scholarly journals The individual course of neuropsychiatric symptoms in people with Alzheimer's and Lewy body dementia: 12-year longitudinal cohort study

2019 ◽  
Vol 216 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Audun Osland Vik-Mo ◽  
Lasse Melvaer Giil ◽  
Miguel Germán Borda ◽  
Clive Ballard ◽  
Dag Aarsland
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuropsychiatric Symptoms ◽  
Personalised Medicine ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Psychotic Symptoms ◽  
Primary Inclusion ◽  
The Individual

IntroductionUnderstanding the natural course of neuropsychiatric symptoms (NPS) in dementia is important for planning patient care and trial design, but few studies have described the long-term course of NPS in individuals.MethodPrimary inclusion of 223 patients with suspected mild dementia from general practice were followed by annual assessment, including the Neuropsychiatric Inventory (NPI), for up to 12 years. Total and item NPI scores were classified as stable, relapsing, single episodic or not present based on 4.96 (s.d. 2.3) observations (98% completeness of longitudinal data) for 113 patients with Alzheimer's disease and 84 patients with LBD (68 dementia with Lewy bodies and 16 Parkinson's disease dementia).ResultsWe found that 80% had stable NPI total ≥1, 50% had stable modest NPI total ≥12 and 25% had stable NPI total ≥24 scores. Very severe NPS (≥48) were mostly single episodes, but 8% of patients with Alzheimer's disease had stable severe NPS. Patients with Alzheimer's disease and the highest 20% NPI total scores had a more stable or relapsing course of four key symptoms: aberrant motor behaviour, aggression/agitation, delusions and irritability (odds ratio 55, P < 0.001). This was not seen in LBD. Finally, 57% of patients with Alzheimer's disease and 84% of patients with LBD had reoccurring psychotic symptoms.ConclusionsWe observed a highly individual course of NPS, with most presenting as a single episode or relapsing; a stable course was less common, especially in LBD. These findings demonstrate the importance of an individualised approach (i.e. personalised medicine) in dementia care.

The ABC of Alzheimer's Disease: Behavioral Symptoms and Their Treatment

2002 ◽  
Vol 14 (S1) ◽  
pp. 27-49 ◽  
Author(s):  
George T. Grossberg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Treatment Options ◽  
Lewy Body Dementia ◽  
Economic Cost ◽  
Brain Regions ◽  
Behavioral Symptoms ◽  
Psychotic Symptoms ◽  
Ache Inhibitors ◽  
Che Inhibitors

Behavioral and psychological symptoms of dementia (BPSD) are a common manifestation of Alzheimer's disease (AD) and other dementia syndromes. Patients experience prominent and multiple symptoms, which are both distressing and a source of considerable social, health, and economic cost. Development of symptoms is in part related to progressive neurodegeneration and cholinergic deficiency in brain regions important in the regulation of behavioral and emotional responses including the cortex, hippocampus, and limbic system. Cholinesterase (ChE) inhibitors offer a mechanism-based approach to therapy to enhance endogenous cholinergic neurotransmission. Studies using ChE inhibitors have demonstrated their clear potential to improve or stabilize existing BPSD. Differences have been noted between selective acetylcholinesterase (AChE) inhibitors (donepezil and galantamine) and dual ChE inhibitors (rivastigmine) in terms of treatment response. While donepezil has shown efficacy in moderate to severe noninstitutionalized AD patients, conflicting results have been obtained in mild to moderate patients and in nursing home patients. Galantamine has been shown to delay the onset of BPSD during a five-month study but has been otherwise poorly studied to-date. Both donepezil and galantamine have not as yet demonstrated efficacy in reducing psychotic symptoms or in reducing levels of concomitant psychotropic medication use. Studies with the dual ChE inhibitor rivastigmine in mild to moderately severe AD and in Lewy body dementia (LBD) have shown improvements in behavioral symptoms including psychosis. Improvements have been maintained over a period of up to two years. In addition, institutionalized patients with severe AD have shown symptomatic benefits with a reduction in the requirement for additional psychotropic drugs following treatment with rivastigmine. The psychotropic properties associated with rivastigmine may in part be mediated through effects on butyrylcholinesterase. Current treatment options are limited for patients with dementia syndromes other than AD. However, data concerning rivastigmine in patients with LBD and preliminary studies in Parkinson's disease dementia and vascular dementia suggest a role for ChE inhibitors across the spectrum of dementia syndromes. Finally, studies that incorporated a delayed start design demonstrate that ChE inhibitors may delay the progression of BPSD.

scholarly journals Neuropsychiatric symptoms correlated with functional trajectories among people living with Alzheimer’s disease dementia and Lewy body dementia

2020 ◽  
Vol 16 (S8) ◽  
Author(s):  
Miguel German Borda ◽  
Dag Aarsland ◽  
Ketil Oppedal ◽  
Lasse Melvær Giil ◽  
Audun Osland Vik‐Mo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Neuropsychiatric Symptoms ◽  
Lewy Body Dementia ◽  
Alzheimer’S Disease Dementia

Increased Cerebrospinal Fluid Concentration of ZnT3 Is Associated with Cognitive Impairment in Alzheimer’s Disease

2020 ◽  
Vol 77 (3) ◽  
pp. 1143-1155
Author(s):  
Daniela Enache ◽  
Joana B. Pereira ◽  
Vesna Jelic ◽  
Bengt Winblad ◽  
Per Nilsson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Cognitive Impairment ◽  
Depressive Symptoms ◽  
Cognitive Decline ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Synaptic Proteins ◽  
Subjective Cognitive Decline

Background: Cognitive deficits arising in the course of Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and Parkinson’s disease with dementia (PDD) are directly linked to synaptic loss. Postmortem studies suggest that zinc transporter protein 3 (ZnT3), AMPA glutamate receptor 3 (GluA3), and Dynamin1 are associated with cognitive decline in AD and Lewy body dementia patients. Objective: We aimed to evaluate the diagnostic value of ZnT3, GluA3, and Dynamin 1 in the cerebrospinal fluid (CSF) of patients with dementia due to AD, DLB, and PDD compared to cognitively normal subjective cognitive decline (SCD) patients in a retrospective study. In addition, we assessed the relationship between synaptic markers and age, sex, cognitive impairment, and depressive symptoms as well as CSF amyloid, phosphorylated tau (p-tau), and total tau (T-tau). Methods: Commercially available ELISA immunoassay was used to measure the levels of proteins in a total of 97 CSF samples from AD (N = 24), PDD (N = 18), DLB (N = 27), and SCD (N = 28) patients. Cognitive impairment was assessed using the Mini-Mental State Examination (MMSE). Results: We found a significant increase in the concentrations of ZnT3, GluA3, and Dynamin1 in AD (p = 0.002) and of ZnT3 and Dynamin 1 in DLB (p = 0.001, p = 0.002) when compared to SCD patients. Changes in ZnT3 concentrations correlated with MMSE scores in AD (p = 0.011), and with depressive symptoms in SCD (p = 0.041). Conclusion: We found alteration of CSF levels of synaptic proteins in AD, PDD, and DLB. Our results reveal distinct changes in CSF concentrations of ZnT3 that could reflect cognitive impairment in AD with implications for future prognostic and diagnostic marker development.

Dementia with Lewy bodies

1998 ◽  
Vol 4 (6) ◽  
pp. 360-363 ◽  
Author(s):  
E. Jane Byrne
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Senile Dementia ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Body Type ◽  
Clinical Criteria ◽  
Dementia Syndrome ◽  
Distinct Disease

Dementia with cortical Lewy bodies (LBD) was first described by Okazakiet alin 1961 and is now recognised as a relatively common cause of the dementia syndrome. The true prevalence of LBD is unknown. In post-mortem studies of patients diagnosed as having dementia in life, the mean frequency of Lewy body dementia is 12.5% (Byrne, 1997). Clinically diagnosed LBD (using operational clinical criteria) is found in 10–23% of patients presenting to, or in the care of, psychogeriatric services (Collertonet al, 1996). What is not yet certain is its nosological status; opinion is divided between regarding it as a variety of Alzheimer's disease (the Lewy body variant), a distinct disease (senile dementia of the Lewy body type) or a spectrum disorder related to both Parkinson's disease and to Alzheimer's disease (Byrne, 1992).

scholarly journals Frequency and subgroups of neuropsychiatric symptoms in mild cognitive impairment and different stages of dementia in Alzheimer's disease

2017 ◽  
Vol 30 (1) ◽  
pp. 103-113 ◽  
Author(s):  
N. Siafarikas ◽  
G. Selbaek ◽  
T. Fladby ◽  
J. Šaltytė Benth ◽  
E. Auning ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Factor Analysis ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Neuropsychiatric Symptoms ◽  
Small Sample ◽  
Psychotic Symptoms ◽  
Cross Sectional

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.

scholarly journals Evidence of compensation in the brain networks of Lewy body dementia and Alzheimer’s disease patients

2017 ◽  
Author(s):  
Luis R. Peraza ◽  
Ruth Cromarty ◽  
Xenia Kobeleva ◽  
Michael J. Firbank ◽  
Alison Killen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Minimum Spanning Tree ◽  
Brain Networks ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Dominant Frequency ◽  
Compensatory Response ◽  
The Brain

AbstractDementia with Lewy bodies (DLB) and Alzheimer’s disease (AD) require differential management despite presenting with symptomatic overlap. A human electrophysiological difference is a decrease of dominant frequency (DF) −the highest power frequency between 4-15Hz– in DLB; a characteristic of Parkinsonian diseases. We analysed electroencephalographic (EEG) recordings from old adults: healthy controls (HCs), AD, DLB and Parkinson’s disease dementia (PDD) patients. Brain networks were assessed with the minimum spanning tree (MST) within six EEG bands: delta, theta, high-theta, alpha, beta and DF. Patients showed lower alpha band connectivity and lower DF than HCs. Lewy body dementias showed a randomised MST compared with HCs and AD in high-theta and alpha but not within the DF. The MST randomisation in DLB and PDD reflects decreased brain efficiency as well as impaired neural synchronisation. However, the lack of network topology differences at the DF indicates a compensatory response of the brain to the neuropathology.

scholarly journals Influencia del estrés en la Enfermedad de Alzheimer. // Stress influence in Alzheimer’s disease

Ciencia Unemi ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 123
Author(s):  
Maria Alejandra Vallejo-Johnson ◽  
Patricia Marcial-Velastegui
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Damage ◽  
The Body ◽  
Daily Routine ◽  
Stressful Situation ◽  
The Individual ◽  
Stress Influences ◽  
The Brain

Existen diversos estudios que proponen las causas de la Enfermedad de Alzheimer (EA), las cuales pueden ser: biológicas, genéticas, cronológicas y ambientales, dentro de ésta última se encuentra el estrés como una influencia para el inicio de dicha patología. Según las distintas teorías del estrés, el sujeto, al encontrarse frente a una situación estresante, sufre diversos cambios en su cuerpo para sobrellevar dicho acontecimiento. El cerebro es el encargado de poner al cuerpo en alerta y en marcha para actuar frente a dicho cambio. El estrés prolongado conlleva a alteraciones en las vías cerebrales, específicamente un daño neuronal del hipocampo, el cual es el encargado de los recuerdos y memoria. Éste al verse afectado, repercute en la memoria del sujeto y por lo tanto empieza a fallar; el sujeto se ve en la incapacidad para recordar y realizar distintas actividades rutinarias. Mediante la investigación documental y encuestas a profesionales de la salud, se obtuvo información tanto del estrés como de la Enfermedad de Alzheimer para luego concluir en la influencia del mismo en el origen de la enfermedad. Se concluye que el estrés perenne repercute en la muerte de neuronas del hipocampo lo que conlleva a la EA. AbstractThere are different studies that propose that the causes of Alzheimer might be biological, genetic, chronological and environmental. Within the environmental aspects, the stress influences the beginning of this pathology. There are several studies that propose the causes of Alzheimer's disease (AD), which can be: biological, genetic, chronological and environmental, within the latter is the stress that influences the beginning of this pathology. According to different theories of stress, the individual, while facing a stressful situation, experiences many changes in the body in order to deal with this situation. The brain is in charge of alerting the body to protect itself against that change. The long-term stress alters the brain pathways, producing specifically a neuronal damage in the hippocampus that is responsible for memories and memory. This affects memory and therefore individual begins to fail, and then, the person cannot remember how to do the daily routine. Through bibliographical research and surveys applied to healthcare professionals, information was obtained on both stress and Alzheimer's disease to establish the influence of that condition on the disease. The study concludes that long-term stress affects the death of neurons in the hippocampus, which leads to AD.

scholarly journals The evaluation of cognitive function in the dementias: methodological and regulatory considerations

2003 ◽  
Vol 5 (1) ◽  
pp. 77-88
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Skills ◽  
Lewy Bodies ◽  
Disease Assessment ◽  
Central Feature ◽  
Memory Problems ◽  
Automated Procedures

Impairment of cognitive function is the central feature of dementia. Although, clinically, the cognitive deficit most often manifests itself as memory problems, a number of other areas of cognition are affected, and memory is but one of the cognitive skills compromised in dementia. Dementia with Lewy bodies, for example, accounts for 15% to 25% of all dementias and does not have memory deficits as a core feature. Our cognitive facilities underlie our abilities to engage successfully in the activities of daily living (ADL) and it follows thai enhancement of cognitive function will facilitate performance of ADL The assessment and understanding of these impairments are crucial to any treatment of the disorder. Unfortunately, the principal instrument used to assess cognitive function in most of the major clinical trials of Alzheimer's disease in recent years, the Alzheimer's Disease Assessment Scale-Cognitive Subsection (ADAS-COG), primarily assesses aspects of memory, which has resulted in other important cognitive deficits in dementia being overlooked. Automated cognitive tests are now available that can identify an earlier onset of improvements in dementia in smaller samples than the ADAS, Regulatory authorities should encourage - or even require - the use of automated procedures alongside the ADAS in pivotal trials to help determine the relative utility of the instruments in the fairest way possible. Whatever the outcome, this will be of long-term benefit to patients, carers, drug developers, clinicians, and regulators in this important area.

scholarly journals Commentary

1998 ◽  
Vol 4 (6) ◽  
pp. 364-366 ◽  
Author(s):  
D. Neill
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Bodies ◽  
Neuronal Loss ◽  
Pathological Process ◽  
Psychotic Symptoms ◽  
Extrapyramidal Features ◽  
Relationship Of ◽  
The Relationship

The article by Byrne gives a general overview of dementia with Lewy bodies (LBD) and discusses treatment in terms of modulation of neurotransmitter systems, treatment of psychotic symptoms and extrapyramidal features. However, as is the case with Alzheimer's disease, the dementia is related to underlying pathological processes which result in death and/or malfunction of neurons. Prevention or amelioration of this neuronal loss is therefore the ultimate aim of treatment. Such treatment is not yet available and the possibility of its development is likely to depend on further elucidation of the underlying pathological process. The relationship of LBD to Alzheimer's disease and Parkinson's disease should be considered, as this is important for the determination of the underlying pathological processes in LBD.

A Clinical Overview of Cholinesterase Inhibitors in Alzheimer's Disease

2002 ◽  
Vol 14 (S1) ◽  
pp. 93-126 ◽  
Author(s):  
Martin Farlow
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Symptomatic Relief ◽  
Disease Process ◽  
Lewy Body Dementia ◽  
Underlying Disease ◽  
Research Experience ◽  
Behavioral Disturbances ◽  
The Individual ◽  
Che Inhibitors

This review provides an overview of the three most widely used cholinesterase (ChE) inhibitors: donepezil, rivastigmine, and galantamine. Differences in pharmacologic profiles will be discussed, and consideration will be given to how such differences may relate to and influence the clinical efficacy and tolerability of the various agents. In addition to providing cognitive benefits in patients with Alzheimer's disease (AD), growing clinical evidence also suggests that ChE inhibitors can produce favorable and clinically relevant effects on neuropsychiatric/behavioral disturbances and activities of daily living. Furthermore, recent data indicate that these agents may be effective at all levels of disease severity and for all rates of disease progression. The clinical utility of ChE inhibitors in a wider spectrum of dementias which share a common cholinergic deficit, such as Lewy body dementia, Parkinson's disease dementia, and vascular dementia, is currently under investigation. Beyond symptomatic relief, data suggest that ChE inhibitors may also slow the underlying disease process. As clinical and research experience with these agents continues to accumulate, the differences in their effects will become more apparent and will help physicians tailor ChE inhibition treatment to the needs of the individual patient.

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