Pathological Correlations of Neuropsychiatric Symptoms in Institutionalized People with Dementia

Antonio, Ester Esteban de; López-Álvarez, Jorge; Rábano, Alberto; Agüera-Ortíz, Luis; Sánchez-Soblechero, Antonio; Amaya, Laura Juliana Dueñas; Portela, Sofía; Cátedra, Carlos; Olazarán, Javier

doi:10.3233/jad-200600

Cited by 11 publications

(4 citation statements)

References 48 publications

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“…Though late-life incidence of NPS and emotional dysregulation may be indicative of disruption in serotonergic and noradrenergic systems that are involved in both the pathogenesis of AD and mood symptoms, the direct connection between NPS and AD pathology is only beginning to be elucidated [4,[9][10][11][12][13][14][15]. While there is substantial breadth of the literature suggesting that NPS predispose individuals to developing dementia, there has been limited examination of the relationship between cortical amyloidbeta (Aβ) burden and NPS [1,8,[16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Neuropsychiatric Profiles and Cerebral Amyloid Burden in Adults without Dementia

Gontrum,

Paolillo,

Lee

et al. 2024

Dement Geriatr Cogn Disord

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Introduction: We comprehensively evaluated how self- and informant-reported neuropsychiatric symptoms (NPS) were differentially associated with cerebral amyloid-beta (Aβ) PET levels in older adults without dementia. Methods: Two hundred and twenty-one participants (48% female, age = 73.4 years ± 8.4, Clinical Dementia Rating = 0 [n = 184] or 0.5 [n = 37]) underwent an Aβ-PET scan (florbetapir or PIB), comprehensive neuropsychological testing, and self-reported (Geriatric Depression Scale – 30 item [GDS-30]) and informant-reported interview (Neuropsychiatric Inventory Questionnaire [NPI-Q]) of NPS. Cerebral Aβ burden was quantified using centiloids (CL). NPI-Q and GDS-30 queried the presence of NPS within 4 subdomains and 6 subscales, respectively. Regression models examined the relationship between NPS and Aβ-PET CL. Results: Both higher self- and informant-reported NPS were associated with higher Aβ burden. Among specific NPI-Q subdomains, informant-reported changes in depression, anxiety, and irritability were all associated with higher Aβ-PET. Similarly, self-reported (GDS-30) subscales of depression, apathy, anxiety, and cognitive concern were associated with higher Aβ-PET. When simultaneously entered, only self-reported cognitive concern was associated with Aβ-PET in the GDS-30 model, while both informant-reported anxiety and depression were associated with Aβ-PET in the NPI-Q model. Clinical status moderated the association between self-reported NPS and Aβ-PET such that the positive relationship between self-perceived NPS and Aβ burden strengthened with increasing functional difficulties. Conclusions: In a cohort of older adults without dementia, both self- and informant-reported measures of global NPS, particularly patient-reported cognitive concerns and informant-reported anxiety and depression, corresponded with cerebral Aβ burden. NPS may appear early in the prodromal disease state and relate to initial AD proteinopathy burden, a relationship further exaggerated in those with greater clinical severity.

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Section: Introductionmentioning

confidence: 99%

Neuropsychiatric Profiles and Cerebral Amyloid Burden in Adults without Dementia

Gontrum,

Paolillo,

Lee

et al. 2024

Dement Geriatr Cogn Disord

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“…The clinical manifestations of PD include muscular rigidity, resting tremor, postural instability, dystonia, and dyskinesias [ 4 ]. In addition, the non-motor symptoms of PD include depression, anxiety, hallucination, personality changes [ 5 ], diarrhea [ 6 ], and sleep disorder [ 7 ]. Due to the complexity in the diagnosis of PD, PD patients are often dissatisfied with the consultation and treatment process [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The Potential Role of Voltage-Dependent Anion Channel in the Treatment of Parkinson’s Disease

Wang

Yang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Parkinson’s disease (PD) is a neurodegenerative disease second only to Alzheimer’s disease in terms of prevalence. Previous studies have indicated that the occurrence and progression of PD are associated with mitochondrial dysfunction. Mitochondrial dysfunction is one of the most important causes for apoptosis of dopaminergic neurons. Therefore, maintaining the stability of mitochondrial functioning is a potential strategy in the treatment of PD. Voltage-dependent anion channel (VDAC) is the main component in the outer mitochondrial membrane, and it participates in a variety of biological processes. In this review, we focus on the potential roles of VDACs in the treatment of PD. We found that VDACs are involved in PD by regulating apoptosis, autophagy, and ferroptosis. VDAC1 oligomerization, VDACs ubiquitination, regulation of mitochondrial permeability transition pore (mPTP) by VDACs, and interaction between VDACs and α-synuclein (α-syn) are all promising methods for the treatment of PD. We proposed that inhibition of VDAC1 oligomerization and promotion of VDAC1 ubiquitination as an effective approach for the treatment of PD. Previous studies have proven that the expression of VDAC1 has a significant change in PD models. The expression levels of VDAC1 are decreased in the substantia nigra (SN) of patients suffering from PD compared with the control group consisting of normal individuals by using bioinformatics tools. VDAC2 is involved in PD mainly through the regulation of apoptosis. VDAC3 may have a similar function to VDAC1. It can be concluded that the functional roles of VDACs contribute to the therapeutic strategy of PD.

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“…This notion has been supported by postmortem studies (12,13) showing the large presence of neurofibrillary tangles in the OFC and ACC of patients with the frontal variant of AD. Indeed, a strict correlation among neuropsychiatric symptoms (NPS), especially aggressiveness, and tau pathology, rather than amyloid, is commonly reported in AD patients (12,14,15). A significant tau pathology in the frontal lobes is also a major postmortem finding in FTD, which is notably characterized by disabling behavioral changes (16,17).…”

Section: Introductionmentioning

confidence: 99%

Agitation and Dementia: Prevention and Treatment Strategies in Acute and Chronic Conditions

et al. 2021

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Agitation is a behavioral syndrome characterized by increased, often undirected, motor activity, restlessness, aggressiveness, and emotional distress. According to several observations, agitation prevalence ranges from 30 to 50% in Alzheimer's disease, 30% in dementia with Lewy bodies, 40% in frontotemporal dementia, and 40% in vascular dementia (VaD). With an overall prevalence of about 30%, agitation is the third most common neuropsychiatric symptoms (NPS) in dementia, after apathy and depression, and it is even more frequent (80%) in residents of nursing homes. The pathophysiological mechanism underlying agitation is represented by a frontal lobe dysfunction, mostly involving the anterior cingulate cortex (ACC) and the orbitofrontal cortex (OFC), respectively, meaningful in selecting the salient stimuli and subsequent decision-making and behavioral reactions. Furthermore, increased sensitivity to noradrenergic signaling has been observed, possibly due to a frontal lobe up-regulation of adrenergic receptors, as a reaction to the depletion of noradrenergic neurons within the locus coeruleus (LC). Indeed, LC neurons mainly project toward the OFC and ACC. These observations may explain the abnormal reactivity to weak stimuli and the global arousal found in many patients who have dementia. Furthermore, agitation can be precipitated by several factors, e.g., the sunset or low lighted environments as in the sundown syndrome, hospitalization, the admission to nursing residencies, or changes in pharmacological regimens. In recent days, the global pandemic has increased agitation incidence among dementia patients and generated higher distress levels in patients and caregivers. Hence, given the increasing presence of this condition and its related burden on society and the health system, the present point of view aims at providing an extensive guide to facilitate the identification, prevention, and management of acute and chronic agitation in dementia patients.

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Pathological Correlations of Neuropsychiatric Symptoms in Institutionalized People with Dementia

Cited by 11 publications

References 48 publications

Neuropsychiatric Profiles and Cerebral Amyloid Burden in Adults without Dementia

Neuropsychiatric Profiles and Cerebral Amyloid Burden in Adults without Dementia

The Potential Role of Voltage-Dependent Anion Channel in the Treatment of Parkinson’s Disease

Agitation and Dementia: Prevention and Treatment Strategies in Acute and Chronic Conditions

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