Differential Cortical Atrophy in Subgroups of Mild Cognitive Impairment

Abstract

To compare gray matter brain volumes in patients diagnosed with subtypes of mild cognitive impairment (MCI) (those with a focal amnestic disorder and those with more diffuse cognitive dysfunction) with those of elderly controls. Design: Magnetic resonance imaging volumetric study of MCI subgroups (MCI-amnestic [MCI-A], and MCImultiple cognitive domain [MCI-MCD]) using a whole brain voxel-based analysis. Setting: Referral dementia clinic. Patients: Thirty-seven patients with MCI (age range, 49-85 years; MCI-A, n=9; MCI-MCD, n=28) and 47 control subjects (age range, 55-81 years). Main Outcome Measures: Volumetric anatomical magnetic resonance imaging differences between MCI subgroups and normal controls, and between patients with MCI who progressed to dementia. Magnetic resonance imaging scans were analyzed using statistical software SPM99. Results: Overall, the patients with MCI had significantly decreased volume in the hippocampus and middle temporal gyrus, bilaterally, compared with control subjects. Compared with patients with MCI-MCD, patients with MCI-A had significant volume loss of the left entorhinal cortex and inferior parietal lobe. Compared with patients with MCI-A, patients with MCI-MCD had significantly reduced volume of the right inferior frontal gyrus, right middle temporal gyrus, and bilateral superior temporal gyrus. Patients with MCI who progressed to Alzheimer disease during follow-up (mean interval 2 years, maximum 4.5 years), showed greater atrophy in the left entorhinal cortex, bilateral superior temporal gyri, and right inferior frontal gyrus compared with those who did not progress. Conclusions: These data provide evidence of distinct brain structural abnormalities in 2 groups of patients with MCI. While both have mesial temporal and cortical volume loss, those with a focal memory deficit have more involvement of the mesial temporal structures and less involvement of the neocortical heteromodal association areas than those patients with MCI with diffuse cognitive dysfunction. Thus, MCI may represent a more heterogeneous group than currently conceived, possibly reflecting 2 different etiological processes to dementia. These data also suggest that these structural abnormalities precede the development of Alzheimer disease.

Cholinesterase inhibitors affect brain potentials in amnestic mild cognitive impairment

“…The degree of memory impairment in the two subtypes did not differ. These and other results (Bell-McGinty et al, 2005) suggest that primary and secondary auditory cortices in the temporal lobe that generate the P50 component (LiegeoisChauvel et al, 1994;Reite et al, 1988) become involved as MCI progresses from isolated memory deficits (singledomain MCI) to additional cognitive dysfunctions involving language functions (multiple-domain MCI).…”

Deficits in face perception in the amnestic form of mild cognitive impairment

“…Neuroimaging studies show structural [4][5][6][7] and functional features [8] in patients with aMCI that are intermediate between those of healthy subjects and AD patients, consistent with neuropathologic evidence of transitional pathologic findings [9,10]. Furthermore, magnetic resonance imaging studies have shown atrophy in not only medial temporal structures but also the inferior and lateral temporal lobes, the cingulate gyrus, and the parietal and frontal lobes, depending on the stage of disease [11][12][13][14]. Some of the earliest changes occur in the anterior medial temporal lobe and fusiform gyrus, as much as 3 years before the diagnosis of AD [15].…”

Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

“…While these psychotherapies have been shown to be effective in the treatment of LLD, as with medication treatments, a significant portion of individuals receiving treatment do not respond to these interventions (14, 23). Given the cognitive demands of psychotherapy and known associations between cognitive deficits and cortical atrophy in older adults (25, 26), as well as the impact of cortical atrophy on antidepressant treatment response (18, 27), there is compelling evidence to suggest that cortical atrophy may have a deleterious impact on psychotherapy treatment outcomes. Further, given recent findings of prominent reductions in right hemisphere cortical thickness associated with familial risk of depression; indices of cortical thickness may be a particularly sensitive phenotypic marker of psychotherapy treatment response in older adults.…”