Late Onset Psychosis. Review

IntroductionSeveral risk factors make older adults more prone to psychosis. The persistent growth in the elderly population makes important the necessity of accurate diagnosis of psychosis, since this population has special features especially regarding to the pharmacotherapy and side effects.ObjectivesTo review the medical literature related to late-life psychosis.MethodsMedline search and ulterior review of the related literature.ResultsReinhard et al. [1] highlight the fact that up to 60% of patients with late onset psychosis have a secondary psychosis, including: metabolic (electrolite abnormalities, vitamines defficiency…); infections (meningitides, encephalitides…); neurological (dementia, epilepsy…); endocrine (hypoglycemia…); and intoxication. Colijn et al. [2] describe the epidemiological and clinical features of the following disorders: schizophrenia (0.3% lifetime prevalence > 65 years); delusional disorder (0.18% lifetime prevalence); psychotic depression (0.35% lifetime prevalence); schizoaffective disorder (0.32% lifetime prevalence); Alzheimer disease (41.1% prevalence of psychotic symptoms); Parkinson's disease (43% prevalence of psychotic symptoms); Parkinson's disease dementia (89% prevalence of visual hallucinations); Lewy body dementia (up to 78% prevalence of hallucinations) and vascular dementia (variable estimates of psychotic symptoms). Recommendations for treatment include risperidone, olanzapine, quetiapine, aripiprazole, clozapine, donepezil and rivastigmine.ConclusionsDifferential diagnosis is tremendously important in elderly people, as late-life psychosis can be a manifestation of organic disturbances. Mental disorders such as schizophrenia or psychotic depression may have different manifestations in comparison with early onset psychosis.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Quetiapine in the elderly with parkinsonism and psychosis

European Psychiatry ◽

10.1016/j.eurpsy.2003.01.001 ◽

2003 ◽

Vol 18 (7) ◽

pp. 372-373 ◽

Cited By ~ 11

Author(s):

H.H Wijnen ◽

F.M.M.A van der Heijden ◽

F.M.E van Schendel ◽

S Tuinier ◽

W.M.A Verhoeven

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Elderly Patients ◽

Prospective Study ◽

The Elderly ◽

Psychotic Symptoms ◽

General Motor ◽

Motor Functioning ◽

Antipsychotic Effect ◽

Open Prospective Study

AbstractIn the present open prospective study the effects of quetiapine were investigated in two elderly patients with parkinsonism and psychosis. Treatment induced a marked antipsychotic effect that coincided with an improvement of general motor functioning. These findings support the idea that quetiapine may be preferentially of use in the elderly with parkinson’s disease and psychotic symptoms.

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Faculty Opinions recommendation of A susceptibility gene for late-onset idiopathic Parkinson's disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1004442.148857 ◽

2002 ◽

Author(s):

John Hardy

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Late Onset ◽

Susceptibility Gene ◽

Idiopathic Parkinson’S Disease ◽

Idiopathic Parkinson's Disease

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Imaging Familial and Sporadic Neurodegenerative Disorders Associated with Parkinsonism

Neurotherapeutics ◽

10.1007/s13311-020-00994-4 ◽

2021 ◽

Author(s):

David J. Brooks

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Disorders ◽

Lewy Body Dementia ◽

Imaging Biomarkers ◽

Imaging Findings ◽

Subclinical Disease ◽

Similarities And Differences ◽

Potential Use

AbstractIn this paper, the structural and functional imaging changes associated with sporadic and genetic Parkinson’s disease and atypical Parkinsonian variants are reviewed. The role of imaging for supporting diagnosis and detecting subclinical disease is discussed, and the potential use and drawbacks of using imaging biomarkers for monitoring disease progression is debated. Imaging changes associated with nonmotor complications of PD are presented. The similarities and differences in imaging findings in Lewy body dementia, Parkinson’s disease dementia, and Alzheimer’s disease are discussed.

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Cross-platform transcriptional profiling identifies common and distinct molecular pathologies in Lewy body diseases

Acta Neuropathologica ◽

10.1007/s00401-021-02343-x ◽

2021 ◽

Author(s):

Rahel Feleke ◽

Regina H. Reynolds ◽

Amy M. Smith ◽

Bension Tilley ◽

Sarah A. Gagliano Taliun ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Diseases ◽

Lewy Body ◽

Molecular Mechanisms ◽

Lewy Bodies ◽

Subsequent Development ◽

Lewy Body Dementia ◽

Anterior Cingulate ◽

Lewy Body Diseases

AbstractParkinson’s disease (PD), Parkinson’s disease with dementia (PDD) and dementia with Lewy bodies (DLB) are three clinically, genetically and neuropathologically overlapping neurodegenerative diseases collectively known as the Lewy body diseases (LBDs). A variety of molecular mechanisms have been implicated in PD pathogenesis, but the mechanisms underlying PDD and DLB remain largely unknown, a knowledge gap that presents an impediment to the discovery of disease-modifying therapies. Transcriptomic profiling can contribute to addressing this gap, but remains limited in the LBDs. Here, we applied paired bulk-tissue and single-nucleus RNA-sequencing to anterior cingulate cortex samples derived from 28 individuals, including healthy controls, PD, PDD and DLB cases (n = 7 per group), to transcriptomically profile the LBDs. Using this approach, we (i) found transcriptional alterations in multiple cell types across the LBDs; (ii) discovered evidence for widespread dysregulation of RNA splicing, particularly in PDD and DLB; (iii) identified potential splicing factors, with links to other dementia-related neurodegenerative diseases, coordinating this dysregulation; and (iv) identified transcriptomic commonalities and distinctions between the LBDs that inform understanding of the relationships between these three clinical disorders. Together, these findings have important implications for the design of RNA-targeted therapies for these diseases and highlight a potential molecular “window” of therapeutic opportunity between the initial onset of PD and subsequent development of Lewy body dementia.

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Identification of sixteen novel candidate genes for late onset Parkinson’s disease

Molecular Neurodegeneration ◽

10.1186/s13024-021-00455-2 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Alessandro Gialluisi ◽

Mafalda Giovanna Reccia ◽

Nicola Modugno ◽

Teresa Nutile ◽

Alessia Lombardi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Candidate Genes ◽

Rare Variants ◽

Late Onset ◽

High Specificity ◽

Diagnostic Tools ◽

Multi Stage ◽

Whole Exome ◽

Family Based

Abstract Background Parkinson’s disease (PD) is a neurodegenerative movement disorder affecting 1–5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD. Methods The study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls). Results Family-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (≥ 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 × 10− 5). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment. Conclusions Besides confirming the extreme genetic heterogeneity of PD, these data provide novel insights into the genetic of the disease and may be relevant for its prediction, diagnosis and treatment.

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