Cognitive impairment in bipolar disorder Neuroprogression or behavioral variant frontotemporal dementia?

Borges, Saulo Queiroz; Corrêa, Thiago Xavier; Trindade, Isabela Oliveira Azevedo; Amorim, Rivadávio Fernandes Batista de; Toledo, Maria Alice de Vilhena

doi:10.1590/1980-57642018dn13-040016

Cited by 13 publications

(15 citation statements)

References 26 publications

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“…У дослідженнях останніх років наголошується на наявності у хворих на БАР виражених когнітивних порушень ймовірно пов'язаних з глибокими структурними морфологічними змінами у структурах мозку [11], які включають дефіцит виконавської функції, уваги та пам›яті [12]. Ці порушення можуть виявлятися не лише на нозологічному [13], а й на донозологічному етапах [14].…”

Section: вступunclassified

Features of cognitive disorders in patients with primary episodes of bipolar affective disorder

Mysula¹

2020

ScienceRise: Medical Science

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Мета роботи-вивчити особливості когнітивних порушень при первинному епізоді біполярного афективного розладу з урахуванням гендерного фактору і клінічного варіанту. Матеріали і методи. За допомогою тесту Струпа обстежено 153 хворих з первинним епізодом біполярного афективного розладу: з переважанням депресивної симптоматики (44 чоловіка і 75 жінок), з переважанням маніакальної симптоматики (15 чоловіків і 8 жінок) та з одночасною наявністю депресивної та маніакальної симптоматики або зі швидкою зміною фаз (6 чоловіків і 5 жінок).

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Section: вступunclassified

Features of cognitive disorders in patients with primary episodes of bipolar affective disorder

Mysula¹

2020

ScienceRise: Medical Science

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“…All these neuronal abnormalities in BD can result in gross morphological changes, such as reduced prefrontal and hippocampal volumes leading to a reorganization of brain circuits, resulting in cognitive, emotional, and functional de cits 2 . Other studies showed that the severity of BD and loss of response to treatment are correlated with the number of previous episodes 3 . Thus, the progressive structural and biochemical changes in the prodromal and early stages of the disease will evolve to more advanced stages, producing a slow evolution of the clinical process, called neuroprogression.…”

Section: Introduction 11 Bipolar Disorder Neuroin Ammation and Neuroprogressionmentioning

confidence: 97%

Can we prevent the neuroinflammation and neuroprogression produced by oxidative stress in euthymic bipolar patients, using mood stabilizers?

Lima

Cyrino

Ferreira

et al. 2022

Preprint

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Bipolar Disorder (BD) is associated with systemic toxicity, represented by changes in the biomarkers, associated with mood episodes, leading to neurological damage, which may reflect on cognitive functions and functionality, and the progression of the disease. We aimed to analyze the effect of four biomarkers superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes, and thiobarbituric acid reactive substances (TBA-RS) related to oxidative stress in BD and to correlate them with cognitive functions and functionality. We studied 50 bipolar patients type I/II, in the euthymic phase, which was divided into two subgroups with 25 patients, (≤3 years and ≥10 years of diagnosis, from the first episode of mania), and 25 control patients. To analyze frontal cognitive functions and functionality, we used the tests: Frontal Assessment Battery (FAB) and Functioning Assessment Short Test (FAST), respectively. The FAST test scores results were ≤3 years (20.63±8.21), ≥10 years (27.80±12.50), and control group (9.80±5.94), p<0.001. Changes occurred in all domains. The FAB test scores were ≤3 years (14.64±2.48), ≥10 years (12.44±2.78), and control group (15.84±1.55), p<0.001, and showed lower scores in four domains. The oxidative stress showed an increase in TBA-RS levels: ≤3 years (3.18±1.17), ≥10 years (3.01±1.03) compared to the control group (1.62±0.28), p<0.0001; and in the CAT enzyme activity we found, ≤3 years (8.10±4.18), ≥10 years (9.41±4.95), compared to the control group (3.47±0.77), p<0.0001. Even during the euthymic phase, bipolar patients showed and maintained an increase in CAT activity and lipid peroxidation with significant changes in the FAB and FAST tests in different groups of patients, demonstrating impairment in cognitive functions and functionality since disease onset.

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“…Progressive structural and biochemical changes in the prodromal and early stages of the disease, produce a slowly evolving clinical process called neuroprogression. The typical patient exhibits a slow decline in behavioral and cognitive functions associated with a weaker response to treatment (Berk et al, 2011 ; Borges et al, 2019 ). This slow progression prevents early diagnosis and rapid initiation of appropriate treatment.…”

Section: Introductionmentioning

confidence: 99%

Concepts of Neuroinflammation and Their Relationship With Impaired Mitochondrial Functions in Bipolar Disorder

Cyrino

Lima

Ullmann

et al. 2021

Front. Behav. Neurosci.

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Bipolar disorder (BD) is a chronic psychiatric disease, characterized by frequent behavioral episodes of depression and mania, and neurologically by dysregulated neurotransmission, neuroplasticity, growth factor signaling, and metabolism, as well as oxidative stress, and neuronal apoptosis, contributing to chronic neuroinflammation. These abnormalities result from complex interactions between multiple susceptibility genes and environmental factors such as stress. The neurocellular abnormalities of BD can result in gross morphological changes, such as reduced prefrontal and hippocampal volume, and circuit reorganization resulting in cognitive and emotional deficits. The term “neuroprogression” is used to denote the progressive changes from early to late stages, as BD severity and loss of treatment response correlate with the number of past episodes. In addition to circuit and cellular abnormalities, BD is associated with dysfunctional mitochondria, leading to severe metabolic disruption in high energy-demanding neurons and glia. Indeed, mitochondrial dysfunction involving electron transport chain (ETC) disruption is considered the primary cause of chronic oxidative stress in BD. The ensuing damage to membrane lipids, proteins, and DNA further perpetuates oxidative stress and neuroinflammation, creating a perpetuating pathogenic cycle. A deeper understanding of BD pathophysiology and identification of associated biomarkers of neuroinflammation are needed to facilitate early diagnosis and treatment of this debilitating disorder.

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Cognitive impairment in bipolar disorder Neuroprogression or behavioral variant frontotemporal dementia?

Cited by 13 publications

References 26 publications

Features of cognitive disorders in patients with primary episodes of bipolar affective disorder

Features of cognitive disorders in patients with primary episodes of bipolar affective disorder

Can we prevent the neuroinflammation and neuroprogression produced by oxidative stress in euthymic bipolar patients, using mood stabilizers?

Concepts of Neuroinflammation and Their Relationship With Impaired Mitochondrial Functions in Bipolar Disorder

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