scholarly journals Exacerbation of psychotic symptoms as clinical presentation of Wernicke encephalopathy in an Alzheimer's disease patient

2020 ◽  
Vol 21 (5) ◽  
pp. 185-187
Author(s):  
Nozomu Uchida ◽  
Mayumi Ishida ◽  
Izumi Sato ◽  
Takao Takahashi ◽  
Daisuke Furuya ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Presentation ◽  
Disease Patient ◽  
Psychotic Symptoms ◽  
Wernicke Encephalopathy

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.

Differentiated clinical presentation of early and late-onset Alzheimer’s disease: is 65 years of age providing a reliable threshold?

2015 ◽  
Vol 262 (5) ◽  
pp. 1238-1246 ◽  
Author(s):  
Antonio Palasí ◽  
Belén Gutiérrez-Iglesias ◽  
Montse Alegret ◽  
Francesc Pujadas ◽  
Mikel Olabarrieta ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Presentation ◽  
Late Onset

Psychotic Symptoms in Alzheimer's Disease and 5-HTTLPR Polymorphism of the Serotonin Transporter Gene: Evidence for an Association

2009 ◽  
Vol 16 (1) ◽  
pp. 173-180 ◽  
Author(s):  
Davide Quaranta ◽  
Alessandra Bizzarro ◽  
Camillo Marra ◽  
Maria Gabriella Vita ◽  
Davide Seripa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Serotonin Transporter ◽  
Serotonin Transporter Gene ◽  
Psychotic Symptoms ◽  
Transporter Gene

scholarly journals A Case Report of a 37-Year-Old Alzheimer's Disease Patient with Prominent Striatum Amyloid Retention

2017 ◽  
Vol 14 (4) ◽  
pp. 521 ◽  
Author(s):  
Yoo Hyun Um ◽  
Woo Hee Choi ◽  
Won Sang Jung ◽  
Young Ha Park ◽  
Chang-Uk Lee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Case Report ◽  
Disease Patient

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 Disclosing a Diagnosis of Alzheimer’s Disease: Patient and Family Experiences

2001 ◽  
Vol 28 (S1) ◽  
pp. S67-S71 ◽  
Author(s):  
André P. Smith ◽  
B. Lynn Beattie
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Family Members ◽  
Disease Patient ◽  
Memory Problems ◽  
Family Conference ◽  
The Family ◽  
Disclosure Of Diagnosis ◽  
Assessment Beliefs ◽  
Collection Methods

Background:Informing patients and families about the diagnosis of Alzheimer’s disease (AD) is a complex ethical and practical issue. This qualitative study explores the psychosocial impact of disclosing a diagnosis of AD on patients and family members.Methods:This study identified 14 patients and their accompanying family members undergoing a multidisciplinary assessment for dementia at an outpatient clinic for AD and related disorders. Of the group, three patients had probable AD and five had possible AD as per NINCDS-ADRDAcriteria. Six patients were not demented as per DSM IIIR criteria. Disclosure of diagnosis occurred, in a family conference, within six to eight weeks of the assessment. Data collection methods included observation of the assessment and the family conference as well as in-depth home interviews with family members and with each patient whenever feasible. The interviews were transcribed verbatim and coded for recurrent themes.Results:A total of 40 individuals across 14 families participated in this study. Only two families chose not to have the patient attend the family conference. The disclosure of a diagnosis of probable AD brought on an experience of relief in three families, marking the end of a lengthy period of confusion about the nature of memory problems. Patients diagnosed with possible AD and their families interpreted how indicative the diagnosis was of the presence of the disease with varying degrees of certainty depending on pre-assessment beliefs about the cause of memory problems. In the group diagnosed as not demented, four patients had complaints of forgetfulness likely related to minor depression. The disclosure of a diagnosis of no dementia did not produce the anticipated relief. Two patients continued to believe their memory problems were caused by the early onset of AD or some other “organic” problem.Interpretation:This study reveals that disclosure of the diagnosis of AD to patients and family members is generally beneficial but that there are variations in the understanding of the diagnostic information, particularly in instances where the assessment results are ambiguous.

scholarly journals STIM1 deficiency is linked to Alzheimer’s disease and triggers cell death in SH-SY5Y cells by upregulation of L-type voltage-operated Ca2+ entry

2018 ◽  
Vol 96 (10) ◽  
pp. 1061-1079 ◽  
Author(s):  
Carlos Pascual-Caro ◽  
Maria Berrocal ◽  
Aida M. Lopez-Guerrero ◽  
Alberto Alvarez-Barrientos ◽  
Eulalia Pozo-Guisado ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Protein Expression ◽  
Transmembrane Domain ◽  
Neuroblastoma Cell ◽  
Disease Patient ◽  
List Type

Abstract STIM1 is an endoplasmic reticulum protein with a role in Ca2+ mobilization and signaling. As a sensor of intraluminal Ca2+ levels, STIM1 modulates plasma membrane Ca2+ channels to regulate Ca2+ entry. In neuroblastoma SH-SY5Y cells and in familial Alzheimer’s disease patient skin fibroblasts, STIM1 is cleaved at the transmembrane domain by the presenilin-1-associated γ-secretase, leading to dysregulation of Ca2+ homeostasis. In this report, we investigated expression levels of STIM1 in brain tissues (medium frontal gyrus) of pathologically confirmed Alzheimer’s disease patients, and observed that STIM1 protein expression level decreased with the progression of neurodegeneration. To study the role of STIM1 in neurodegeneration, a strategy was designed to knock-out the expression of STIM1 gene in the SH-SY5Y neuroblastoma cell line by CRISPR/Cas9-mediated genome editing, as an in vitro model to examine the phenotype of STIM1-deficient neuronal cells. It was proved that, while STIM1 is not required for the differentiation of SH-SY5Y cells, it is absolutely essential for cell survival in differentiating cells. Differentiated STIM1-KO cells showed a significant decrease of mitochondrial respiratory chain complex I activity, mitochondrial inner membrane depolarization, reduced mitochondrial free Ca2+ concentration, and higher levels of senescence as compared with wild-type cells. In parallel, STIM1-KO cells showed a potentiated Ca2+ entry in response to depolarization, which was sensitive to nifedipine, pointing to L-type voltage-operated Ca2+ channels as mediators of the upregulated Ca2+ entry. The stable knocking-down of CACNA1C transcripts restored mitochondrial function, increased mitochondrial Ca2+ levels, and dropped senescence to basal levels, demonstrating the essential role of the upregulation of voltage-operated Ca2+ entry through Cav1.2 channels in STIM1-deficient SH-SY5Y cell death. Key messages STIM1 protein expression decreases with the progression of neurodegeneration in Alzheimer’s disease. STIM1 is essential for cell viability in differentiated SH-SY5Y cells. STIM1 deficiency triggers voltage-regulated Ca2+ entry-dependent cell death. Mitochondrial dysfunction and senescence are features of STIM1-deficient differentiated cells.

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