In the present study, we demonstrated that dementia patients with higher MTA (≥ 3) and Koedam (≥ 2) score were more likely to have a poor cognitive function. This finding is applicable to various types of dementia, encompassing not only Alzheimer's disease but also vascular and mixed dementia.
The findings in the present study corroborates previous study that showed a relationship between the results of the VRS examination and the severity of cognitive function in dementia patients [13]. A higher MTA score is significantly correlated with the Mini Mental State Examination (MMSE) score of dementia patients (p = 0,00095) and a higher Koedam score is associated with a worse Clinical Dementia Rating (CDR) score (p < 0,05) [13, 14]. Nonetheless, the conclusions drawn in previous studies were limited in scope, as they exclusively pertained to patients with Alzheimer's dementia.
MTA assesses hippocampal atrophy within 5 points, where the higher degree of atrophy indicates a higher MTA score. Previous studies have shown that the MTA score is associated with memory impairment in patients with Alzheimer's dementia and the amnestic type of Mild Cognitive Impairment (MCI). MTA is correlated significantly with the memory domain or memory recall with R2 = 0,100 (p = 0.043) [23, 24].
The MTA score has a sensitivity of 85% and a specificity of 82% in diagnosing patients with Alzheimer's Dementia. A higher MTA score will be associated with a lower MMSE score (B=-0,2; p < 0,01). In the present study, the relationship between a high MTA score with poor cognitive among dementia patients, including patients with vascular dementia (VaD), may indicate a pre-existing Alzheimer’s pathology in those with VaD. Furthermore, knowing the MTA score could also assist clinicians in predicting the progression of dementia disease [18].
In addition to the role of MTA score, previous studies have also shown that posterior atrophy is also associated with dementia progression with an HR of 2,24 (95% CI: 1.49–3.36) [3]. Posterior atrophy, measured by Koedam score, is a potential biomarker in the early onset of Alzheimer's dementia and atypical Alzheimer's dementia including posterior cortical atrophy (PCA). Examination of the Koedam score is very helpful for clinicians in diagnosing dementia, particularly in patients with atypical symptoms. It also helps differentiate the types of dementia with a sensitivity of 57% and a specificity of 95%. In addition, previous studies have shown that the Koedam score is associated with a lower working memory score (R2 = 0,106; p = 0,043) and MMSE score (B=-1,8, p < 0,01) [18, 23, 24]. Similar with MTA score, most studies investigating the role of the Koedam score in aiding the diagnosis of dementia have primarily focused on patients with Alzheimer's disease. However, research focusing on the relationship between Koedam score and cognitive function in VaD patients is still scarce. In the present study, a higher Koedam score corresponds with cognitive functioning in all type of dementia, including VaD, may also indicate a pre-existing Alzheimer’s pathology.
Nevertheless, some studies demonstrated a contradictory finding about the association between Medial Temporal Atrophy (MTA) and Koedam score with cognitive function in dementia patients [13, 18]. Previous studies showed that The Koedam score is complementary, which the posterior atrophy is more related to non-cognitive symptoms in dementia [25–27]. Different patterns of atrophy will also lead to different domains of cognitive impairment [24, 28, 29]. This discrepancy could also be attributed to variations in methodologies employed, which may yield divergent results. Furthermore, when considering vascular dementia, cognitive outcomes are likely to be influenced not solely by brain atrophy but, more significantly, by factors such as the size and location of infarcts, along with the presence of other vascular risk factors [30–32].
Limitations of the study
This study has several limitations. First, the result could not be generalized to all population due to relatively small sample size. Second, we did not analyze the effect of medication in this study because almost all participants received similar standard treatment for dementia. In addition, we did not analyze the relationship between each domain of the cognitive function with the MTA and Koedam score. Finally, this present study exclusively relied on cross-sectional data, preventing the establishment of a causal link between MTA and Koedam score with cognitive impairment. However, the observed direction of influence was consistent with prior studies.