Age and dementia-associated atrophy predominates in the hippocampal head and amygdala in Parkinson's disease

Bouchard, Thomas; Malykhin, Nikolai; Martin, W. R. Wayne; Hanstock, Christopher C.; Emery, Derek; Fisher, Nancy; Camicioli, Richard

doi:10.1016/j.neurobiolaging.2007.02.002

Cited by 147 publications

(139 citation statements)

References 75 publications

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“…However, although functional disruption of the hippocampal recall-related circuits will result from ventral tegmental area degeneration even if the hippocampus remains largely structurally intact, there is also evidence that indicates there is hippocampal neuropathology in nondementing PD with volume loss particularly associated with the CA2-4 subfields/dentate gyrus (Pereria et al, 2013). Volumetric imaging studies in nondementing PD also report an association between recall but not recognition and c o r t e x x x x ( 2 0 1 5 ) 1 e1 7 hippocampal neuropathology (e.g., Bouchard, et al, 2008;Carlesimo et al, 2012;Filoteo, Reed, Litvan, & Harrington, 2014;Ibbarretxe-Bilbao, et al, 2008;Junque, et al, 2005;Laakso, et al, 1996;Riekkinen et al, 1998; however, for a counter argument see Apostolova, et al, 2010;Camicioli et al, 2003;Nagano-Saito, et al, 2005;Tam, Burton, McKeith, Burn, & O'Brien, 2005) Q10 . However, the overall pattern of our data (for example, the statistically weaker correlational evidence, which should be taken as suggestive rather than conclusive) indicates that our main findings do not eliminate the possibility that there is a weak contribution from impaired dysexecutive processing driven by prefrontal dysfunction.…”

Section: Q9mentioning

confidence: 99%

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Edelstyn

John

Shepherd

et al. 2015

Cortex

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Familiarity Medial temporal lobe Prefrontal cortexParkinson's disease a b s t r a c t Medicated, non-dementing mild-to-moderate Parkinson's disease (PD) patients usually show recall/recollection impairments but have only occasionally shown familiarity impairments. We aimed to assess two explanations of this pattern of impairment.Recollection typically improves when effortful planning of encoding and retrieval processing is engaged. This depends on prefrontally-dependent executive processes, which are often disrupted in PD. Relative to an unguided encoding and retrieval of words condition (C1), giving suitable guidance at encoding alone (C2) or at encoding and retrieval (C3) should, if executive processes are disrupted, improve PD recollection more than control recollection and perhaps raise it to normal levels. Familiarity, being a relatively automatic kind of memory, whether impaired or intact, should be unaffected by guidance. According to the second explanation, PD deficits are amnesia-like and caused by medial temporal lobe dysfunction and although poorer recollection, which is caused by hippocampal disruption, may be improved by guidance, it should not improve more than control recollection. Familiarity impairment will also occur if the perirhinal cortex is disrupted, but will be unimproved by guidance. Without guidance, recollection/ recall was impaired in thirty PD patients relative to twenty-two healthy controls and remained relatively equally impaired when full guidance was provided (C1 vs C3), both groups improving to broadly the same extent. Although impaired, and markedly less so than recollection, familiarity was not improved by guidance in both groups.The patients showed elevated rates of subclinical depressive symptoms, which weakly correlated with recall/recollection in all three conditions. PD executive function was also deficient and correlated with unguided/C1 recollection only. Our results are * Corresponding author. School of Psychology, Keele University, Keele, Staffordshire ST5 5BG, UK.E-mail address: n.edelstyn@keele.ac.uk (N.M.J. Edelstyn).Available online at www.sciencedirect.com ScienceDirectJournal homepage: www.elsevier.com/locate/cortex 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125 126 127 128

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Section: Q9mentioning

confidence: 99%

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Edelstyn

John

Shepherd

et al. 2015

Cortex

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“…There is evidence that the hippocampal head and body undergo increased atrophy in mild cognitive impairment (MCI) (Martin et al, 2010), and these subregions are correlated with neuropsychological measures of memory (Hackert et al, 2002;Chen et al, 2010). Differential atrophy within the head, body, and tail of the hippocampus have additionally been reported in other disease states, such as hippocampal sclerosis (Bronen et al, 1995), Parkinson's disease (Bouchard et al, 2008), temporal lobe epilepsy (Bernasconi et al, 2003), and schizophrenia (Witthaus et al, 2010), further suggesting that these hippocampal subregions may be sensitive to detecting progression to different disease states, including AD.…”

Section: Introductionmentioning

confidence: 99%

Hippocampal Subregions are Differentially Affected in the Progression to Alzheimer's Disease

Greene

Killiany

2011

The Anatomical Record

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Atrophy within the hippocampus (HP) as measured by magnetic resonance imaging (MRI) is a promising biomarker for the progression to Alzheimer's disease (AD). Subregions of the HP along the longitudinal axis have been found to demonstrate unique function, as well as undergo differential changes in the progression to AD. Little is known of relationships between such HP subregions and other potential biomarkers, such as neuropsychological (NP), genetic, and cerebral spinal fluid (CSF) beta amyloid and tau measures. The purpose of this study was to subdivide the hippocampus to determine how the head, body, and tail were affected in normal control, mild cognitively impaired, and AD subjects, and investigate relationships with HP subregions and other potential biomarkers. MRI scans of 120 participants of the Alzheimer's Disease Neuroimaging Initiative were processed using FreeSurfer, and the HP was subdivided using 3D Slicer. Each subregion was compared among groups, and correlations were used to determine relationships with NP, genetic, and CSF measures. Results suggest that HP subregions are undergoing differential atrophy in AD, and demonstrate unique relationships with NP and CSF data. Discriminant function analyses revealed that these regions, when combined with NP and CSF measures, were able to classify by diagnostic group, and classify MCI subjects who would and would not progress to AD within 12 months. Anat Rec,

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“…While a few studies have demonstrated atrophy in the medial temporal lobes, 16 amygdala, 17 and frontal and parietal regions, 18 others have reported no significant GM reductions in PD populations without dementia. 19 In addition, cortical thinning in PD represents a relatively new area of research, and it has been reported to be more sensitive than voxel-based morphometry.…”

mentioning

confidence: 99%

Subcortical Atrophy Is Associated with Cognitive Impairment in Mild Parkinson Disease: A Combined Investigation of Volumetric Changes, Cortical Thickness, and Vertex-Based Shape Analysis

Mak

Bergsland

Dwyer

et al. 2014

AJNR Am J Neuroradiol

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Age and dementia-associated atrophy predominates in the hippocampal head and amygdala in Parkinson's disease

Cited by 147 publications

References 75 publications

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Evidence of an amnesia-like cued-recall memory impairment in nondementing idiopathic Parkinson's disease

Hippocampal Subregions are Differentially Affected in the Progression to Alzheimer's Disease

Subcortical Atrophy Is Associated with Cognitive Impairment in Mild Parkinson Disease: A Combined Investigation of Volumetric Changes, Cortical Thickness, and Vertex-Based Shape Analysis

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