Strongly reduced volumes of putamen and thalamus in Alzheimer's disease: an MRI study

Jong, Laura W. de; Hiele, Karin van der; Veer, Ilya M.; Houwing, Jeanine J; Westendorp, Rudi G.J.; Bollen, E.; Bruin, Paul W. de; Middelkoop, Huub A. M.; Buchem, Mark A. van; Grond, Jeroen van der

doi:10.1093/brain/awn278

Cited by 451 publications

(356 citation statements)

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“…Only recently, the latter have been identified as regions with a high susceptibility for AD pathology. 25 Our findings of a progressive MTR reduction in the basal ganglia and thalamus are in line with the observation of a significant atrophy of the putamen and thalamus in AD. 25 We would also have expected to find MTR reductions in the cortex.…”

Section: Discussionsupporting

confidence: 90%

“…25 Our findings of a progressive MTR reduction in the basal ganglia and thalamus are in line with the observation of a significant atrophy of the putamen and thalamus in AD. 25 We would also have expected to find MTR reductions in the cortex. 16,26 However, due to limited image resolution and partial volume effects, we unfortunately were not able to obtain reliable and reproducible MTR values in the cortex, and therefore abstained from such analysis.…”

Section: Discussionsupporting

confidence: 90%

“…The origin of this asymmetry, which has also been observed in volumetric analyses, 25 has not been resolved so far, but it is quite plausible that structural damage of the left hemisphere is more relevant for the cognitive functions assessed. Thus, our MTR findings parallel the observation that volume loss of the left putamen and thalamus is a strong predictor for cognitive decline in AD, while the volume of the caudate nucleus was not associated with cognition.…”

Section: Discussionmentioning

confidence: 99%

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Longitudinal Magnetization Transfer Imaging in Mild to Severe Alzheimer Disease

Ropele

Schmidt²,

Enzinger³

et al. 2011

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE: MTI has been proposed as a sensitive technique for studying microstructural brain tissue changes in patients with AD, but the course of these changes over time is largely unknown. We therefore used a placebo-controlled study of memantine to follow the evolution of tissue damage in AD by means of MTR measurements and investigated how MTR changes were related to brain atrophy and cognition.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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Longitudinal Magnetization Transfer Imaging in Mild to Severe Alzheimer Disease

Ropele

Schmidt²,

Enzinger³

et al. 2011

AJNR Am J Neuroradiol

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“…The diffuse projections of these subcortical structures may account for the wide range of cognitive findings and cortical damage exhibited across the C9ORF72 mutation cohort here. Involvement of thalamus and cerebellar connections could underpin the prominent neuropsychiatric features shown by these cases (Andreasen et al, 1996;Schmahmann, 2005;Goossens et al, 2007;Straube et al, 2007;Schmahmann and Pandya, 2008;Tedesco et al, 2011), as well as episodic memory deficits ( Van der Werf et al, 2003;de Jong et al, 2008) somatic complaints, hallucinations and delusions (Kessler et al, 2009;Tedesco et al, 2011). Although none of our cases had frank cerebellar ataxia, this has been described in previous cases of chromosome 9 linked FTLD (Pearson et al, 2011).…”

Section: Discussionsupporting

confidence: 67%

O1‐05‐01: Frontotemporal dementia with the C9ORF72 hexanucleotide repeat expansion: Clinical, neuroanatomical and neuropathological features

Mahoney¹,

Beck²,

Rohrer

et al. 2012

Alzheimer's & Dementia

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An expanded hexanucleotide repeat in the C9ORF72 gene has recently been identified as a major cause of familial frontotemporal lobar degeneration and motor neuron disease, including cases previously identified as linked to chromosome 9. Here we present a detailed retrospective clinical, neuroimaging and histopathological analysis of a C9ORF72 mutation case series in relation to other forms of genetically determined frontotemporal lobar degeneration ascertained at a specialist centre. Eighteen probands (19 cases in total) were identified, representing 35% of frontotemporal lobar degeneration cases with identified mutations, 36% of cases with clinical evidence of motor neuron disease and 7% of the entire cohort. Thirty-three per cent of these C9ORF72 cases had no identified relevant family history. Families showed wide variation in clinical onset (43-68 years) and duration (1.7-22 years). The most common presenting syndrome (comprising a half of cases) was behavioural variant frontotemporal dementia, however, there was substantial clinical heterogeneity across the C9ORF72 mutation cohort. Sixty per cent of cases developed clinical features consistent with motor neuron disease during the period of follow-up. Anxiety and agitation and memory impairment were prominent features (between a half to two-thirds of cases), and dominant parietal dysfunction was also frequent. Affected individuals showed variable magnetic resonance imaging findings; however, relative to healthy controls, the group as a whole showed extensive thinning of frontal, temporal and parietal cortices, subcortical grey matter atrophy including thalamus and cerebellum and involvement of long intrahemispheric, commissural and corticospinal tracts. The neuroimaging profile of the C9ORF72 expansion was significantly more symmetrical than progranulin mutations with significantly less temporal lobe involvement than microtubule-associated protein tau mutations. Neuropathological examination in six cases with C9ORF72 mutation from the frontotemporal lobar degeneration series identified histomorphological features consistent with either type A or B TAR DNA-binding protein-43 deposition; however, p62-positive (in excess of TAR DNA-binding protein-43 positive) neuronal cytoplasmic inclusions in hippocampus and cerebellum were a consistent feature of these cases, in contrast to the similar frequency of p62 and TAR DNA-binding protein-43 deposition in 53 control cases with frontotemporal lobar degeneration-TAR DNA-binding protein. These findings corroborate the clinical importance of the C9ORF72 mutation in frontotemporal lobar degeneration, delineate phenotypic and neuropathological features that could help to guide genetic testing, and suggest hypotheses for elucidating the neurobiology of a culprit subcortical network.

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“…Volumetric loss in the thalamus has been proposed as a predictor of dementia, 46 while studies have demonstrated thalamic atrophy in PD with dementia compared with healthy individuals. 14,16 Previous studies have also demonstrated the relation of thalamic atrophy to cognitive performance in other neurologic disorders, including Alzheimer disease, 47 Huntington disease, 48 and multiple sclerosis. 49 Considered in light of those findings, the volumetric reduction of the thalamus observed in our PD-MCI group may reflect an intermediary stage of cognitive dysfunction.…”

Section: Discussionmentioning

confidence: 99%