Hippocampal volumes in Alzheimer's disease, Parkinson's disease with and without dementia, and in vascular dementia

Abstract

Hippocampal atrophy detected by volumetric MRI is a sensitive feature of early Alzheimer's disease (AD), but there are no studies evaluating hippocampal atrophy by MR volumetry in other dementing diseases. We therefore compared hippocampal volumes in a total of 113 subjects: 50 patients with mild to moderate AD, 9 patients with vascular dementia (VaD), 12 patients with idiopathic Parkinson's disease (PD) without dementia, 8 patients with PD and dementia (PDD), and 34 elderly control subjects. Thin, coronal, contiguous images were obtained by a 1.5-T MR imager. All patient groups had significantly smaller volumes of the hippocampus compared with the control group. In the PDD group, the absolute volumes were even smaller than in the AD group. In the PD group, the volumes were diminished to a lesser but significant extent. The volumes in the VaD group varied: of nine patients, two had no atrophy, three had unilateral, and four had bilateral atrophy. We postulate that hippocampal atrophy does not seem to be a specific phenomenon of dementia in AD but also occurs in VaD and PDD, and even in PD when no dementia is present. However, coexistence of AD pathology in our PD and VaD patients cannot be ruled out. Further studies with access to neuropathologic data are needed.

The use of biomarkers for the etiologic diagnosis of MCI in Europe: An EADC survey

“…Last, hippocampal atrophy is known to lack specificity, as it can be present in non-AD forms of dementia, like vascular dementia [19,20], semantic dementia [21], Parkinson's dementia [20], and frontotemporal lobar degeneration [22]. Interestingly, EADC centers seem to endorse the notion that the amyloid cascade stays at the core of the pathophysiology of AD.…”

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

“…However, whether these neuropathologies result directly and solely from atrophy of midbrain dopaminergic structures remains uncertain (e.g., Laakso, et al, 1996). Whatever the source of dysfunctionality of the hippocampus, the dual process view proposes that this structure's impaired efficiency disrupts recollection and other kinds of recall selectively, leaving familiarity intact, and recognition intact to the extent that it is supported by familiarity (see Aggleton & Brown, 1999;Edelstyn, Grange, Ellis, & Mayes, 2015;.…”

“…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.…”

Age effects on hippocampal structural changes in old men: The HAAS

“…Furthermore, most studies of VaD have been compared with other disease groups rather than to non-demented group to find how the different pathologies affect the volumetric differences of brain structures (e.g. hippocampus, entorhinal cortex) (Laakso et al, 1996, Barber et al, 2000, Mungas et al, 2001, Du et al, 2002, Swartz et al, 2002, Wolf et al, 2004.…”