Memory impairment patterns can be divided into two subtypes that show either encoding (EF) or retrieval failure (RF). This subtype classification of MCI may have utility as an easily accessible tool, and additional classifications based on AD pathology to amnestic MCI may be more successful. There are different rates of progression among subtypes of MCI, and approximately 80% of patients with amnestic MCI convert to AD dementia within 6 years. Many studies have suggested that the subtypes have different etiologies and future outcomes and risk of progress to AD may be influenced by the subtype of MCI.

MCI is subdivided into non-amnestic and amnestic types and single and multiple domains.

It is impossible to perform these studies on all patients with MCI, and simpler methods may be more valuable in practice. However, these biomarkers are not easily accessible due to high cost, invasiveness, and restricted availability. The evidence of Alzheimer pathology in cerebrospinal fluid (CSF) or positron emission tomography (PET) and neurodegeneration in multimodal neuroimaging may provide information about disease progression. Because the preclinical or prodromal stage of AD has become a major focus in research regarding disease-modifying therapy, identifying individuals at the risk of developing AD would be needed for researchers. The early recognition of disease progression to AD in patients with MCI is an important topic of interest for clinicians in terms of early intervention and patient education. MCI is a heterogeneous disorder with different prognosis from progression to Alzheimer’s disease (AD) or non-AD dementias to the maintenance or even improvement of cognitive decline. Mild cognitive impairment (MCI) is considered an intermediate stage in the trajectory from normal cognition to dementia. Additionally, insufficient sample size may lead to ambiguous statistical findings in direct comparisons, and a larger patient cohort could more robustly identify differences in GM volume reductions between the EF and the RF group. Since this study is a cross-sectional study, prospective follow-up studies are needed to investigate whether different types of memory impairments can predict the underlying pathology of amnestic MCI. The EF findings are structurally and functionally more consistent with the prodromal Alzheimer’s disease stage than the RF findings. MCI differs functionally and structurally according to their specific memory impairments. However, when compared to normal control, GM volume reductions due to EF in the left thalamus and bilateral hippocampi and reductions due to RF in the left thalamus, right superior frontal lobe, right superior temporal lobe, and right middle cingulum were observed ( p < 0.05, family-wise error correction). There was no statistically significant difference in GM volume between the EF and RF. QEEG showed higher frontal theta and lower beta2 band power, and higher theta connectivity in the EF.

Voxel-based morphometric analysis of the gray matter (GM) in the MCI groups and 71 cognitive normal controls was also done using the Computational Anatomy Toolbox 12 ( ). We compared quantitative electroencephalography (qEEG) power spectra and connectivity between 87 MCI patients with EF and 78 MCI with RF using iSyncBrain® (iMediSync Inc., Republic of Korea) ( ). We explored the differences structurally and functionally.

The memory impairments in mild cognitive impairment (MCI) can be classified into encoding (EF) and retrieval (RF) failure, which can be affected by underlying pathomechanism.

Amnestic disorder vs dementia