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Decreases in low-frequency power (2-30 Hz) alongside high-frequency power increases (>40 Hz) have been demonstrated to predict successful memory formation. Parsimoniously, this change in the frequency spectrum can be explained by one factor, a change in the tilt of the power spectrum (from steep to flat) indicating engaged brain regions. A competing view is that the change in the power spectrum contains several distinct brain oscillatory fingerprints, each serving different computations. Here, we contrast these two theories in a parallel magnetoencephalography (MEG)-intracranial electroencephalography (iEEG) study in which healthy participants and epilepsy patients, respectively, studied either familiar verbal material or unfamiliar faces. We investigated whether modulations in specific frequency bands can be dissociated in time and space and by experimental manipulation. Both MEG and iEEG data show that decreases in alpha/beta power specifically predicted the encoding of words but not faces, whereas increases in gamma power and decreases in theta power predicted memory formation irrespective of material. Critically, these different oscillatory signatures of memory encoding were evident in different brain regions. Moreover, high-frequency gamma power increases occurred significantly earlier compared to low-frequency theta power decreases. These results show that simple "spectral tilt" cannot explain common oscillatory changes and demonstrate that brain oscillations in different frequency bands serve different functions for memory encoding.
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http://dx.doi.org/10.1371/journal.pbio.3000403 | DOI Listing |
Fish Physiol Biochem
September 2025
Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM's Narsee Monjee Institute of Management Studies, Mumbai, 56, India.
Zebrafish models have been used to research Alzheimer's disease and other neurodegenerative disorders because of their similarities to the human genetic composition and behavior. Researchers have detected iron accumulation in the post-mortem brain sections of neurodegenerative disorder patients. Therefore, the development an animal model to simulate these clinical pathological findings is important.
View Article and Find Full Text PDFElife
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.
Innate immune cells can acquire a memory phenotype, termed trained immunity, but the mechanism underlying the regulation of trained immunity remains largely elusive. Here, we demonstrate that inhibition of Aurora kinase A (AurA) dampens trained immunity induced by β-glucan. ATAC-seq and RNA-seq analysis reveal that AurA inhibition restricts chromatin accessibility of genes associated with inflammatory pathways such as JAK-STAT, TNF, and NF-κB pathways.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Department of Anesthesiology, The First Medical Center of Chinese PLA General Hospital, 100853 Beijing, China.
Neurocognitive disorders represent a significant global health challenge and are characterized by progressive cognitive decline across conditions including Alzheimer's disease, mild cognitive impairment, and diabetes-related cognitive impairment. The hippocampus is essential for learning and memory and requires intact neuroplasticity to maintain cognitive function. Recent evidence has identified the brain insulin signaling pathway as a key regulator of hippocampal neuroplasticity through multiple cellular processes including synaptic plasticity, neurotransmitter regulation, and neuronal survival.
View Article and Find Full Text PDFThe human mind constructs and updates models of events during comprehension. Event models are multidimensional, multi-timescale, and structured. They enable prediction, shape memory formation, and facilitate action control.
View Article and Find Full Text PDFBackground: Perioperative neurocognitive disorders (PND) is a significant clinical syndrome and neuroinflammation is an important pathological process. Matrix metalloproteinase 9 (MMP9) as a Zn2+-dependent matrix enzyme, not only maintains the integrity of the blood-brain barrier and synaptic plasticity, but also plays a key regulatory factor in peripheral and central nervous inflammation. This study aimed to investigate the effects of MMP9-mediated microglial polarization on surgery-induced neuroinflammation in aged rats and to provide novel targets for prevention and treatment of PND.
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