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Functional neuroanatomy of the dementia syndrome (CROSBI ID 613092)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | domaća recenzija

Šimić, Goran Functional neuroanatomy of the dementia syndrome // Book of abstracts 4th Croatian Congress of Neuroscience / Croatian Society for Neuroscience (ur.). Zagreb: Croatian Insitute for Brain Research, 2013. str. 23-23

Podaci o odgovornosti

Šimić, Goran

engleski

Functional neuroanatomy of the dementia syndrome

Dementia is a multidimensional syndrome, which makes diagnosis and testing of novel treatments for primary causes of dementia (most notably Alzheimer's disease, AD) complicated. Recent advances in functional and structural MRl, including DTI tractography, have enabled the precise delineation of multiple large- scale distributed brain networks as well as identification of patterns of neuronal dysfunction in progressive neurodegenerative diseases. One of the main insights common to all studies is that, compared to baseline brain activity, only a small percentage of neurons is required to respond to an external stimulus (such task-related activation usually accounts for about only 1-5% of the total BOLD signal). Most of baseline activity is mediated by neurons that are constantly active and participate in the default mode network (DMN, also known as the resting state or task-negative network) (Deco et al., TINS, 2013). The DMN is anatomically defined by interconnections among several epicenters that include parts of the medial temporal lobe, parts of the medial prefrontal cortex and the posterior cingulate cortex and adjacent ventral precuneus and parietal cortex. It seems that DMN connectivity reflects the level of consciousness (Vanhaudenhuyse et al., Brain, 2010), generates spontaneous thoughts, and preferentially activates when individuals engage in internal tasks such as daydreaming, envisioning the future, and retrieving memories, while it is negatively correlated with brain systems that focus on external visual signals. The DMN undergoes developmental changes and is characterized by coherent neuronal oscillations at a rate lower than 0.1 Hz that become more consistent in children aged 9-12 years and in older subjects. As has been amply documented by structural (atrophy patterns of normal and AD patients) and functional MRI, the activity of DMN is severely deficient in AD compared to healthy elderly controls, so this measure has been recently proposed as a promising clinical marker of AD (Damoiseaux et al., Neurobiol. Aging, 2012 ; Greicius et al., curr. opin. Neurol., 2012 ; Lehmann et al., PNAS, 2013). During my talk I will attempt to reconcile these novel findings with known neuropathological data in support of an emerging etiopathogenetic mechanism by which β- amyloid in the common, late-onset form of sporadic AD may be released into the extracellular space from non-junctional varicosities of axons generated from abnormal tau-containing neurons of brainstem nuclei projecting to the DMN neurons (Šimić et al., Neuropathol. Appl. Neurobiol., 2009 ; Braak and Del Tredici, Acta Neuropathol., 2013).

Dementia; default mode network; functional MRl

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Podaci o prilogu

23-23.

2013.

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objavljeno

Podaci o matičnoj publikaciji

Book of abstracts 4th Croatian Congress of Neuroscience

Croatian Society for Neuroscience

Zagreb: Croatian Insitute for Brain Research

Podaci o skupu

4th Croatian Congress of Neuroscience

ostalo

20.09.2013-21.09.2013

Zagreb, Hrvatska

Povezanost rada

Temeljne medicinske znanosti, Kliničke medicinske znanosti