Cerebral perfusion (HMPAO-SPECT) in patients with depression with cognitive impairment versus those with mild cognitive impairment and dementia of Alzheimer’s type: a semiquantitative and automated evaluation

Staffen, Wolfgang; Bergmann, Jürgen; Schönauer, U.; Zauner, Harald; Kronbichler, Martin; Golaszewski, Stefan; Ladurner, G

doi:10.1007/s00259-008-1028-2

Cited by 42 publications

(31 citation statements)

References 52 publications

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“…We hypothesize that this compromised neurovasculature, together with widespread fibrin deposition, might lead to deficits in cerebral blood flow in these mice. Since hypoperfusion can lead to cognitive decline [36, 37], our current findings support our previous report that plg−/− mice exhibit memory deficits [5]. Our results also correlate well with what is observed in chronic neurodegenerative diseases in humans, such as MS and AD.…”

Section: Discussionsupporting

confidence: 92%

“…Studies on postmortem tissue from these patients often show reduced neurovascular integrity and leakage of fibrin into the brain parenchyma [1–3]. AD and MS patients also present with hypoperfusion [37, 38], which could ultimately lead to their cognitive deficits. Future studies that examine the role of plasmin in neurodegenerative disease pathophysiology may be warranted as plasmin may have a significant impact on neurovascular integrity.…”

Section: Discussionmentioning

confidence: 99%

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Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain

Hultman

Cortes‐Canteli

Bounoutas

et al. 2014

Journal of Thrombosis and Haemostasis

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Background Excess fibrin in blood vessels is cleared by plasmin, the key proteolytic enzyme in fibrinolysis. Neurological disorders and head trauma can result in the disruption of the neurovasculature and the entry of fibrin and other blood components into the brain, which may contribute to further neurological dysfunction. Objectives While chronic fibrin deposition is often implicated in neurological disorders, the pathological contributions attributable specifically to fibrin have been difficult to ascertain. An animal model that spontaneously acquires fibrin deposits could allow researchers to better understand the impact of fibrin in neurological disorders. Methods Brains of plasminogen (plg)- and tissue plasminogen activator (tPA)-deficient mice were examined and characterized with regard to fibrin accumulation, vascular and neuronal health, and inflammation. Furthermore, the inflammatory response following intrahippocampal lipopolysaccharide (LPS) injection was compared between plg−/− and wild type (WT) mice. Results and Conclusions Both plg−/− and tPA−/− mice exhibited brain parenchymal fibrin deposits that appear to result from reduced neurovascular integrity. Markers of neuronal health and inflammation were not significantly affected by proximity to the vascular lesions. A compromised neuroinflammatory response was also observed in plg−/− compared to WT mice following intrahippocampal LPS injection. These results demonstrate that fibrin does not affect neuronal health in the absence of inflammation and suggest that plasmin may be necessary for a normal neuroinflammatory response in the mouse CNS.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain

Hultman

Cortes‐Canteli

Bounoutas

et al. 2014

Journal of Thrombosis and Haemostasis

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“…One previous SPECT study found that patients with aMCI showed hypometabolism in the frontal and subcortical areas and their abnormal social behaviors may be attributed to the impaired frontalsubcortical circuits [31]. Furthermore, [32] these studies also found that frontal cortical In our study, the loss of gray matter volume and reduction of ALFF were observed in the superior temporal gyrus and insula, which is consistent with the Xenon-enhanced computed tomography PET study [33]. A previous PET study also suggested that loss of metabolism also occurs at these two regions in the prodromal stage of AD [34].…”

Section: Discussionmentioning

confidence: 99%

Early morphological brain abnormalities in patients with amnestic mild cognitive impairment

Yin¹,

Jia

et al. 2014

Translational Neuroscience

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Patients with amnestic mild cognitive impairment (aMCI) are at an increased risk of further deterioration and eventually developing Alzheimer's disease (AD). Therefore, the identification of specific markers for this disease such as radiological markers is of great diagnostic and clinical significance. Our previous work has shown that magnetic resonance imaging (MRI) is a powerful tool to identify unique imaging features in patients with aMCI. Herein, we calculated the gray matter volume by structural magnetic resonance imaging (sMRI), and spontaneous low frequency fluctuations (LFF) using resting-state functional MRI (rs-fMRI) in 11 patients with aMCI and 22 normal control patients. Compared with the control group, patients with aMCI showed significant reduction of gray matter volume in the inferior frontal gyrus, inferior parietal lobule, anterior cingulated cortex, and insula and superior temporal gyrus. Patients with aMCI also showed significantly lower amplitudes of low-frequency fluctuations (ALFF) in the posterior cingulate cortex, precuneus, temporal gyrus and inferior parietal lobule when compared with the control group. However, in several other brain regions including the occipital lobe and cerebellum, the ALFF in patients with aMCI was significantly increased. The variation in ALFF between the two groups remained significant after adjustment for structural differences. Our results obtained in this pilot study are consistent with our previous finding and collectively show that patients with aMCI have abnormal MRI imaging findings. The pathological basis of these imaging features in patients with aMCI needs to be further explored.

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“…For this reason, the significance of abnormalities in MCI, usually defined as subjective and objective cognitive impairment without functional impairment, are difficult to assess: unless brains come to pathological examination shortly after the scan, intervening illness is likely to blur the picture. At best, patterns of hypoperfusion in MCI patients that are typical of AD will predict later conversion to dementia [56][57][58][59]. Of greatest interest is, of course, whether imaging can inform treatment decisions.…”

Section: Sensitivity and Specificitymentioning

confidence: 99%

Is there Still a Place for Perfusion SPECT in the Diagnosis of Dementia?

Ebmeier

2010

TONMEDJ

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Abstract:Although research interest within functional imaging has moved towards applications of MRI, such as BOLD and perfusion imaging, there is a wealth of clinical experience in emission tomographic imaging techniques that make the use of these modalities relevant for the decades to come. This review touches upon the technical and practical issues that distinguish SPECT from PET, describes perfusion and metabolic changes observed in the dementias, compares the clinical utility of the two techniques, and reports data on clinical sensitivity and specificity, as well as diagnostic head-to head comparisons in dementia, and specifically Alzheimer's disease. While few centres have a genuine choice between PET and SPECT, either appears to be good enough to help with the differential diagnosis of dementia in difficult cases.

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Cerebral perfusion (HMPAO-SPECT) in patients with depression with cognitive impairment versus those with mild cognitive impairment and dementia of Alzheimer’s type: a semiquantitative and automated evaluation

Cited by 42 publications

References 52 publications

Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain

Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain

Early morphological brain abnormalities in patients with amnestic mild cognitive impairment

Is there Still a Place for Perfusion SPECT in the Diagnosis of Dementia?

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