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Background and Objectives: Cognitive impairment affects memory, reasoning, and problem-solving, with early detection being critical for effective management. The amygdala, a key structure in emotional processing and memory, may play a pivotal role in detecting cognitive decline. This study examines differences in amygdala nuclei volumes in patients with varying levels of cognitive performance to evaluate its potential as a biomarker. Material and methods: This cross-sectional study of 35 participants was conducted and classified into three groups: the normal (≥26), moderate (15–25), and low (≤14) cognitive performance groups based on the Montreal Cognitive Assessment (MoCA) scores. High-resolution magnetic resonance imaging at 3.0 T scanner was used to assess amygdala nuclei volumes. Results: Significant amygdala atrophy was observed in multiple amygdala nuclei across cognitive performance groups, with more pronounced changes in the low-performance group. The right hemisphere nuclei, including the lateral and basal nuclei, showed more significant differences, indicating their sensitivity to cognitive decline. Conclusions: This study highlights the potential of amygdala nuclei atrophy as a biomarker for cognitive impairment. Additional research with larger sample sizes and longitudinal designs is needed to confirm these findings and determine their diagnostic value. [ABSTRACT FROM AUTHOR]

Background and Objectives: Cognitive impairment affects memory, reasoning, and problem-solving, with early detection being critical for effective management. The amygdala, a key structure in emotional processing and memory, may play a pivotal role in detecting cognitive decline. This study examines differences in amygdala nuclei volumes in patients with varying levels of cognitive performance to evaluate its potential as a biomarker. Material and methods: This cross-sectional study of 35 participants was conducted and classified into three groups: the normal (≥26), moderate (15–25), and low (≤14) cognitive performance groups based on the Montreal Cognitive Assessment (MoCA) scores. High-resolution magnetic resonance imaging at 3.0 T scanner was used to assess amygdala nuclei volumes. Results: Significant amygdala atrophy was observed in multiple amygdala nuclei across cognitive performance groups, with more pronounced changes in the low-performance group. The right hemisphere nuclei, including the lateral and basal nuclei, showed more significant differences, indicating their sensitivity to cognitive decline. Conclusions: This study highlights the potential of amygdala nuclei atrophy as a biomarker for cognitive impairment. Additional research with larger sample sizes and longitudinal designs is needed to confirm these findings and determine their diagnostic value.

Previous research has emphasized the unique impact of Alzheimer’s Disease (AD) pathology on the medial temporal lobe (MTL), a reflection that tau pathology is particularly striking in the entorhinal and transentorhinal cortex (ERC, TEC) early in the course of disease. However, other brain regions are affected by AD pathology during its early phases. Here, we use longitudinal diffeomorphometry to measure the atrophy rate from MRI of the amygdala compared with that in the ERC and TEC in cognitively unimpaired (CU) controls, CU individuals who progressed to mild cognitive impairment (MCI), and individuals with MCI who progressed to dementia of the AD type (DAT), using a dataset from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Our results show significantly higher atrophy rates of the amygdala in both groups of ‘converters’ (CU→MCI, MCI→DAT) compared to controls, with rates of volume loss comparable to rates of thickness loss in the ERC and TEC. We localize atrophy within the amygdala within each of these groups using fixed effects modeling. Controlling for the familywise error rate highlights the medial regions of the amygdala as those with significantly higher atrophy in both groups of converters than in controls. Using our recently developed method, referred to as Projective LDDMM, we map measures of neurofibrillary tau tangles (NFTs) from digital pathology to MRI atlases and reconstruct dense 3D spatial distributions of NFT density within regions of the MTL. The distribution of NFTs is consistent with the spatial distribution of MR measured atrophy rates, revealing high densities (and atrophy) in the amygdala (particularly medial), ERC, and rostral third of the MTL. The similarity of the location of NFTs in AD and shape changes in a well-defined clinical population suggests that amygdalar atrophy rate, as measured through MRI may be a viable biomarker for AD.

MRI volumetric findings were correlated with seizure patterns and EEGs in 14 patients with intractable seizures, porencephaly and hippocampal sclerosis (HS) in a study at the University of Alabama, Birmingham, AL.