Orientation dependence in spatial memory has often been interpreted in terms of accessibility: Object locations are encoded relative to a reference orientation that affords the most accurate access to spatial memory. An open question, however, is whether people naturally use this "preferred" orientation whenever recalling the space. We tested this question by asking participants to locate buildings on a familiar campus from various imagined locations, without specifying the heading to be assumed. We then used these pointing judgments to infer the approximate heading participants assumed at each location. Surprisingly, each location showed a unique assumed heading that was consistent across participants and seemed to reflect episodic or visual properties of the space. This result suggests that although locations are encoded relative to a reference orientation, other factors may influence how people choose to access the stored information and whether they appeal to long-term spatial memory or other more sensory-based stores.
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http://dx.doi.org/10.1037/a0030905 | DOI Listing |
Eur J Nucl Med Mol Imaging
January 2025
Laboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocenter and Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Purpose: As dual-phase amyloid-PET can evaluate amyloid (A) and neurodegeneration (N) with a single tracer injection, dual-phase tau-PET might be able to provide both tau (T) and N. Our study aims to assess the association of early-phase tau-PET scans and F-fluorodeoxyglucose (FDG) PET and their comparability in discriminating Alzheimer's disease (AD) patients and differentiating neurodegenerative patterns.
Methods: 58 subjects evaluated at the Geneva Memory Center underwent dual-phase F-Flortaucipir-PET with early-phase acquisition (eTAU) and F-FDG-PET within 1 year.
Behav Brain Res
January 2025
Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD 57007. Electronic address:
The astroglial glutamate transporter in the hippocampus and anterior cingulate cortex (ACC) is critically involved in chronic pain-induced cognitive and psychiatric abnormalities. We have previously reported that LDN-212320, a glutamate transporter-1 (GLT-1) activator, attenuates complete Freund's adjuvant (CFA)-induced acute and chronic nociceptive pain. However, the cellular and molecular mechanisms underlying GLT-1 modulation in the hippocampus and ACC during chronic pain-induced cognitive deficit-like and anxiety-like behaviors remain unknown.
View Article and Find Full Text PDFNeurotoxicology
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, 11566, Egypt. Electronic address:
Doxorubicin (DOX)-induced chemobrain has been reported in several studies. Its main culprit is the induction of massive amounts of reactive oxygen species (ROS), hence triggering damage to brain tissues and thus leading to neuroinflammation. Biochanin A (BIO-A) is known to be an antioxidant, anti-inflammatory, and neuroprotective agent.
View Article and Find Full Text PDFPhytomedicine
January 2025
Department of Gynecology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. Electronic address:
People with mild cognitive impairment (MCI) carry a considerable risk of developing dementia. Studies have shown that female sex hormones have long-lasting neuroprotective and anti-aging properties, and the increased risk of MCI and AD is associated with the lack of estrogen during menopause. Previous studies have shown that Tiao Geng Decoction (TGD) may have antioxidant and anti apoptotic properties, which may prevent neurodegenerative diseases.
View Article and Find Full Text PDFCell Rep
January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
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