (n = 18), comorbid LLD and aMCI (n = 13), and controls (n = 25)] completed neuropsychiatric assessments. Graph theoretical methods were employed on resting-state functional connectivity magnetic resonance imaging data. Results LLD and aMCI comorbidity was associated with the greatest disruptions in functional integration measures (decreased global efficiency and increased path length); both LLD groups showed abnormal functional segregation (reduced local efficiency). The modular network organization was most variable in the comorbid group, followed by LLD-only patients. Decreased mean global, local and nodal efficiency metrics were associated with greater depressive symptom severity but not memory performance. Conclusions Consider the whole brain as a complex network may provide unique insights on the neurobiological underpinnings of LLD with and without cognitive impairment.

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“…There are hints that the cognitive decline found in the two disorders may at least partially share an underlying pathophysiology: when the neuropathological hallmarks of AD - i.e., amyloid plaques and intracellular tau tangles - spread from the entorhinal cortex into the limbic system, patients are prone to develop anxiety and depressive symptoms. Moreover, MDD has been discussed as a risk factor for the development of AD [1, 2]. Essentially, discriminating between AD and MDD is a prerequisite for an optimal clinical and pharmacological treatment [3].…”

Section: Introductionmentioning

confidence: 99%

“…Many studies have employed neuropsychological test profiles to discriminate between AD and MDD [1, 2, 4, 5], yielding differences between healthy controls, patients with mild cognitive impairment (MCI) due to AD, and AD patients. However, this approach is less successful in distinguishing patients with early stages of AD from MDD patients with cognitive deficits or other disorders [2].…”

Section: Introductionmentioning

confidence: 99%

Neurogranin and BACE1 in CSF as Potential Biomarkers Differentiating Depression with Cognitive Deficits from Early Alzheimer’s Disease: A Pilot Study

Schipke

Vos²,

Fuentes

et al. 2018

Dement Geriatr Cogn Disord Extra

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Background/Aims: Major depressive disorder (MDD) can cooccur with early Alzheimer’s disease (AD) or may cause memory problems independently of AD. Previous studies have suggested that the AD-related cerebrospinal fluid (CSF) biomarkers tau and Aβ(1–42) could help discriminate between early AD and depression unrelated to AD. Moreover, the postsynaptic protein neurogranin and presynaptic BACE1 have increasingly gained attention as potential new AD biomarkers, but they have not yet been investigated concerning depression. Methods: Using ELISAs, we studied CSF neurogranin and BACE1 levels in patients with mild (n = 21) and moderate (n = 19) AD, as well as in MDD patients with (n = 20) and without (n = 20) cognitive deficits. The clinical examinations included analyses of t-tau, Aβ(1–42), and Aβ(1–40), besides neuropsychological tests and cranial magnetic resonance imaging. Depressive symptom severity was assessed using the Geriatric Depression Scale (GDS). Results: Along with classic AD biomarkers, neurogranin and BACE1 CSF levels differed between moderate AD and MDD (p ≤ 0.01). MDD associated with cognitive deficits was distinguished from mild AD through the CSF neurogranin/BACE1 ratio (p < 0.05), which was strongly correlated with GDS scores (ρ = –0.656; p < 0.01). Conclusion: The neurogranin/BACE1 ratio in CSF can distinguish between depression and AD among patients with similar cognitive deficits, along with the classic AD biomarkers. Further longitudinal studies are ongoing to identify which biomarkers have prognostic value.

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Depression in Mild Cognitive Impairment is associated with Progression to Alzheimer's Disease: A Longitudinal Study

Abstract: Depressive symptoms in MCI appear to be predictors for progression to AD.

Cited by 113 publications

References 66 publications

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment

Cortical Amyloid β Deposition and Current Depressive Symptoms in Alzheimer Disease and Mild Cognitive Impairment

Disrupted small world topology and modular organisation of functional networks in late-life depression with and without amnestic mild cognitive impairment

Neurogranin and BACE1 in CSF as Potential Biomarkers Differentiating Depression with Cognitive Deficits from Early Alzheimer’s Disease: A Pilot Study

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