Patterns of Striatal Degeneration in Frontotemporal Dementia

Halabi, Cathra; Halabi, Anasheh; Dean, David L.; Wang, Pei Ning; Boxer, Adam L.; Trojanowski, John Q.; DeArmond, Stephen J.; Miller, Bruce L.; Kramer, Joel H.; Seeley, William W.

doi:10.1097/wad.0b013e31824a7df4

Cited by 55 publications

(50 citation statements)

References 55 publications

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“…These findings further corroborate the specificity of the VMPFC [5] and striatum [40,41] in bvFTD. VMPFC changes, in particular in orbitofrontal and anterior cingulate cortices in bvFTD [42,43], that have been associated with many of the classical behavioural features in the disease, notably disinhibition, apathy, loss of insight and reduced empathy [44][45][46].…”

Section: Sv-ppa Vs Bvftdsupporting

confidence: 76%

Grey and white matter brain network changes in frontotemporal dementia subtypes

Nguyen

Bertoux

O’Callaghan

et al. 2013

Translational Neuroscience

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Grey and whIte matter braIn network chanGes In frontotemporal dementIa subtypes abstract Background: Frontotemporal dementia (FTD) comprises of three clinical syndromes, behavioural-variant frontotemporal dementia (bvFTD), semantic dementia (SV-PPA), and progressive nonfluent aphasia (NFV-PPA) with unique underlying neuroanatomical deficits. To date, however, grey matter structural differences and their connecting white matter tracts in this network have been mostly characterised in comparison to controls, whereas within FTD subtype comparisons in the same patients have not been explored. Methodology: In 94 participants, including bvFTD (n = 16), SV-PPA (n = 16) and NFV-PPA (n = 16), as well as an age-matched control group (n = 46), we employed voxel-based morphometry (VBM) and diffusion tensor imaging (DTI) to examine grey and white matter key signatures in each of the three FTD subtypes. Results: Our results showed that bvFTD had specific ventromedial prefrontal cortex and striatum grey matter atrophy along with their connecting white matter tracts compared to other FTD subtypes. By contrast, SV-PPA showed additional temporal pole grey matter damage to bvFTD and grey and white matter temporal, amygdala and insula changes compared to NFV-PPA. Finally, NFV-PPA showed mild insula grey and white matter changes compared to bvFTD but differed from SV-PPA only on anterior corpus callosum white matter changes. Conclusions: Our findings clearly indicate that not only grey matter regions of the FTD network but also their white matter connecting tracts have specific signatures for each FTD subtype. These promising findings highlight how neural network approaches can shed new light on neurodegenerative conditions and FTD in particular, which will inform future diagnostic and disease management. keywords

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Section: Sv-ppa Vs Bvftdsupporting

confidence: 76%

Grey and white matter brain network changes in frontotemporal dementia subtypes

Nguyen

Bertoux

O’Callaghan

et al. 2013

Translational Neuroscience

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“…This was further corroborated by structural neuroimaging studies that identified striatal atrophy in FTD, again with the most severe changes seen in bvFTD 78 79. In both bvFTD and PPA-nfv, atrophy has been shown in the caudate and putamen, as well as nucleus accumbens, with putaminal atrophy in bvFTD being more right lateralised and less severe than caudate atrophy 78 79.…”

Section: Disorders With Less Described Striatal Dysfunctionmentioning

confidence: 56%

“…By comparison, bvFTD patients have been reported to show a 25% caudate volume reduction compared with age-matched controls 91. Similarly, the nucleus accumbens and putamen appeared to be relatively spared in AD,78 80 although some studies have reported putaminal volume loss, in particular for the left putamen 92…”

Section: Disorders With Less Described Striatal Dysfunctionmentioning

confidence: 99%

Beyond and below the cortex: the contribution of striatal dysfunction to cognition and behaviour in neurodegeneration

O’Callaghan

Bertoux

Hornberger

2013

Journal of Neurology, Neurosurgery & Psychiatry

101

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Investigations of cognitive and behavioural changes in neurodegeneration have been mostly focussed on how cortical changes can explain these symptoms. In the proposed review, we will argue that the striatum has been overlooked as a critical nexus in understanding the generation of such symptoms. Although the striatum is historically more associated with motor dysfunction, there is increasing evidence from functional neuroimaging studies in the healthy that striatal regions modulate behaviour and cognition. This should not be surprising, as the striatum has strong anatomical connections to many cortical regions including the frontal, temporal and insula lobes, as well as some subcortical regions (amygdala, hippocampus). To date, however, it is largely unclear to what extent striatal regions are affected in many neurodegenerative conditions-and if so, how striatal dysfunction can potentially influence cognition and behaviour. The proposed review will examine the existing evidence of striatal changes across selected neurodegenerative conditions (Parkinson's disease, progressive supranuclear palsy, Huntington's disease, motor neuron disease, frontotemporal dementia and Alzheimer's disease), and will document their link with the cognitive and behavioural impairments observed. Thus, by reviewing the varying degrees of cortical and striatal changes in these conditions, we can start outlining the contributions of the striatal nexus to cognitive and behavioural symptoms. In turn, this knowledge will inform future studies investigating corticostriatal networks and also diagnostic strategies, disease management and future therapeutics of neurodegenerative conditions.

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“…While not yet described in FTD models, repetitive grooming has been described in several knockout mouse lines. 118–120 Again, there are interesting neuroanatomic parallels, as the striatum seems to be highly involved in both FTD-associated repetitive behavior 121,122 and repetitive grooming in mutant mice. 119,120 …”

Section: Future Opportunities With Ftd Modelsmentioning

confidence: 99%

Mouse models of frontotemporal dementia

Roberson

2012

Annals of Neurology

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The pace of discovery in frontotemporal dementia (FTD) has accelerated dramatically with the discovery of new genetic causes and pathological substrates of the disease. MAPT/Tau, GRN/progranulin, and C9ORF72 have emerged as common FTD genes, and TARDBP/TDP-43, VCP, FUS, and CHMP2B have been identified as less common genetic causes. TDP-43 and FUS have joined Tau as common neuropathological substrates of the disease. Mouse models provide an important tool for understanding the role of these molecules in FTD pathogenesis. Here, we review recent progress with mouse models based on Tau, TDP-43, progranulin, VCP, and CHMP2B. We also consider future prospects for FTD models, including developing new models to address unanswered questions. There are also opportunities for capitalizing on conservation of the salience network, which is selectively vulnerable in FTD, and the availability of FTD-related behavioral paradigms to analyze mouse models of the disease.

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Patterns of Striatal Degeneration in Frontotemporal Dementia

Cited by 55 publications

References 55 publications

Grey and white matter brain network changes in frontotemporal dementia subtypes

Grey and white matter brain network changes in frontotemporal dementia subtypes

Beyond and below the cortex: the contribution of striatal dysfunction to cognition and behaviour in neurodegeneration

Mouse models of frontotemporal dementia

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