Aphasia is an acquired language disorder following brain injury; dyslexia is a developmental reading disorder. Both affect left-hemisphere language networks but differ in etiology and deficit profiles. This PRISMA-guided review synthesizes neuroimaging and behavioral evidence comparing phonological, syntactic, and semantic impairments and their neuroanatomical substrates. PubMed, Scopus, and Web of Science were searched (2015–2024) using aphasia/dyslexia terms combined with phonological/syntactic/semantic and fMRI/DTI/lesion keywords. Two reviewers screened 1,247 records, yielding 47 studies (25 aphasia-based, n=1,248 patients; 22 dyslexia-based, n=1,112 patients). Quality was assessed with Newcastle–Ottawa Scale (mean 7.6/9). Aphasia-based studies showed lesions in left inferior frontal gyrus and insula correlating with phonemic paraphasias (r=0.68, 95% CI 0.42–0.85, p=0.002) and reduced mean length of utterance (3.4±1.2 vs 7.3±0.8 words, p<0.001). Dyslexia-based studies reported reduced superior temporal gyrus–angular gyrus connectivity (t=4.21, p<0.001) with preserved oral syntax but slower reading (4.7±1.1s vs 2.4±0.6s, p<0.001). Limitations include diagnostic heterogeneity, cross-sectional designs, and English-language restriction. Evidence suggests aphasia disrupts dorsal-stream production networks via focal lesions, whereas dyslexia reflects disrupted temporoparietal connectivity underlying phoneme–grapheme integration. Preliminary neuromodulation trials warrant larger randomized controlled studies.
This review synthesizes current evidence on posttraumatic stress disorder (PTSD) neurobiology and evaluates ketamine’s potential mechanisms, with particular emphasis on region-specific alterations in synaptic plasticity and glutamatergic transmission as avenues for symptom relief. PTSD is a complex psychiatric condition characterized by intrusive flashbacks, emotional dysregulation, and heightened physiological arousal following exposure to trauma. Conventional treatments, such as cognitive behavioral therapy (CBT) and selective serotonin reuptake inhibitors (SSRIs), offer some symptom relief but for many patients, efficacy is limited, highlighting the urgent need for alternative interventions. Clinical studies suggest that ketamine can produce rapid reductions in PTSD symptoms, positioning it as a potential intervention for patients who do not respond adequately to conventional treatments; however, the neurobiological mechanisms underlying these effects remain insufficiently understood. Acknowledging this, this review specifically addresses the potential mechanisms by which ketamine may reduce symptoms through the incorporation and exploration of PTSD’s neurobiological underpinnings, aiming to both synthesize the current literature and identify priorities for further research. Overall, current evidence suggests that ketamine may reduce PTSD symptoms through changes in α-amino-3-hydroxy-5-methyl-4-iso xazolepropionic acid receptor (AMPAR) dependent plasticity and modulation of glutamatergic transmission, though questions remain regarding long-term safety, durability, and precise molecular mechanisms.
Alterations in neuronal and glial metabolism contribute to numerous neurodegenerative diseases. The crosstalk between these two cell types (i.e., axoglial metabolic coupling) is at the center of extensive investigation. Metabolic alterations frequently culminate in mitochondrial dysfunction, but it has proven challenging to obtain cell-type-specific metabolic data from neuronal or glial mitochondria in mouse models of injury or disease. Magnetic immunocapture of genetically tagged mitochondria has emerged as a powerful strategy. However, existing immunocapture methods are either incompatible with sensitive downstream multi-omic workflows or not yet tested in complex tissues with highly heterogeneous cell populations. In the present study, the research team refined the MITO-Tag approach, which leverages a Cre-dependent 3×HA-EGFP-OMP25 epitope tag localized to the outer mitochondrial membrane. Following enzymatic and mechanical dissociation, mitochondria were rapidly immunopurified from cortical neurons, oligodendrocyte lineage cells, and—accomplished here for the first time—peripheral nerve axons using anti-hemagglutinin magnetic beads in liquid chromatography-tandem mass spectrometry (LC-MS/MS)-compatible KPBS buffer. This method yields specific and structurally intact mitochondria, as confirmed by live-organelle imaging and Western blotting for compartment-specific markers (COXIV, VDAC, citrate synthase), with minimal contamination from other organelles. Proteomic analysis of brainderived immunoprecipitates revealed mitochondrial enrichment comparable to existing magnetic immunopurification workflows. As the first isolation strategy which enables multi-omic profiling of mitochondria from lower-abundance cell types, this method provides a versatile tool for investigating mitochondrial involvement in neurological disease and injury in vivo. Notably, isolation of axonal mitochondria permits characterization of the metabolic shifts occurring in axons after injury and in disease models, including shifts associated with axoglial metabolic coupling. Given that axon death is preceded by bioenergetic failure, defining the mitochondrial mechanisms involved could reveal novel targets for neuroprotective therapies.
This manuscript provides a comprehensive overview of the role of auto-associative networks (AANs) in the neurobiological process of cognitive behavior. The structural organization of the brain is largely governed by the Hebbian postulate, “cells that fire together, wire together.” This organization is supported by assemblies that use both ascending feedforward and descending feedback projections, as well as recursive loops that allow for the enhancement of human capacity for such cognition. Detailed analysis reveals that AANs enable the prime and functional retrieval of human memory and language. Their attractor system facilitates pattern completion from noisy and partial cues, enabling reliable recall of stored information. This winner-take-all approach calls for the closest match to be pulled from prior expectations. Oscillatory controls, long-term potentiation, and NMDA gating all contribute to this process, pushing our brains to not only replay events but also predict and simulate those of the future. This can be conceptualized from a symbolic standpoint using real-world items (RWIs), tokens that represent abstractions and can be paired via spreading activation. AANs support language by organizing symbolic RWIs into stable, retrievable assemblies. This context suggests that these associative dynamics are the foundation for driving the fluidity of human memory, language, and predictive thought.
Prescription stimulants such as medication for Attention-Deficit Hyperactivity Disorder (ADHD) can be detrimental when misused. Illicit ADHD medication usage, or non-prescription use, is prevalent across college students in pursuit of an academic advantage, increased focus, and recreation. Similarly, cannabis use has increased among college students, often as a result of legalization in various states. The purpose of this study was to investigate associations among prescribed and illicit ADHD medication use, grade point average (GPA) and mental distress as well as the relationship among cannabis use, mental distress and grade point average (GPA). Responses from 702 undergraduate college students from universities across the United States were included. An anonymous cross-sectional survey assessed self-reported drug usage, GPA and mental health. The results of the study revealed that 71.4% of study participants who reported ADHD medication use were using the medication illicitly. Statistically significant (p<0.01) positive correlations between illicit ADHD dependence and both a marked decrease (~ -1.0) and slight decrease (~ -0.5) in GPA were found,. There was a positive correlation among ADHD medication use and feeling worthless (p<0.05) as well as a negative correlation among very frequent use (40+ times annually) and GPA (p<0.01). While non-frequent cannabis usage (no usage in the last 12 months) showed negative correlations with symptoms of mental distress (p<0.05), very frequent cannabis usage showed positive correlations with mental distress (p<0.05). The findings suggest that ADHD medication usage has a negative impact on academic performance and that very frequent use of cannabis has a negative impact on mental well-being. Study results add to understanding of the relationship among prescribed and illicit ADHD medication use, GPA, and mental distress as well as cannabis use, GPA and mental distress in college students.
