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1.
Neurobiol Learn Mem ; 185: 107529, 2021 Sep 29.
Artigo em Inglês | MEDLINE | ID: mdl-34597816

RESUMO

There is evidence suggesting that online consolidation during retrieval-mediated learning interacts with offline consolidation during subsequent sleep to transform memory. Here we investigate whether this interaction persists when retrieval-mediated learning follows post-training sleep and whether the direction of this interaction is conditioned by the quality of encoding resulting from manipulation of the amount of sleep on the previous night. The quality of encoding was determined by computing the degree of similarity between EEG-activity patterns across restudy of face pairs in two groups of young participants, one who slept the last 4 h of the pre-training night, and another who slept 8 h. The offline consolidation was assessed by computing the degree of coupling between slow oscillations (SOs) and spindles (SPs) during post-training sleep, while the online consolidation was evaluated by determining the degree of similarity between EEG-activity patterns recorded during the study phase and during repeated recognition of either the same face pair (i.e., specific similarity) or face pairs sharing sex and profession (i.e., categorical similarity) to evaluate differentiation and generalization, respectively. The study and recognition phases were separated by a night of normal sleep duration. Mixed-effects models revealed that the stability of neural encoding moderated the relationship between sleep- and retrieval-mediated consolidation processes over left frontal regions. For memories showing lower encoding stability, the enhanced SO-SP coupling was associated with increased reinstatement of category-specific encoding-related activity at the expense of content-specific activity, whilst the opposite occurred for memories showing greater encoding stability. Overall, these results suggest that offline consolidation during post-training sleep interacts with online consolidation during retrieval the next day to favor the reorganization of memory contents, by increasing specificity of stronger memories and generalization of the weaker ones.

2.
Alzheimers Res Ther ; 13(1): 150, 2021 09 06.
Artigo em Inglês | MEDLINE | ID: mdl-34488875

RESUMO

BACKGROUND: Aging is associated with declining protective immunity and persistent low-grade inflammatory responses, which significantly contribute to Alzheimer's disease (AD) pathogenesis. Detecting aging-related cerebral vulnerability associated with deterioration of the immune system requires from non-invasive biomarkers able to detect failures in the brain-immunity connection. Reduced levels of salivary lactoferrin (sLF), an iron-binding protein with immunomodulatory activity, have been related to AD diagnosis. However, it remains unknown whether decreased sLF is associated with increased cortical amyloid-beta (Aß) load and/or with loss of cortical integrity in normal aging. METHODS: Seventy-four cognitively normal older adults (51 females) participated in the study. We applied multiple linear regression analyses to assess (i) whether sLF is associated with cortical Aß load measured by 18F-Florbetaben (FBB)-positron emission tomography (PET), (ii) whether sLF-related variations in cortical thickness and cortical glucose metabolism depend on global Aß burden, and (iii) whether such sLF-related cortical abnormalities moderate the relationship between sLF and cognition. RESULTS: sLF was negatively associated with Aß load in parieto-temporal regions. Moreover, sLF was related to thickening of the middle temporal cortex, increased FDG uptake in the posterior cingulate cortex, and poorer memory. These associations were stronger in individuals showing the highest Aß burden. CONCLUSIONS: sLF levels are sensitive to variations in cortical Aß load, structural and metabolic cortical abnormalities, and subclinical memory impairment in asymptomatic older adults. These findings provide support for the use of sLF as a non-invasive biomarker of cerebral vulnerability in the general aging population.


Assuntos
Doença de Alzheimer , Lactoferrina , Idoso , Envelhecimento , Doença de Alzheimer/diagnóstico por imagem , Peptídeos beta-Amiloides/metabolismo , Feminino , Humanos , Tomografia por Emissão de Pósitrons
3.
J Gerontol A Biol Sci Med Sci ; 76(10): 1839-1845, 2021 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-33522564

RESUMO

BACKGROUND: Determining susceptibility to Alzheimer's disease (AD) in asymptomatic individuals requires from noninvasive, simple, and inexpensive markers that can be easily obtained in primary care settings. While saliva meets all these requirements, there is a lack of evidence linking salivary constituents to in vivo AD pathology in aging. METHODS: We examined the potential of salivary total antioxidant capacity (TAC) for identifying global cortical amyloid-beta (Aß) burden, deficits in regional glucose uptake, and poorer cognition in 71 cognitively normal older adults. We further assessed whether salivary TAC-related cognitive performance was associated with higher Aß load and lower cortical glucose consumption. RESULTS: Linear regression analyses adjusted by age, sex, years of education, and ApoE4 status showed that salivary TAC was associated with slower processing speed and poorer sustained attention, as well as with higher Aß load and lower glucose metabolism in cortical regions vulnerable to cognitive aging and AD. Results also revealed that lower scores in processing speed and sustained attention were associated with greater Aß burden and lower regional glucose consumption, respectively. CONCLUSIONS: Together, these findings support the use of salivary TAC for preventive screening and detection of cerebral vulnerability to AD. Further research is needed to evaluate the utility of salivary TAC as a clinical marker.

4.
Aging (Albany NY) ; 12(21): 21004-21022, 2020 11 04.
Artigo em Inglês | MEDLINE | ID: mdl-33147571

RESUMO

Identifying cerebral vulnerability in late life may help prevent or slow the progression of aging-related chronic diseases. However, non-invasive biomarkers aimed at detecting subclinical cerebral changes in the elderly are lacking. Here, we have examined the potential of plasma total tau (t-tau) for identifying cerebral and cognitive deficits in normal elderly subjects. Patterns of cortical thickness and cortical glucose metabolism were used as outcomes of cerebral vulnerability. We found that increased plasma t-tau levels were associated with widespread reductions of cortical glucose uptake, thinning of the temporal lobe, and memory deficits. Importantly, tau-related reductions of glucose consumption in the orbitofrontal cortex emerged as a determining factor of the relationship between cortical thinning and memory loss. Together, these results support the view that plasma t-tau may serve to identify subclinical cerebral and cognitive deficits in normal aging, allowing detection of individuals at risk for developing aging-related neurodegenerative conditions.


Assuntos
Envelhecimento/sangue , Cognição , Disfunção Cognitiva/sangue , Proteínas tau/sangue , Fatores Etários , Idoso , Envelhecimento/psicologia , Peptídeos beta-Amiloides/metabolismo , Córtex Cerebral/diagnóstico por imagem , Córtex Cerebral/metabolismo , Envelhecimento Cognitivo , Disfunção Cognitiva/diagnóstico por imagem , Disfunção Cognitiva/psicologia , Feminino , Glucose/metabolismo , Humanos , Imageamento por Ressonância Magnética , Masculino , Memória , Pessoa de Meia-Idade , Testes Neuropsicológicos , Fragmentos de Peptídeos/metabolismo , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Fatores de Risco
5.
Sci Adv ; 6(35): eaba1394, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32923622

RESUMO

Alzheimer's disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ε4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ε4-carriers during a virtual navigation task. We report a selective impairment in APOE ε4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations when no compensatory strategies were available, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ε4-carriers. Furthermore, posterior cingulate/retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.

6.
Brain Struct Funct ; 225(2): 841-851, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32048020

RESUMO

Identifying cerebral vulnerability in late life is of paramount importance to prevent pathological trajectories of aging before the onset of symptoms. Considerable evidence suggests that impaired antioxidant mechanisms are a fingerprint of aging-related conditions, but there is a lack of human research linking total antioxidant capacity (TAC) measured in peripheral blood to in vivo brain changes and other factors featuring accelerated aging. To address this issue, we have assessed in cognitively normal elderly subjects (N = 100) correlations between serum TAC, using the oxygen radical absorbance capacity assay, surface-based cortical thickness, surface-based 18F-fluorodeoxyglucose positron emission tomography cortical uptake, and different factors associated with accelerated aging [i.e., serum homocysteine (HCY), self-reported memory problems, and self-reported patterns of physical activity]. While no relationship was observed between serum TAC and variations in cortical thickness, decreased TAC level was significantly associated with lower FDG uptake in temporal lobes bilaterally. Remarkably, decreased TAC level was linked to increased HCY concentrations, more subjective memory complaints, and lower frequency of physical activity. Overall, our results suggest that decreased serum TAC level may be helpful to detect vulnerable trajectories of aging.


Assuntos
Envelhecimento/sangue , Antioxidantes/metabolismo , Encéfalo/metabolismo , Glucose/metabolismo , Idoso , Feminino , Fluordesoxiglucose F18 , Homocisteína/sangue , Humanos , Masculino , Pessoa de Meia-Idade , Capacidade de Absorbância de Radicais de Oxigênio , Tomografia por Emissão de Pósitrons
7.
Sci Rep ; 10(1): 1449, 2020 01 29.
Artigo em Inglês | MEDLINE | ID: mdl-31996775

RESUMO

Sleep is thought to play a complementary role in human memory processing: sleep loss impairs the formation of new memories during the following awake period and, conversely, normal sleep promotes the strengthening of the already encoded memories. However, whether sleep can strengthen deteriorated memories caused by insufficient sleep remains unknown. Here, we showed that sleep restriction in a group of participants caused a reduction in the stability of EEG activity patterns across multiple encoding of the same event during awake, compared with a group of participants that got a full night's sleep. The decrease of neural stability patterns in the sleep-restricted group was associated with higher slow oscillation-spindle coupling during a subsequent night of normal sleep duration, thereby suggesting the instantiation of restorative neural mechanisms adaptively supporting cognition and memory. Importantly, upon awaking, the two groups of participants showed equivalent retrieval accuracy supported by subtle differences in the reinstatement of encoding-related activity: it was longer lasting in sleep-restricted individuals than in controls. In addition, sustained reinstatement over time was associated with increased coupling between spindles and slow oscillations. Taken together, these results suggest that the strength of prior encoding might be an important moderator of memory consolidation during sleep. Supporting this view, spindles nesting in the slow oscillation increased the probability of correct recognition only for weakly encoded memories. Current results demonstrate the benefit that a full night's sleep can induce to impaired memory traces caused by an inadequate amount of sleep.


Assuntos
Cognição/fisiologia , Consolidação da Memória/fisiologia , Transtornos da Memória/terapia , Memória/fisiologia , Privação do Sono/terapia , Adolescente , Adulto , Feminino , Humanos , Masculino , Modalidades de Fisioterapia , Recuperação de Função Fisiológica , Fases do Sono , Sono de Ondas Lentas , Adulto Jovem
8.
Cereb Cortex ; 30(4): 2083-2098, 2020 04 14.
Artigo em Inglês | MEDLINE | ID: mdl-31799623

RESUMO

Evidence suggests that the basal forebrain (BF) cholinergic system degenerates early in the course of Alzheimer's disease (AD), likely due to the vulnerability of BF cholinergic neurons to tau pathology. However, it remains unclear whether the presence of tauopathy is the only requirement for initiating the BF degeneration in asymptomatic subjects at risk for AD (AR-AD), and how BF structural deficits evolve from normal aging to preclinical and prodromal AD. Here, we provide human in vivo magnetic resonance imaging evidence supporting that abnormal cerebrospinal fluid levels of phosphorylated tau (T+) are selectively associated with bilateral volume loss of the nucleus basalis of Meynert (nbM, Ch4) in AR-AD individuals. Spreading of atrophy to medial septum and vertical limb of diagonal band Broca (Ch1-Ch2) occurred in both preclinical and prodromal AD. With the exception of A+, all groups revealed significant correlations between volume reduction of BF cholinergic compartments and atrophy of their innervated regions. Overall, these results support the central role played by tauopathy in instigating the nbM degeneration in AR-AD individuals and the necessary coexistence of both AD proteinopathies for spreading damage to larger BF territories, thus affecting the core of the BF cholinergic projection system.

9.
Transl Neurodegener ; 8: 34, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31700619

RESUMO

Background: Previous studies have shown that expression levels of miR-181c are downregulated by amyloid-ß (Aß) deposition and chronic cerebral hypoperfusion, both factors largely associated with the development of AD. Moreover, reduced 2-[18F]fluoro-2-deoxy-D-glucose (FDG)-PET brain metabolism and volume loss of regions of the medial temporal lobe have been generally recognized as hallmarks of AD. Based on this evidence, we have here investigated potential associations between serum levels of miR-181c-5p and these AD signatures in asymptomatic elderly subjects. Methods: Ninety-five normal elderly subjects underwent clinical, cognitive, structural MRI, and FDG-PET explorations. Serum expression levels of miR-181c-5p and plasma Aß concentrations were further analyzed in this cohort. Regression analyses were performed to assess associations between serum miR-181c-5p levels and cognitive functioning, plasma Aß, structural and metabolic brain changes. Results: Decreased serum expression of miR-181c-5p was associated with increased plasma levels of Aß1-40, deficits in cortical glucose metabolism, and volume reduction of the entorhinal cortex. No significant associations were found between lower miR-181c-5p levels and cognitive deficits or cortical thinning. Conclusions: These findings suggest that deregulation of serum miR-181c-5p may indicate cerebral vulnerability in late life.

10.
Cereb Cortex ; 29(10): 4426-4437, 2019 09 13.
Artigo em Inglês | MEDLINE | ID: mdl-30590432

RESUMO

Evidence has shown that microRNAs (miRNAs) are involved in molecular pathways responsible for aging and prevalent aging-related chronic diseases. However, the lack of research linking circulating levels of miRNAs to changes in the aging brain hampers clinical translation. Here, we have investigated if serum expression of brain-enriched miRNAs that have been proposed as potential biomarkers in Alzheimer's disease (AD) (miR-9, miR-29b, miR-34a, miR-125b, and miR-146a) are also associated with cognitive functioning and changes of the cerebral cortex in normal elderly subjects. Results revealed that candidate miRNAs were linked to changes in cortical thickness (miR-9, miR-29b, miR-34a, and miR-125b), cortical glucose metabolism (miR-29b, miR-125b, and miR-146a), and cognitive performance (miR-9, miR-34a, and miR-125b). While both miR-29b and miR-125b were related to aging-related structural and metabolic cortical changes, only expression levels of miR-125b were associated with patterns of glucose consumption shown by cortical regions that correlated with executive function. Together, these findings suggest that serum expression of AD-related miRNAs are biologically meaningful in aging and may play a role as biomarkers of cerebral vulnerability in late life.


Assuntos
Envelhecimento/metabolismo , Doença de Alzheimer/sangue , Córtex Cerebral/anatomia & histologia , Cognição/fisiologia , MicroRNAs/sangue , Idoso , Biomarcadores/sangue , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Tomografia por Emissão de Pósitrons
11.
CorSalud ; 10(4): 330-335, oct.-dic. 2018. graf
Artigo em Espanhol | LILACS | ID: biblio-1089699

RESUMO

RESUMEN La asociación de dos tumores de diferente origen en un mismo paciente es cada vez más frecuente en la práctica clínica actual. Se presenta un caso con una rara asociación de mixoma cardíaco e hipernefroma, previamente tratado. Ante la presencia de manifestaciones neurológicas, inicialmente se planteó el diagnóstico de metástasis cerebral del tumor renal; luego, con el hallazgo ecocardiográfico de una masa intracardíaca, se pensó en la posibilidad de trombo, por lo que se decidió practicar cirugía cardíaca con carácter urgente para resecarla. El estudio anatomopatológico confirmó la existencia de un mixoma cardíaco, por lo que se trata de un enfermo con dos enfermedades tumorales cuya coincidencia ha sido pocas veces descrita.


ABSTRACT The association of two tumors of different origin in the same patient is becoming more frequent in the current clinical practice. Here is presented a case with a rare association of cardiac myxoma and hypernephroma, previously treated. Due to the presence of neurological symptoms, there was initially set a diagnosis of brain metastasis from the renal tumor; then, with the echocardiographic finding of an intracardiac mass, the possibility of thrombus was considered, therefore a cardiac surgery was decided to be performed urgently in order to resect it. The pathologic examination confirmed the existence of a cardiac myxoma, then, we have a patient with two tumor diseases whose coincidence has been rarely described.


Assuntos
Mixoma , Carcinoma de Células Renais , Embolia , Neoplasias Primárias Múltiplas
12.
Sleep Med Rev ; 42: 171-183, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30241997

RESUMO

Aging is characterized by a progressive increase in proinflammatory status. This state, known as inflammaging, has been associated with cognitive decline in normal and pathological aging. However, this relationship has been inconsistently reported, likely because it is conditioned by other factors also affected by the aging process. Sleep and adiposity are two factors in particular that show significant alterations with aging and have been related to both cognitive decline and inflammaging. Given the consequences this state also has for brain integrity and cognition, we discuss here evidence supporting the potential mediating role of chronic low-grade systemic inflammation in the complex relationship between impaired sleep, dysfunctional adiposity, and cognitive decline through the common pathway of neuroinflammation. This review proposes a multi-factor model of aging-related cognitive decline that highlights the reciprocal interactions between sleep, the circadian system, and inflammation on the one hand, and between sleep, adiposity, and hormone resistance on the other. The model identifies sleep and adiposity as modifiable lifestyle factors that can be targeted to maximize cognitive function and quality of life in the elderly.


Assuntos
Adiposidade/fisiologia , Envelhecimento , Disfunção Cognitiva/fisiopatologia , Inflamação/imunologia , Sono/fisiologia , Adiposidade/imunologia , Humanos , Sono/imunologia
13.
Cortex ; 101: 136-153, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29475078

RESUMO

In mild cognitive impairment (MCI), the APOE4 genotype is associated with accelerated memory decline, likely due to the impact of neuropathology on main cerebral networks required for successful memory retrieval and/or to decreased capacity for recruiting secondary networks that might compensate for that brain damage. Here, we tested this hypothesis in twenty-six healthy older adults and thirty-four MCI patients, of which sixteen were APOE4 carriers. Compared to controls, MCI showed hippocampal volume reduction, cortical thinning in frontal, temporal and parietal regions, and dysfunctional EEG oscillations across fronto-temporal networks. But importantly, APOE4 status was the critical factor in determining the impact of temporal lobe degeneration on memory in MCI individuals. Specifically, path analyses revealed that hippocampal damage in MCI was responsible for memory deterioration in APOE4 carriers, a relationship mediated by the serial intervention of three related factors in noncarriers. Temporal cortical thickness (first mediator) accounted for activation of functional networks through synchronized theta activity across temporal regions (second mediator), which, in turn, coordinated memory reactivation through desynchronized alpha/beta activity across sensorimotor areas (third mediator). Results revealed that, contrary to APOE4-carrier patients, noncarriers are successful in recruiting secondary cortical networks to improve memory performance as long as the integrity and functionality of the temporal lobe is preserved, a fact primarily dependent on hippocampal degeneration.


Assuntos
Apolipoproteína E4/genética , Associação , Disfunção Cognitiva/genética , Disfunção Cognitiva/fisiopatologia , Memória , Lobo Temporal/patologia , Idoso , Análise de Variância , Mapeamento Encefálico , Distribuição de Qui-Quadrado , Eletroencefalografia , Feminino , Lobo Frontal/diagnóstico por imagem , Lobo Frontal/patologia , Genótipo , Hipocampo/diagnóstico por imagem , Hipocampo/patologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Rede Nervosa/fisiopatologia , Testes Neuropsicológicos , Lobo Parietal/diagnóstico por imagem , Lobo Parietal/patologia , Lobo Temporal/diagnóstico por imagem
14.
Neurobiol Aging ; 64: 58-67, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29331877

RESUMO

The diagnostic value of cerebrospinal fluid (CSF) biomarkers is well established in Alzheimer's disease, but our current knowledge about how abnormal CSF levels affect cerebral integrity, at local and network levels, is incomplete in asymptomatic older adults. Here, we have collected CSF samples and performed structural magnetic resonance imaging scans in cognitively normal elderly as part of a cross-sectional multicenter study (SIGNAL project). To identify group differences in cortical thickness, white matter volume, and properties of structural networks, participants were split into controls (N = 20), positive amyloid-ß (Aß1-42+) (N = 19), and positive phosphorylated tau (N = 18). The Aß1-42+ group exhibited thickening of middle temporal regions, while positive phosphorylated tau individuals showed thinning in the superior parietal and orbitofrontal cortices. Subjects with abnormal CSF biomarkers further showed regional white matter atrophy and more segregated cortical networks, the Aß1-42+ group showing heightened isolation of cingulate and temporal cortices. Collectively, these findings highlight the relevance of combining structural brain imaging and connectomics for in vivo tracking of Alzheimer's disease lesions in asymptomatic stages.


Assuntos
Doença de Alzheimer/diagnóstico , Doença de Alzheimer/patologia , Córtex Cerebral/patologia , Substância Cinzenta/patologia , Rede Nervosa/patologia , Idoso , Peptídeos beta-Amiloides/líquido cefalorraquidiano , Atrofia , Biomarcadores/líquido cefalorraquidiano , Córtex Cerebral/diagnóstico por imagem , Estudos Transversais , Feminino , Substância Cinzenta/diagnóstico por imagem , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Fragmentos de Peptídeos/líquido cefalorraquidiano , Sintomas Prodrômicos , Risco , Proteínas tau/líquido cefalorraquidiano
15.
Brain Struct Funct ; 223(2): 597-607, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28900721

RESUMO

Considerable evidence suggests that circadian rhythmicity is progressively disrupted in senescence. Among clock genes, Period3 (PER3) has been associated with circadian phenotypes, homeostatic regulation of sleep, and cognitive performance in young adults. However, the effects of PER3 genotype on aging-related changes in both cognitive function and cortical integrity remain largely unknown. To shed light into this issue, we have investigated differences in cognitive performance, patterns of cortical thickness, and cortical glucose consumption in normal elderly subjects homozygous carriers of the short (PER34/4, n = 32) and long repeat alleles (PER35/5, n = 32). Relationships between cognitive performance and cortical thickness/metabolism were further explored for each PER3 genotype. We found that PER35/5 carriers had poorer cognitive performance (attention, executive function, semantic memory, and verbal fluency) and lower cortical integrity (structural and functional) than PER34/4. PER35/5 further showed thinning of temporo-parietal areas, and reductions of glucose consumption in fronto-temporo-parietal regions bilaterally. Moreover, PER35/5 subjects exhibited significant correlations between decreased glucose metabolism in fronto-parietal regions and poorer cognitive flexibility, though only correlations with lower glucose consumption of the supramarginal gyrus distinguished PER35/5 from PER34/4 groups. Overall, these findings enhance our understanding on the gene-brain interaction in aging, and may have further implications for the detection of subclinical cognitive decline associated with PER3 genotypes in late life.


Assuntos
Envelhecimento/genética , Córtex Cerebral/fisiologia , Cognição/fisiologia , Proteínas Circadianas Period/genética , Polimorfismo de Nucleotídeo Único/genética , Idoso , Córtex Cerebral/diagnóstico por imagem , Córtex Cerebral/metabolismo , Ritmo Circadiano/genética , Correlação de Dados , Feminino , Humanos , Processamento de Imagem Assistida por Computador , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Testes Neuropsicológicos , Tomografia por Emissão de Pósitrons , Estatísticas não Paramétricas
16.
Sci Rep ; 7(1): 7719, 2017 08 10.
Artigo em Inglês | MEDLINE | ID: mdl-28798397

RESUMO

Tremendous progress has been made over the last few years in understanding how sleep and amyloid-ß (Aß) cooperate to speed up the progression of Alzheimer's disease (AD). However, it remains unknown whether sleep deficits also interact with other risk factors that exacerbate the pathological cascade of AD. Based on evidence showing that higher levels of homocysteine (HCY) and sleep loss increase oxidative damage, we here investigate whether the relationship between HCY and total antioxidant capacity (TAC) is mediated by changes in objective sleep in healthy older (HO, N = 21) and mild cognitive impairment (MCI, N = 21) subjects. Results revealed that reduced TAC levels in MCI was significantly correlated with increased HCY, shorter sleep duration, lower sleep efficiency, and reduced volume of temporal regions. However, only the HCY-TAC association showed diagnostic value, and this relationship was mediated by poorer sleep quality in MCI patients. We further showed that HCY-related cerebral volume loss in MCI depended on the serial relationship between poorer sleep quality and lower TAC levels. These findings provide novel insights into how impaired sleep may contribute to maintain the relationship between HCY and oxidative stress in prodromal AD, and offer empirical foundations to design therapeutic interventions aimed to weaken this link.


Assuntos
Disfunção Cognitiva/etiologia , Disfunção Cognitiva/metabolismo , Homocisteína/metabolismo , Estresse Oxidativo , Sono , Idoso , Biomarcadores , Mapeamento Encefálico , Córtex Cerebral/diagnóstico por imagem , Córtex Cerebral/metabolismo , Córtex Cerebral/fisiopatologia , Cognição , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/psicologia , Suscetibilidade a Doenças , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade
17.
CorSalud ; 9(1)ene.-mar. 2017. ilus
Artigo em Espanhol | CUMED | ID: cum-69296

RESUMO

La endocarditis infecciosa es una enfermedad que involucra con más frecuencia a las válvulas cardíacas, pero también puede ocurrir sobre cuerdas tendinosas, o sobre el endocardio mural. Su lesión característica, la vegetación, consiste en una masa de plaquetas, fibrina, microcolonias de microorganismos y escasas células inflamatorias. Se presenta el caso de un hombre joven, diagnosticado con endocarditis infecciosa e insuficiencia valvular mitral con ruptura de las cuerdas tendinosas, que presentó paro cardiorrespiratorio y requirió reanimación cerebro-cardio-pulmonar con la que se logró la recuperación de la circulación espontánea. Finalmente fue llevado de emergencia al quirófano donde se realizó sustitución valvular mitral y conservación de las cuerdas tendinosas, con resultado satisfactorio y sin secuelas pulmonares o neurológicas(AU)


Assuntos
Humanos , Masculino , Adulto , Endocardite , Insuficiência da Valva Mitral , Parada Cardíaca , Anestesia , Reanimação Cardiopulmonar/métodos
18.
Cereb Cortex ; 27(8): 3881-3889, 2017 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-27371762

RESUMO

Extensive research suggests that basal forebrain (BF) cholinergic neurons are selectively vulnerable to Alzheimer's disease (AD). However, it remains unknown whether volume loss of BF cholinergic compartments parallels structural changes of their innervated regions in prodromal AD. To this aim, we have correlated volume of each BF compartment with cortical thickness and hippocampus/amygdala volume in 106 healthy older (HO) adults and 106 amnestic mild cognitive impairment (aMCI) patients. Correlations were limited to regions affected by atrophy in aMCI. The volume of the nucleus basalis of Meynert (NBM/Ch4) was positively correlated with thickness of the temporal cortex in aMCI, and with volume of amygdala in HO and aMCI, separately. Volume of the medial septum/diagonal band of Broca (Ch1-Ch3) was also positively correlated with volume of the hippocampus within the 2 groups. Only correlations between the NBM and their innervated regions showed diagnostic value. Unlike men, aMCI women showed a stronger association between volume of the NBM and thickness of the temporal lobe when compared with HO women. Altogether, these results reveal, for the first time in humans, that atrophy of NBM is associated with structural changes of their innervated regions in prodromal AD, being this relationship more evident in women.


Assuntos
Núcleo Basal de Meynert/diagnóstico por imagem , Disfunção Cognitiva/diagnóstico por imagem , Idoso , Tonsila do Cerebelo/diagnóstico por imagem , Tonsila do Cerebelo/patologia , Atrofia , Núcleo Basal de Meynert/patologia , Disfunção Cognitiva/patologia , Feminino , Hipocampo/diagnóstico por imagem , Hipocampo/patologia , Humanos , Processamento de Imagem Assistida por Computador , Imageamento por Ressonância Magnética , Masculino , Tamanho do Órgão , Caracteres Sexuais , Lobo Temporal/diagnóstico por imagem , Lobo Temporal/patologia
19.
Sci Rep ; 6: 31859, 2016 08 22.
Artigo em Inglês | MEDLINE | ID: mdl-27546195

RESUMO

Synaptic dysfunction, a key pathophysiological hallmark of Alzheimer's disease (AD), may account for abnormal memory-related EEG patterns in prodromal AD. Here, we investigate to what extent oscillatory EEG changes during memory encoding and/or retrieval enhance the accuracy of medial temporal lobe (MTL) atrophy in predicting conversion from amnestic mild cognitive impairment (aMCI) to AD. As expected, aMCI individuals that, within a 2-year follow-up period, developed dementia (N = 16) compared to healthy older (HO) (N = 26) and stable aMCI (N = 18) showed poorer associative memory, greater MTL atrophy, and lower capacity to recruit alpha oscillatory cortical networks. Interestingly, encoding-induced abnormal alpha desynchronized activity over the posterior cingulate cortex (PCC) at baseline showed significantly higher accuracy in predicting AD than the magnitude of amygdala atrophy. Nevertheless, the best accuracy was obtained when the two markers were fitted into the model (sensitivity = 78%, specificity = 82%). These results support the idea that synaptic integrity/function in the PCC is affected during prodromal AD and has the potential of improving early detection when combined with MRI biomarkers.


Assuntos
Doença de Alzheimer/complicações , Tonsila do Cerebelo/patologia , Giro do Cíngulo/fisiopatologia , Transtornos da Memória/diagnóstico por imagem , Idoso , Ritmo alfa , Doença de Alzheimer/fisiopatologia , Atrofia , Feminino , Giro do Cíngulo/diagnóstico por imagem , Humanos , Imageamento por Ressonância Magnética , Masculino , Transtornos da Memória/fisiopatologia , Pessoa de Meia-Idade
20.
J Gerontol A Biol Sci Med Sci ; 71(9): 1210-5, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-26946100

RESUMO

BACKGROUND: Evidence suggests a link between the presence of subjective memory complaints (SMC) and lower volume of the hippocampus, one of the first regions to show neuropathological lesions in Alzheimer's disease. However, it remains unknown whether this pattern of hippocampal atrophy is regionally specific and whether SMC are also paralleled by changes in peripheral levels of amyloid-beta (Aß). METHODS: The volume of hippocampal subregions and plasma Aß levels were cross-sectionally compared between elderly individuals with (SMC(+); N = 47) and without SMC (SMC(-); N = 48). Significant volume differences in hippocampal subregions were further correlated with plasma Aß levels and with objective memory performance. RESULTS: Individuals with SMC exhibited significantly higher Aß1-42 concentrations and lower volumes of CA1, CA4, dentate gyrus, and molecular layer compared with SMC(-) participants. Regression analyses further showed significant associations between lower volume of the dentate gyrus and both poorer memory performance and higher plasma Aß1-42 levels in SMC(+) participants. CONCLUSIONS: The presence of SMC, lower volumes of specific hippocampal regions, and higher plasma Aß1-42 levels could be conditions associated with aging vulnerability. If such associations are confirmed in longitudinal studies, the combination may be markers recommending clinical follow-up in nondemented older adults.


Assuntos
Envelhecimento , Doença de Alzheimer/diagnóstico , Peptídeos beta-Amiloides/sangue , Hipocampo/patologia , Transtornos da Memória/diagnóstico , Idoso , Doença de Alzheimer/sangue , Doença de Alzheimer/epidemiologia , Atrofia , Biomarcadores/sangue , Encéfalo/patologia , Estudos Transversais , Diagnóstico Diferencial , Feminino , Hipocampo/diagnóstico por imagem , Humanos , Imageamento por Ressonância Magnética , Masculino , Transtornos da Memória/sangue , Transtornos da Memória/epidemiologia , Pessoa de Meia-Idade , Testes Neuropsicológicos , Valor Preditivo dos Testes , Sensibilidade e Especificidade
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