Cognitive and Behavioral Determinants of Psychotic Symptoms in Alzheimer's Disease

2015 ◽  
Vol 39 (3-4) ◽  
pp. 194-206 ◽  
Author(s):  
Davide Quaranta ◽  
Maria Gabriella Vita ◽  
Alessandra Bizzarro ◽  
Carlo Masullo ◽  
Chiara Piccininni ◽  
...  

Aims: To investigate the relationship between psychotic symptoms and cognitive impairment in Alzheimer's disease (AD). Methods: A total of 108 subjects affected by AD were subdivided into subjects without delusions (ND), subjects with paranoid delusions (PD), subjects with delusional misidentifications (DM), subjects with both DM and PD (DM+PD), subjects with visual hallucinations (v-HALL), and subjects without visual hallucinations (N-HALL). Results: PD and ND subjects performed similarly on neuropsychological tests, while DM patients performed significantly worse than PD and ND patients. v-HALL patients performed worse than N-HALL patients on memory, visuospatial, and executive functions. As for behavioral features, DM and v-HALL subjects reported higher scores on the abnormal motor behavior subscale of the neuropsychiatric inventory (NPI); PD subjects reported higher scores on the disinhibition subscale of the NPI. The severity of PD was predicted by the severity of disinhibition (B = 0.514; p = 0.016) but not by neuropsychological performances. The severity of DM was predicted by age (B = 0.099; p = 0.048) and MMSE (B = -0.233; p = 0.001). The severity of v-HALL was predicted by age (B = 0.052; p = 0.037) and scores on an immediate visual memory task (B = -0.135; p = 0.007). Conclusions: The occurrence of PD may require the relative sparing of cognitive functions and be favored by frontal lobe dysfunction, while DM is associated with the overall level of cognitive impairment. Finally, v-HALL are associated with the impairment of visuospatial abilities.

NeuroImage ◽  
2012 ◽  
Vol 59 (4) ◽  
pp. 4132-4140 ◽  
Author(s):  
Ryu Kurimoto ◽  
Ryouhei Ishii ◽  
Leonides Canuet ◽  
Koji Ikezawa ◽  
Masao Iwase ◽  
...  

2009 ◽  
Vol 120 (5) ◽  
pp. e155
Author(s):  
Ryu Kurimoto ◽  
Ryouhei Ishii ◽  
Koji Ikezawa ◽  
Leonides Canuet ◽  
Masao Iwase ◽  
...  

2003 ◽  
Vol 15 (2) ◽  
pp. 171-179 ◽  
Author(s):  
Mun Tran ◽  
Michel Bédard ◽  
D. William Molloy ◽  
Sacha Dubois ◽  
Judith A. Lever

Background: Alzheimer's disease (AD) is associated with dependence in activities of daily living (ADL). In addition to the cognitive impairment resulting from AD, the presence of psychotic symptoms may further increase this dependence. The objective of this study was to quantify the additional contribution of psychotic symptoms to dependence in ADL. Method: We analyzed data from 558 individuals with AD referred to a memory clinic. Information on ADL, psychotic symptoms, depression symptoms, and cognition was collected with standardized instruments. Results: The frequency of psychotic symptoms was correlated with dependence in ADL (r = −.44, p < .001). The independent contribution of psychotic symptoms to ADL (basic and instrumental) after consideration for cognitive impairment and depression symptoms was assessed with hierarchical regression models. Twenty-five percent of basic ADL variance was explained by cognition; psychotic symptoms accounted for an additional 7% of the variance (b = −0.12, p < .001). Cognitive impairment explained 31% of instrumental ADL variance; psychotic symptoms accounted for an additional 6% (b = −0.21, p < .001). Discussion: Psychotic symptoms are associated with dependence in ADL after controlling for cognitive impairment and depression symptoms. Future research should investigate possible causal linkages between psychotic symptoms and dependence in ADL. This may have implications regarding interventions to maintain independent living in people with AD.


2017 ◽  
Vol 30 (1) ◽  
pp. 103-113 ◽  
Author(s):  
N. Siafarikas ◽  
G. Selbaek ◽  
T. Fladby ◽  
J. Šaltytė Benth ◽  
E. Auning ◽  
...  

ABSTRACTBackground:Neuropsychiatric symptoms (NPS), such as depression, apathy, agitation, and psychotic symptoms are common in mild cognitive impairment (MCI) and dementia in Alzheimer's disease (AD). Subgroups of NPS have been reported. Yet the relationship of NPS and their subgroups to different stages of cognitive impairment is unclear. Most previous studies are based on small sample sizes and show conflicting results. We sought to examine the frequency of NPS and their subgroups in MCI and different stages of dementia in AD.Methods:This was a cross-sectional study using data from a Norwegian national registry of memory clinics. From a total sample of 4,571 patients, we included those with MCI or AD (MCI 817, mild AD 883, moderate–severe AD 441). To compare variables across groups ANOVA or χ2-test was applied. We used factor analysis of Neuropsychiatric Inventory Questionnaire (NPI-Q) items to identify subgroups of NPS.Results:The frequency of any NPS was 87.2% (AD 91.2%, MCI 79.5%; p < 0.001) and increased with increasing severity of cognitive decline. The most frequent NPS in MCI was depression. Apathy was the most frequent NPS in AD across different stages of severity. The factor analysis identified three subgroups in MCI and mild AD, and a fourth one in moderate–severe AD. We labelled the subgroups “depression,” “agitation,” “psychosis,” and “elation.”Conclusions:The frequency of NPS is high in MCI and AD and increases with the severity of cognitive decline. The subgroups of NPS were relatively consistent from MCI to moderate-severe AD. The subgroup elation appeared only in moderate-severe AD.


2020 ◽  
pp. 1-9
Author(s):  
Calum A. Hamilton ◽  
Fiona E. Matthews ◽  
Paul C. Donaghy ◽  
John-Paul Taylor ◽  
John T. O'Brien ◽  
...  

Abstract Background Mild cognitive impairment (MCI) may gradually worsen to dementia, but often remains stable for extended periods of time. Little is known about the predictors of decline to help explain this variation. We aimed to explore whether this heterogeneous course of MCI may be predicted by the presence of Lewy body (LB) symptoms in a prospectively-recruited longitudinal cohort of MCI with Lewy bodies (MCI-LB) and Alzheimer's disease (MCI-AD). Methods A prospective cohort (n = 76) aged ⩾60 years underwent detailed assessment after recent MCI diagnosis, and were followed up annually with repeated neuropsychological testing and clinical review of cognitive status and LB symptoms. Latent class mixture modelling identified data-driven sub-groups with distinct trajectories of global cognitive function. Results Three distinct trajectories were identified in the full cohort: slow/stable progression (46%), intermediate progressive decline (41%) and a small group with a much faster decline (13%). The presence of LB symptomology, and visual hallucinations in particular, predicted decline v. a stable cognitive trajectory. With time zeroed on study end (death, dementia or withdrawal) where available (n = 39), the same subgroups were identified. Adjustment for baseline functioning obscured the presence of any latent classes, suggesting that baseline function is an important parameter in prospective decline. Conclusions These results highlight some potential signals for impending decline in MCI; poorer baseline function and the presence of probable LB symptoms – particularly visual hallucinations. Identifying people with a rapid decline is important but our findings are preliminary given the modest cohort size.


2004 ◽  
Vol 115 (6) ◽  
pp. 1332-1339 ◽  
Author(s):  
Y.A.L. Pijnenburg ◽  
Y. vd Made ◽  
A.M. van Cappellen van Walsum ◽  
D.L. Knol ◽  
Ph. Scheltens ◽  
...  

2003 ◽  
Vol 8 (3) ◽  
pp. 148-159 ◽  
Author(s):  
Rocío Fernández-Ballesteros ◽  
María Dolores Zamarrón ◽  
Lluís Tárraga ◽  
Rosa Moya ◽  
Julio Iñiguez

Cognitive plasticity, learning potential, and rehabilitation potential are new constructs, which are understood as expressions of neural plasticity. They are assessed through dynamic assessment (or testing-the-limits), using experimental test-training-posttest, a form of evaluation closely related to functional or stress testing in medicine. This research strategy has been used for increasing knowledge about several target populations with intellectual handicaps (socially mentally retarded, brain-impaired, schizophrenia patients, etc.), including older people whose fluid intellectual capacity has declined. Recently, cognitive plasticity has been applied to the study of dementia ( Baltes & Baltes, 1997 ), but there are very few other studies in this area. The basic objective of this research program is to test the extent to which learning potential can be a predictor of the course of dementia. The first specific objective of the research is to test whether learning can discriminate healthy people from those diagnosed with Mild Cognitive Impairment (MCI) and with Alzheimer's Disease (AD). In order to assess cognitive plasticity, a Battery of Learning Potential for Assessing Dementia (BEPAD) was developed, incorporating four tests for assessing visuo-spatial and verbal memory, executive function, and verbal fluency. Two hundred subjects participated in the study: 100 healthy elderly, 50 diagnosed with MCI and 50 with AD. All learning strategies included in the four tests making up the BEPAD appear to be effective: All three groups improved their performance in visual memory, verbal learning, and executive function.


Brain ◽  
2019 ◽  
Vol 142 (8) ◽  
pp. 2492-2509 ◽  
Author(s):  
Anne Maass ◽  
David Berron ◽  
Theresa M Harrison ◽  
Jenna N Adams ◽  
Renaud La Joie ◽  
...  

Abstract Alzheimer’s disease researchers have been intrigued by the selective regional vulnerability of the brain to amyloid-β plaques and tau neurofibrillary tangles. Post-mortem studies indicate that in ageing and Alzheimer’s disease tau tangles deposit early in the transentorhinal cortex, a region located in the anterior-temporal lobe that is critical for object memory. In contrast, amyloid-β pathology seems to target a posterior-medial network that subserves spatial memory. In the current study, we tested whether anterior-temporal and posterior-medial brain regions are selectively vulnerable to tau and amyloid-β deposition in the progression from ageing to Alzheimer’s disease and whether this is reflected in domain-specific behavioural deficits and neural dysfunction. 11C-PiB PET and 18F-flortaucipir uptake was quantified in a sample of 131 cognitively normal adults (age: 20–93 years; 47 amyloid-β-positive) and 20 amyloid-β-positive patients with mild cognitive impairment or Alzheimer’s disease dementia (65–95 years). Tau burden was relatively higher in anterior-temporal regions in normal ageing and this difference was further pronounced in the presence of amyloid-β and cognitive impairment, indicating exacerbation of ageing-related processes in Alzheimer’s disease. In contrast, amyloid-β deposition dominated in posterior-medial regions. A subsample of 50 cognitively normal older (26 amyloid-β-positive) and 25 young adults performed an object and scene memory task while functional MRI data were acquired. Group comparisons showed that tau-positive (n = 18) compared to tau-negative (n = 32) older adults showed lower mnemonic discrimination of object relative to scene images [t(48) = −3.2, P = 0.002]. In a multiple regression model including regional measures of both pathologies, higher anterior-temporal flortaucipir (tau) was related to relatively worse object performance (P = 0.010, r = −0.376), whereas higher posterior-medial PiB (amyloid-β) was related to worse scene performance (P = 0.037, r = 0.309). The functional MRI data revealed that tau burden (but not amyloid-β) was associated with increased task activation in both systems and a loss of functional specificity, or dedifferentiation, in posterior-medial regions. The loss of functional specificity was related to worse memory. Our study shows a regional dissociation of Alzheimer’s disease pathologies to distinct memory networks. While our data are cross-sectional, they indicate that with ageing, tau deposits mainly in the anterior-temporal system, which results in deficits in mnemonic object discrimination. As Alzheimer’s disease develops, amyloid-β deposits preferentially in posterior-medial regions additionally compromising scene discrimination and anterior-temporal tau deposition worsens further. Finally, our findings propose that the progression of tau pathology is linked to aberrant activation and dedifferentiation of specialized memory networks that is detrimental to memory function.


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