bioRxiv Subject Collection: Neuroscience's Journal
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Thursday, November 14th, 2024
| Time |
Event |
| 1:45p |
We are the sensors of consciousness! A review and analysis on how awakenings during sleep influence dream recall.
Purpose: Since the 1930s, researchers have awakened people from different stages of sleep to record what they have experienced. While some aspects, including asking whether participants had dreams or thoughts before awakening, largely remain the same, others, such as the method of awakening, vary greatly. In addition, it is often assumed that the influence of participant characteristics, such as personality traits, motivation, memory, and attention, is reduced by collecting experiences immediately after they occur, rather than through delayed morning recall. However, the extent to which these variables influence dream recall upon awakening has not yet been thoroughly investigated. Materials and methods: To explore possible contextual and individual influences, this review analyzed 69 awakening studies conducted between 2000 and 2024 and utilized the DREAM database. Differences between sleep stages were quantified and experiences analyzed using the categories 'with recall', 'without recall', and 'no report'. Results: Similar levels of null reports were found in NREM stage 2 and stage 3. Significant factors affecting dream recall included the method of awakening (lower recall with an alarm compared to calling the participant's name), the number of study days (reduced recall for multiple days) and the sleep environment (higher recall at home compared to the laboratory), along with participant characteristics beyond age, sex and study design. Recall rates from NREM sleep are particularly sensitive to the method of awakening and interindividual differences. Conclusion: Both the awakening procedure and participant characteristics influence the amount of reported sleep experiences, which can impact study outcomes, such as the identification of neural correlates of consciousness. Therefore, greater emphasis needs to be placed on how experiences are collected and on participant characteristics, such as openness to experience or familiarity with different states of consciousness. | | 4:34p |
Brain Aging Among Individuals with Classical Trigeminal Neuralgia
Trigeminal neuralgia (TN) is a complex orofacial neuropathic pain condition with limited understanding of underlying mechanisms and therapeutic options. Emerging evidence suggests the involvement of the brain in persons with TN including widespread brain changes when employing a widely used brain aging biomarker that estimates a predicted brain age difference or brain age gap. The aim of the present cross-sectional study was to assess the predicted brain age difference (brain-PAD) or brain age gap across two discrete TN subtypes (classical TN, and secondary/idiopathic TN) in comparison with age-and sex-matched pain-free controls and its association with several clinical and psychological characteristics. Thirty-four individuals diagnosed with Classical TN, 17 diagnosed with secondary/idiopathic TN were age- and sex-matched to pain-free controls (n=54). All participants underwent a T1 brain MRI and completed clinical and psychological measures. There were significant differences in brain-PAD among TN subtypes (ANCOVA p = 0.0078, effect size f2 = 0.282), with individuals diagnosed with Classical TN having a brain-PAD significantly greater than the controls by 3.87 years (p = 0.01, Bonferroni-corrected). There were no significant brain-PAD differences between secondary/idiopathic TN and pain-free controls. Brain-PAD had a significant positive association with both pain catastrophizing (p = 0.032) and pain-related anxiety (p = 0.041), but no significant association with disease duration (p = 0.519) or usual pain intensity (p = 0.443). We report here accelerated brain aging processes in patients with classical TN, but not in persons diagnosed with secondary/idiopathic TN. Our study replicates previous findings and adds to the literature that accelerated brain aging may not occur across all TN subtypes. Given the increased use of MRI for TN diagnostics, combined with our own recent work deriving our brain aging biomarker from clinical-grade scans, future studies within clinical settings are feasible and needed to understand this debilitating condition. | | 5:45p |
Caveolin-1 and Aquaporin-4 as Mediators of Fibrinogen-Driven Cerebrovascular Pathology in Hereditary Cerebral Amyloid Angiopathy
Hereditary Cerebral Amyloid Angiopathy (HCAA) is a rare inherited form of CAA, characterized by increased vascular deposits of amyloid peptides. HCAA provides a unique opportunity to study the pathogenic mechanisms linked to CAA, as it is associated with severe cerebrovascular pathology. Some of HCAA-associated amyloid-{beta} (A{beta}) mutations significantly enhance the interaction between fibrinogen and A{beta}, resulting in altered fibrin structure and co-deposition with A{beta} in the perivascular space. However, the mechanisms underlying perivascular fibrinogen deposition and the associated cerebrovascular pathology in HCAA remain unclear. To investigate this, we analyzed TgSwDI transgenic mice carrying HCAA-associated mutations and observed a significant age-dependent increase in fibrin(ogen) extravasation and fibrin(ogen)-A{beta} colocalization in the perivascular space. Moreover, Caveolin-1, a protein involved in non-specific transcytosis across the endothelium, significantly increased with age in TgSwDI mice and correlated with fibrin(ogen) extravasation. Additionally, we noted significant aquaporin-4 (AQP4) depolarization in the CAA-laden blood vessels of TgSwDI mice, which also correlated with fibrin(ogen) extravasation and fibrin(ogen)-A{beta} colocalization. Given that AQP4 plays a crucial role in A{beta} clearance via the glymphatic pathway, its depolarization may disrupt this critical clearance mechanism, thereby exacerbating CAA pathology. To further explore the relationship between fibrin(ogen) and these factors, we depleted fibrinogen in TgSwDI mice using siRNA against fibrinogen. This intervention resulted in decreased CAA, reduced caveolin-1 levels, attenuated microglial activation, restored polarized expression of AQP4, and improved spatial memory in fibrinogen-depleted TgSwDI mice. These findings suggest that targeting fibrinogen could be a promising strategy for mitigating CAA pathology and its associated cerebrovascular pathology. |
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