Cerebrometabolic Aspects of Delirium in Relationship to Dementia

Blass, John P.; Gibson, Gary E.

doi:10.1159/000017165

Cited by 62 publications

(51 citation statements)

References 8 publications

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“…are sufficient to induce mental and neurological impairments similar to those of AD, it is evident that mitochondrial dysfunction may play a role in the onset of AD [173]. Characteristics of AD include damaged mitochondria and increased oxidative stress, which is consistent with the finding that damaged mitochondria produce more ROS and less ATP compared to their normal counterparts [174].…”

Section: Role Of Mitochondrial Dysfunction and Oxidative Stress In Adsupporting

confidence: 73%

Role of Environmental and Inflammatory Toxicity in Neuronal Cell Death

Somayajulu-Nitu¹,

Domazet-Damjanov²,

Matei³

et al. 2008

TOTOXIJ

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Section: Role Of Mitochondrial Dysfunction and Oxidative Stress In Adsupporting

confidence: 73%

Role of Environmental and Inflammatory Toxicity in Neuronal Cell Death

Somayajulu-Nitu¹,

Domazet-Damjanov²,

Matei³

et al. 2008

TOTOXIJ

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“…Five of eight (62.5%) patients in the prolonged delirium group who were able to ambulate outdoors were housebound at final followup (p = 0.003). similar causative factors, such as excitotoxic neuronal damage and neuron death [1,5,11].…”

Section: Discussionmentioning

confidence: 99%

Frequency, Risk Factors, and Prognosis of Prolonged Delirium in Elderly Patients After Hip Fracture Surgery

Lee

et al. 2011

Clinical Orthopaedics &Amp; Related Research

101

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Background Delirium in elderly patients after hip fracture surgery is believed to be a transient event, although it frequently lasts for more than 4 weeks. Questions/purposes We determined the incidence, risk factors, morbidity, and mortality of prolonged delirium in elderly patients after hip fracture surgery. Patients and Methods We evaluated 232 elderly patients (older than 65 years) (232 hips) who underwent hip fracture surgery for the development and duration of delirium and categorized them into three groups; nondelirium group, transient (B 4 weeks) delirium group, and prolonged ([ 4 weeks) delirium group. Patients underwent a global geriatric evaluation, which included postoperative complications, mortality, and functional and mental status evaluations. The three groups were compared with respect to these variables. Results Seventy patients (30.2%) had delirium develop, and among these, 14 (20%) had prolonged delirium with a total incidence of 6%. Multivariate analysis showed preinjury dementia was a risk factor of prolonged delirium. At the final followup, five (62.5%) of the eight patients who were ambulatory outdoors in the prolonged delirium group became housebound, whereas only 18 (16.4%) of the 110 patients who were ambulatory outdoors in the nondelirium group became housebound. Survival at 40 months was 81.0% (95% confidence interval, 72.6%-89.3%) in the nondelirium group and 63.6% (95% confidence interval, 35.2%-92.

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“…The reaction requires either NAD+ or NADP+ as coenzyme, yielding NADH and NADPH, respectively. Significant decreases were observed in the activities of NADs in addition to the α-ketoglutarate dehydrogenase complex, which have also been observed in AD brains [40]. It is not known whether isocitrate dehydrogenases specific for NAD+ play a role in cellular defense against oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

“…However, since it is involved in the oxidation of glucose in the brain, it is possible that decreased glucose metabolism in prion diseases may precedes clinical changes. In addition, diminished brain metabolism is by itself a well-documented cause of cognitive abnormalities of the types associated with Creutzfeldt-Jakob disease and AD [40]. A recent study on PrP C knockout mice has shown that PrP C in β-cells is involved in glucoregulation [41].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of β-Soluble N-Ethylmaleimide-Sensitive Factor Attachment Protein: Proteomics-Based Identification in Early-Stage Prion Disease

et al. 2015

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Prion diseases are known as neurodegenerative diseases of the central nervous system with a long incubation period. Alzheimer's disease (AD) and prion diseases share the hallmark of severe neuronal loss, although their pathogenic mechanisms are similarly incomplete. It appears that these two neurodegenerative diseases share a complex deterioration of function involved in the onset of neuronal loss. To investigate presymptomatic biochemical changes indicative of the initial stage of prion diseases and decipher the pathophysiological mechanisms of these two neurodegenerative diseases, we performed a differential proteomic analysis on brain tissues of 263K-infected hamsters during the presymptomatic period and transgenic APPSWE, PSEN1dE9 mice (a mouse model of AD). We identified 7 differentially expressed proteins including the β-soluble N-ethylmaleimide-sensitive factor attachment protein (β-SNAP) by 2-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The β-SNAP expression patterns in the brains of cases and controls were further quantified by Western blotting. β-SNAP showed an early decrease followed by a progressive depletion. The expression of β-SNAP was also significantly downregulated in the mouse model of AD. β-SNAP is brain-specific and known to bind to the SNAP receptors and is therefore involved in the control of neurotransmitter release as well as in constitutive vesicular transport. Our results suggest that presynaptic failure and abnormalities in neurotransmission may be early events in the development of neuronal dysfunction.

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Cerebrometabolic Aspects of Delirium in Relationship to Dementia

Cited by 62 publications

References 8 publications

Role of Environmental and Inflammatory Toxicity in Neuronal Cell Death

Role of Environmental and Inflammatory Toxicity in Neuronal Cell Death

Frequency, Risk Factors, and Prognosis of Prolonged Delirium in Elderly Patients After Hip Fracture Surgery

Downregulation of β-Soluble N-Ethylmaleimide-Sensitive Factor Attachment Protein: Proteomics-Based Identification in Early-Stage Prion Disease

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