scholarly journals Neuropsychiatric Symptoms Exacerbate the Cognitive Impairments in Patients With Late-Life Depression

2021 ◽  
Vol 12 ◽  
Author(s):  
Min Zhang ◽  
Ben Chen ◽  
Xiaomei Zhong ◽  
Huarong Zhou ◽  
Qiang Wang ◽  
...  
Keyword(s):  
Factor Score ◽  
Cognitive Impairments ◽  
Neuropsychiatric Symptoms ◽  
Late Life ◽  
Behavioral Symptoms ◽  
Late Life Depression ◽  
Clinical Prognosis ◽  
Negatively Associated ◽  
Mediation Analyses ◽  
Behavioral Factor

Background: Neuropsychiatric symptoms (NPS) and cognitive impairments are both common in patients with late-life depression (LLD). However, the relationship between NPS and cognitive functions in LLD patients remains unclear. The current study aims to explore the effects of NPS on cognitive impairments in LLD patients.Methods: Two hundred and sixty-two LLD patients and 141 normal controls (NC) were recruited. Exploratory factor analysis was used to extract factors from the Neuropsychiatric Inventory (NPI). Correlation, mediation, and moderation analyses were used to explore whether NPS exacerbated the cognitive impairments in LLD and whether NPS exhibited different effects on cognitive impairments in acute-state LLD (aLLD) and recovery-state LLD (rLLD).Results: Three main factors were extracted from the NPI, including emotional, behavioral, and psychotic factors. The patients with LLD exhibited worse cognition and higher NPI scores, and the scores of NPI-total and three extracted factors were negatively associated with cognitive scores. The mediation analyses exhibited that NPI-total and behavioral factor scores increase the difference in cognition scores between LLD and NC groups. The mediation analyses exhibited that behavioral factor score played a greater effect on impairing MMSE in the rLLD group than in the aLLD group. Additionally, behavioral factor score was in a trend to be negatively associated with Mini-Mental State Examination (MMSE) score changes at a one-year follow-up (p = 0.051).Conclusions: NPS, especially behavioral symptoms, exacerbate cognitive impairments in LLD and may contribute to residual cognitive impairment in rLLD patients. Early intervention for behavioral symptoms in LLD patients may be beneficial to their long-term clinical prognosis.

The Cerebrovascular Model of Depression in Late Life

CNS Spectrums ◽  
2002 ◽  
Vol 7 (10) ◽  
pp. 712-715 ◽  
Author(s):  
Jeffrey M. Lyness
Keyword(s):  
Stroke Risk ◽  
Age Of Onset ◽  
Cognitive Impairments ◽  
Late Life ◽  
Executive Dysfunction ◽  
Brain Disease ◽  
Future Research ◽  
Late Life Depression ◽  
Vascular Depression ◽  
Cerebrovascular Risk

ABSTRACTDepression in older people, especially depression with an older age of onset, may be a manifestation of acquired brain disease. The cerebrovascular model of depression, often referred to as “vascular depression,” hypothesizes that otherwise clinically occult small vessel brain disease contribute to the pathogeneses of some late-life depressive conditions. This paper reviews several lines of evidence supporting the cerebrovascular model and addresses the limitations of the existing literature. Several directions for future research are noted, including empirical testing of the notion that cerebrovascular disease might underlie the pathogeneses of depression with prominent executive dysfunction or other cognitive impairments. At this time, there are no specific therapeutic options for patients with suspected vascular depression beyond standard approaches to depression treatments, although education about the possibly greater risks of chronicity should be included in treatment planning. Therapy of cerebrovascular risk factors and stroke-risk reduction are important as consistent with general practice guidelines, although it is not known whether this will reduce the incidence or improve the outcome of late-life depression.

Behavioral Phenomenology in Alzheimer's Disease, Frontotemporal Dementia, and Late-Life Depression: A Retrospective Analysis

1997 ◽  
Vol 10 (2) ◽  
pp. 67-74 ◽  
Author(s):  
J. Randolph Swartz ◽  
Bruce L. Miller ◽  
Ira M. Lesser ◽  
Ruth Booth ◽  
Amy Darby ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Discriminant Analysis ◽  
Frontotemporal Dementia ◽  
Diagnostic Category ◽  
Late Life ◽  
Behavioral Symptoms ◽  
Stepwise Discriminant Analysis ◽  
Late Life Depression ◽  
Behavioral Abnormalities

Often patients in the early stages of Alzheimer's disease (AD), frontotemporal dementia (FTD), and late-life depression can be difficult to differentiate clinically. Although subtle cognitive distinctions exist between these disorders, noncognitive behavioral phenomenology may provide additional discriminating power. In 19 subjects with AD, 19 with FTD, 16 with late-life psychotic depression (LLPD), and 19 with late-life nonpsychotic depression (LLNPD), noncognitive behavioral symptoms were quantified retrospectively using the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) and compared using both a one-way ANOVA and a multivariate stepwise discriminant analysis, which utilized a jackknife procedure. The FTD group showed the highest mean total SCAN score, while the AD group showed the lowest. ANOVA showed significant differences in the mean total SCAN scores between the four diagnostic groups ( P < .0001). With the discriminant analysis, the four disorders demonstrated different clusters of behavioral abnormalities and were differentiated by these symptoms ( P < .0001). A subset of 14 SCAN item group symptoms was identified that collectively classified correctly the following percentages of subjects in each diagnostic category: AD 94.7%, FTD 100%, LLPD 87.5%, and LLNPD 100%. These results indicate that AD, FTD, LLPD, and LLNPD were distinguished retrospectively by the SCAN without using cognitive data. Better definition of the longitudinal course of noncognitive behavioral symptoms in different dementias and psychiatric disorders will be valuable both for diagnosis and to help define behavioral syndromes that are associated with selective neuroanatomic and neurochemical brain pathology.

scholarly journals The additive effect of late-life depression and olfactory dysfunction on the risk of dementia was mediated by hypersynchronization of the hippocampus/fusiform gyrus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ben Chen ◽  
Xiaomei Zhong ◽  
Min Zhang ◽  
Naikeng Mai ◽  
Zhangying Wu ◽  
...  
Keyword(s):  
Interactive Effect ◽  
Low Frequency ◽  
Late Life ◽  
Fusiform Gyrus ◽  
Interactive Effects ◽  
Late Life Depression ◽  
Mediation Analyses ◽  
Left Hippocampus ◽  
Global Cognition ◽  
The Relationship

AbstractEarly detection of patients with late-life depression (LLD) with a high risk of developing dementia contributes to early intervention. Odor identification (OI) dysfunction serves as a marker for predicting dementia, but whether OI dysfunction increases the risk of dementia in LLD patients remains unclear. The present study aimed to explore the interactive effect of LLD and OI dysfunction on the risk of dementia and its underlying neuroimaging changes. One hundred and fifty-seven LLD patients and 101 normal controls were recruited, and data on their OI, cognition, activity of daily living (ADL), and resting-state functional magnetic resonance imaging were collected. Two × two factorial analyses were used to analyze the interactive effects of LLD and OI dysfunction on neuropsychological and neuroimaging abnormalities. Mediation analyses were used to explore whether abnormalities detected by neuroimaging mediated the the associations between OI and cognition/ADL. The results suggested that LLD and OI dysfunction exhibited additive effects on reduced ADL, global cognition and memory scores, as well as neuroimaging variables including (i) increased fractional amplitude of low-frequency fluctuation (fALFF) in the right orbitofrontal cortex and right precentral cortex, and (ii) increased regional homogeneity (ReHo) in the left hippocampus/fusiform gyrus, etc. In addition, these increased fALFF and ReHo values were associated with reduced neuropsychological scores (ADL, global cognition, memory, and language). Moreover, ReHo of the left hippocampus/fusiform gyrus completely mediated the relationship between OI and ADL, and partially mediated the relationship between OI and global cognition. Overall, mediated by the hypersynchronization of the left hippocampus/fusiform gyrus, OI dysfunction may increase the risk of dementia in LLD patients.

scholarly journals 110 - Investigations of Risk, Resilience and Novel Therapeutics of Late Life Neuropsychiatric Disease

2020 ◽  
Vol 32 (S1) ◽  
pp. 22-22
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Imaging ◽  
Animal Models ◽  
Cognitive Decline ◽  
Cognitive Deficits ◽  
Neuropsychiatric Symptoms ◽  
Late Life ◽  
Late Life Depression ◽  
Neuropsychiatric Disease

Converging data from multiple domains of preclinical and human studies has underscored the importance of focusing on genetic, synaptic and neural circuity as critical neurobiological mechanisms of late life neuropsychiatric disease. These complementary research approaches have been applied to identify novel molecular mechanisms that may represent early intervention targets, as well as promising new treatments. The symposium will include four speakers who span the range of studies in animal models, post-mortem brain tissue, molecular imaging and clinical trials combined with biomarkers. Dr Etienne Sibille will present his research on the procognitive, neurotrophic and neurogenic effects of novel compounds augmenting dendritic inhibition and restoring neuronal connectivity, which is affected in aging and in neurodegenerative disorders, such as Alzheimer’s disease. Dr. Robert Sweet will present new GWAS and human postmortem findings regarding risk/resilience to psychosis in Alzheimer's Disease, with an emphasis on synaptic mechanisms of resilience. Dr Helen Lavretsky will present a study of the neuroimaging, genetic and epigenetic effects of memantine and escitalopram treatment in late life depression. The strategy of incorporating biological measures into a clinical trial is an important opportunity to understanding the neurobiological mechanisms. Dr Gwenn Smith will present multi-modality molecular imaging data to understand the synaptic changes associated with Alzheimer’s Disease pathology in late life depression and mild cognitive impairment. Consideration of interdisciplinary research approaches and applications to different neuropsychiatric conditions may have particular relevance to understanding the neurobiological mechanisms underlying neuropsychiatric symptoms as risk factors or complications of neurodegenerative disease.Molecular imaging methods to visualize the neuropathology of Alzheimer’s disease (AD) in vivo provide an unprecedented opportunity to understand the neuropsychiatric (NPS) and cognitive symptoms observed in early stage AD by testing hypotheses informed by human neuropathology and animal models. A fuller understanding of the neurobiology of early AD and its clinical progression is essential to identify individuals at risk and to identify targets for prevention and treatment. Numerous neuroimaging studies have shown that beta-amyloid and tau is necessary but not sufficient to explain cognitive decline and that models to explain cognitive decline must also include measures associated with synaptic dysfunction (eg cerebral glucose metabolism or brain volumes). Human data and animal models support the further investigation of serotonin (5-HT) degeneration. Relative to other molecular targets, there is stronger evidence for 5-HT loss in both cognitive deficits and neuropsychiatric symptoms (NPS) in Alzheimer’s Disease. 5-HT compounds are the only agents with preclinical evidence of multiple therapeutic mechanisms relevant to prevention and symptomatic treatment: blockade of amyloid precursor protein processing or neuroprotection, synaptic plasticity and improvement in both cognitive deficits and NPS. Multi-radiotracer PET studies of beta-amyloid (Aβ), tau and 5-HT have been performed longitudinally in amnestic, multi -domain, MCI (aMCI-MD) and cognitively normal elderly. Cortical and limbic 5-HT degeneration was a more powerful predictor of longitudinal memory decline than Aβ or Tau. Elucidating the role of 5-HT, in relation to Tau and Aβ in cognitive decline in aMCI-MD will have fundamental implications for the design of prevention and intervention studies targeting 5-HT.

scholarly journals Repetitive transcranial magnetic stimulation in patients with late life depression influences phenylalanine metabolism

Pteridines ◽  
2018 ◽  
Vol 29 (1) ◽  
pp. 87-90
Author(s):  
F Leblhuber ◽  
K Steiner ◽  
Jm Gostner ◽  
D Fuchs
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Phenylalanine Hydroxylase ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Neuropsychiatric Symptoms ◽  
Late Life ◽  
Additional Treatment ◽  
Symptom Improvement ◽  
Therapeutic Effects ◽  
Late Life Depression

AbstractRepetitive transcranial magnetic stimulation (rTMS) is used to treat different neuropsychiatric conditions like Parkinson’s disease, essential tremor, stroke, cognitive decline, dementia and depression. rTMS may exert its therapeutic effects by influencing the biochemistry of neurotransmitters. In this exploratory study, safety symptom improvement and changes in the availability of neurotransmitter precursor amino acids were studied following prefrontal cortex (PFC) stimulation using repetitive transcranial stimulation with TheraCell apparatus R (Guth Meditec, Salach, Germany) as an additional treatment in ten patients with late life depression. Treatment was well tolerated with no serious adverse effects being observed. rTMS induced a significant improvement in the symptoms of depression and a significant decrease in the HAMD-7 (p <0.03). At the same time, the serum phenylalanine to tyrosine ratio declined significantly (p <0.04). No significant influence of rTMS on tryptophan breakdown and serum neopterin concentrations was observed. These preliminary findings indicate that rTMS may influence the activity of the enzyme phenylalanine hydroxylase (PAH) which plays a key role in the biosynthesis of neurotransmitter precursors related to neuropsychiatric symptoms in late life depression. However, results were obtained from only 10 patients. Larger studies are therefore required to support these conclusions

Refining Evidence-Based Treatments for Late-Life Depression

GeroPsych ◽  
2015 ◽  
Vol 28 (2) ◽  
pp. 67-76
Author(s):  
Grace C. Niu ◽  
Patricia A. Arean
Keyword(s):  
Older Adults ◽  
Mental Illness ◽  
Brain Plasticity ◽  
Late Life ◽  
Aging Population ◽  
The United States ◽  
Future Research ◽  
Evidence Based ◽  
Late Life Depression ◽  
Evidence Based Treatments

The recent increase in the aging population, specifically in the United States, has raised concerns regarding treatment for mental illness among older adults. Late-life depression (LLD) is a complex condition that has become widespread among the aging population. Despite the availability of behavioral interventions and psychotherapies, few depressed older adults actually receive treatment. In this paper we review the research on refining treatments for LLD. We first identify evidence-based treatments (EBTs) for LLD and the problems associated with efficacy and dissemination, then review approaches to conceptualizing mental illness, specifically concepts related to brain plasticity and the Research Domain Criteria (RDoc). Finally, we introduce ENGAGE as a streamlined treatment for LLD and discuss implications for future research.

Scholarship and Politics in the Examination of Late-Life Depression

1996 ◽  
Vol 41 (5) ◽  
pp. 491-493 ◽  
Author(s):  
Antonette M. Zeiss
Keyword(s):  
Late Life ◽  
Late Life Depression
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