CT-Detected MTA Score Related to Disability and Behavior in Older People with Cognitive Impairment

Abstract

Our study aims to investigate the relationship between medial temporal lobe atrophy (MTA) score, assessed by computed tomography (CT) scans, and functional impairment, cognitive deficit, and psycho-behavioral disorder severity. Overall, 239 (M = 92, F = 147; mean age of 79.3 ± 6.8 years) patients were evaluated with cognitive, neuropsychiatric, affective, and functional assessment scales. MTA was evaluated from 0 (no atrophy) to 4 (severe atrophy). The homocysteine serum was set to two levels: between 0 and 10 µmol/L, and > 10 µmol/L. The cholesterol and glycemia blood concentrations were measured. Hypertension and atrial fibrillation presence/absence were collected. A total of 14 patients were MTA 0, 44 patients were MTA 1, 63 patients were MTA 2, 79 patients were MTA 3, and 39 patients were MTA 4. Cognitive (p < 0.0001) and functional (p < 0.0001) parameters decreased according to the MTA severity. According to the diagnosis distribution, AD patient percentages increased by MTA severity (p < 0.0001). In addition, the homocysteine levels increased according to MTA severity (p < 0.0001). Depression (p < 0.0001) and anxiety (p = 0.001) increased according to MTA severity. This study encourages and supports the potential role of MTA score and CT scan in the field of neurodegenerative disorder research and diagnosis.

Mild behavioral impairment domains are longitudinally associated with pTAU and metabolic biomarkers in dementia‐free older adults

“…25,41 The frequency of hyperhomocysteinemia (> 10 μmol/L) was linked to medial temporal lobe atrophy 42 and with NPS severity (p < .0001) and functional impairment. 43 Additionally, brain structural changes such as medial temporal atrophy (MTA) by computed tomography (CT) scans have been correlated to plasma homocysteine, with more severe MTA associated with higher plasma homocysteine, 42 with similar findings for diffusion-tensor imaging (DTI). 44 The findings regarding hyperhomocysteinemia and abnormal perception might be explained by (1) an indirect mechanism through tau phosphorylation because hyperhomocysteinemia, when caused by low vitamin B12 levels, promotes tau phosphorylation through the regulation of GSK3beta and PP2A 45 and (2) genotype-derived enzymatic deficiency given by the A1298C genetic variant of the methylenetetrahydrofolate (MTHFR) reductase.…”

“…High plasma homocysteine can present in 10% to 20% of older adults, 40 with higher prevalence in psychogeriatric patients 25,41 . The frequency of hyperhomocysteinemia (> 10 μmol/L) was linked to medial temporal lobe atrophy 42 and with NPS severity ( p < .0001) and functional impairment 43 . Additionally, brain structural changes such as medial temporal atrophy (MTA) by computed tomography (CT) scans have been correlated to plasma homocysteine, with more severe MTA associated with higher plasma homocysteine, 42 with similar findings for diffusion‐tensor imaging (DTI) 44 …”