Demencia con cuerpos de Lewy y enfermedad de Alzheimer: diagnóstico diferencial mediante estudio de la inervación simpática cardíaca con MIBG

Estorch, Montserrat; Camacho, Valle; Fuertes, Jordi; Rodríguez-Revuelto, A; Hernández, M. Ángeles; Flotats, Albert; Kulisevsky, Jaime; Carrió, I

doi:10.1157/13090655

Cited by 9 publications

(1 citation statement)

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“…Although sympathetic denervation may lead to postsynaptic supersensitivity due to lack of neural uptake for norepinephrine [37], to what extent adrenergic denervation or desensitization contributes to myocardial complications in AD patients remains controversial. Several reports have been seen to discriminate changes in cardiac sympathetic innervation of AD patients from other neurodegenerative disease such as dementia with Lewy bodies and vascular dementia [38]–[40]. These studies measured cardiac uptake of metaiodobenzylguanidine (MIBG), a physiologic analogue of norepinephrine [41], as a mean of noninvasive index of the integrity of sympathetic neurotransmission in the heart of AD patients.…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocyte Contractile Dysfunction in the APPswe/PS1dE9 Mouse Model of Alzheimer's Disease

et al. 2009

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ObjectivesAmple clinical and experimental evidence indicated that patients with Alzheimer's disease display a high incidence of cardiovascular events. This study was designed to examine myocardial histology, cardiomyocyte shortening, intracellular Ca2+ homeostasis and regulatory proteins, electrocardiogram, adrenergic response, endoplasmic reticulum (ER) stress and protein carbonyl formation in C57 wild-type (WT) mice and an APPswe/PS1dE9 transgenic (APP/PS1) model for Alzheimer's disease.MethodsCardiomyocyte mechanical properties were evaluated including peak shortening (PS), time-to-PS (TPS), time-to-relengthening (TR), maximal velocity of shortening and relengthening (±dL/dt), intracellular Ca2+ transient rise and decay.ResultsLittle histological changes were observed in APP/PS1 myocardium. Cardiomyocytes from APP/PS1 but not APP or PS1 single mutation mice exhibited depressed PS, reduced±dL/dt, normal TPS and TR compared with WT mice. Rise in intracellular Ca2+ was lower accompanied by unchanged resting/peak intracellular Ca2+ levels and intracellular Ca2+ decay in APP/PS1 mice. Cardiomyocytes from APP/PS1 mice exhibited a steeper decline in PS at high frequencies. The responsiveness to adrenergic agonists was dampened although β1-adrenergic receptor expression was unchanged in APP/PS1 hearts. Expression of the Ca2+ regulatory protein phospholamban and protein carbonyl formation were downregulated and elevated, respectively, associated with unchanged SERCA2a, Na+-Ca2+ exchanger and ER stress markers in APP/PS1 hearts. Our further study revealed that antioxidant N-acetylcysteine attenuated the contractile dysfunction in APP/PS1 mice.ConclusionsOur results depicted overt cardiomyocyte mechanical dysfunction in the APP/PS1 Alzheimer's disease model, possibly due to oxidative stress.

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Section: Discussionmentioning

confidence: 99%