The medial temporal lobe (MTL) is crucial for episodic memory. Tau pathology is a hallmark of Alzheimer’s disease (AD) and accumulates in layer-specific patterns in the MTL during aging. It is, however, unclear whether early AD pathology relates to mesoscale network signatures distinct from non-pathological aging. To address this gap, we acquired 7 Tesla submillimeter-resolution resting-state fMRI, plasma-based AD biomarkers, glial fibrillary acidic protein (GFAP) levels, APOE genotype, regional [18F]PI-2620 tau PET burden, and longitudinal episodic memory data in 75 cognitively unimpaired older adults. Older age was associated with lower perirhinal– hippocampal connectivity and lower network segregation, whereas higher plasma-based AD pathology was associated with higher perirhinal–hippocampal connectivity. Furthermore, temporal-lobe tau burden was related to altered connectivity patterns in tau-vulnerable MTL subfields and layers, dependent on GFAP levels. Retrosplenial tau burden was associated with higher hippocampal-retrosplenial connectivity consistent with tau spread along canonical hippocampal output pathways. Finally, higher connectivity within the hippocampus attenuated the negative association between temporal-lobe tau burden and memory performance but predicted unfavorable memory trajectories. Our findings show differential associations of age and AD pathology with mesoscale MTL-connectivity patterns. Importantly, increased hippocampal connectivity may support memory function in the short term while contributing to subsequent memory decline.
Larissa Fischer, N. Vockert, Joseph Höpker Fernandes et al.· bioRxiv· 0 citations
OBJECTIVE
The detection of subtle epileptogenic lesions such as focal cortical dysplasias (FCDs) is a clinical challenge in the management of drug-resistant focal epilepsy (DRFE). Ultra-high-field (UHF) magnetic resonance imaging (MRI) offers increased signal-to-noise ratios and spatial resolution compared to 3-T MRI and may improve diagnostic yield.
METHODS
We recruited n = 21 DRFE patients (with 3-T MRI findings: two positive, three equivocal, 16 negative) undergoing presurgical workup and n = 20 healthy controls for 9.4-T MRI (.8 mm isotropic magnetization-prepared 2 rapid acquisition gradient echo [MP2RAGE], slabs of .375 × .375 × .8 mm T2*-weighted gradient echo) and 3-T MRI (magnetization prepared rapid acquisition gradient echo [MPRAGE], magnetization-prepared 2 rapid acquisition gradient echo [MP2RAGE], fluid-attenuated inversion recovery [FLAIR]) acquisitions. Visual review for possible epileptogenic lesions was performed by clinical experts. For histopathologically confirmed FCDs, we extracted surface-based quantitative features (cortical thickness, quantitative T1, FLAIR, T2*, and quantitative susceptibility mapping values) across cortical depths and distances from the lesion center and performed high-resolution cortical profiling of 9.4-T T2* values.
RESULTS
In two patients with histopathologically confirmed FCD IIb, lesions were visible with distinct qualitative and quantitative features at both field strengths. One of these type IIb FCDs showed a focal cortical T2* reduction at 9.4 T that could be quantified via automated cortical profiling, consistent with the previously described "black line sign." No new epileptogenic lesions were identified at 9.4 T in 3-T MRI-negative patients, who also had no histological evidence of such lesions.
SIGNIFICANCE
9.4-Tesla MRI findings in epileptogenic lesions underlying DRFE are consistent with those on 3-T MRI. UHF T2*-weighted sequences may be useful to detect the black line sign and thereby refine surgical or ablation targeting for some FCDs. Assessment of the diagnostic yield of 9.4-T MRI was limited by the lack of 3-T MRI-negative but histopathologically confirmed cases and by the unavailability of parallel transmit and FLAIR at 9.4 T. Further optimization of UHF protocols and analysis methods on larger cohorts may enhance clinically applicable diagnostic benefits.
Cornelius Kronlage, Pascal Martin, Benjamin Bender et al.· Epilepsia· 0 citations
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