Life

Memory constitutes a fundamental cognitive domain, and converging evidence suggests that its dysfunction represents a prominent, though not exclusive, transdiagnostic dimension across major psychiatric disorders. This review aimed to integrate neurobiological, cognitive, and clinical evidence on domain-specific memory impairments in mood, anxiety, obsessive–compulsive, post-traumatic stress, and psychotic disorders. A comprehensive search was conducted on PubMed, Scopus, and Web of Science up to November 2025 for peer-reviewed studies examining short-term, working, long-term, episodic, semantic, and prospective memory, prioritizing both landmark and recent contributions. Two recurrent transdiagnostic patterns emerged: (i) consistent impairments in working-memory control, and (ii) reduced episodic/autobiographical specificity, while procedural memory appeared relatively preserved. Disorder-specific profiles include overgeneral autobiographical memory in major depression, enduring working and episodic deficits in bipolar disorder, variable impairments in anxiety disorders, functional rather than structural memory inefficiencies in obsessive–compulsive disorder, broad mnemonic disorganization in post-traumatic stress disorder, and pervasive working and episodic deficits in schizophrenia and related psychoses. Across conditions, converging neurobiological data implicate fronto-hippocampal dysconnectivity, altered plasticity, and impaired consolidation processes. Unlike previous reviews, this work syntetisizes evidence across multiple memory systems and across major psychiatric categories, linking neurobiological mechanisms with cognitive and clinical manifestations to support a dimensional, transdiagnostic interpretation of memory dysfunction. These findings could suggest that memory dysfunction represents a recurrent and clinically relevant dimension across psychiatric conditions, warranting further mechanistic and longitudinal investigation.

Fascia research suffers from definitional fragmentation, with no universal agreement about what fascia actually is, why it matters, or how to define it. Researchers often pursue lines of inquiry based on their existing expertise, yet traditional and newer approaches that might resolve these issues frequently conflict. To address this challenge, the authors use a hermeneutic framework to integrate their combined half century of anatomical experience with a narrative literature synthesis. They propose that fascia functions as a stochastic morphogenetic field rather than a discrete anatomical system, a stochastic process displaying opportunistic dynamics at atomic, molecular, and cellular scales that produces deterministic mechanical properties at macroscopic tissue levels. Four key conclusions emerge: (1) anatomical “virtual spaces” are hyaluronic acid (HA)–tissue manifolds tightly coupled with calcium coordination; (2) fascia functions as a stochastic morphogenetic field where clinically and educationally relevant deterministic patterns emerge; (3) a conceptual framework for context-flexible fascial nomenclature; (4) hermeneutic approaches enable synthesis across theoretical domains. The conclusions support the understanding of HA-mediated EMT/MET plasticity and its “Go or Grow” phenotypes as central conduits for both healing and cancer progression. Understanding the stochastic nature of fascia is thus essential for physicians as well as clinicians in the allied health setting. Optimal fascia-aware movement and manual therapy interventions are those that recognize fascia as a self-adapting morphogenetic field.

Purpose: This study aimed to investigate the associations between serum per- and polyfluoroalkyl substances (PFAS) and reproductive hormones, including follicle-stimulating hormone (FSH), anti-Müllerian hormone (AMH), estradiol, and progesterone, in U.S. women. Approach and Results: We conducted a cross-sectional study using data from the National Health and Nutrition Examination Survey (NHANES) 2017–2018. The study included 612 women aged ≥18 years with available PFAS and sex hormone measurements. Serum concentrations of four major PFASs (linear perfluorooctanoic acid [n-PFOA], perfluorooctane sulfonic acid [PFOS], perfluorononanoic acid [PFNA], and perfluorohexane sulfonic acid [PFHxS]) were analyzed, along with serum levels of FSH, AMH, estradiol, and progesterone measured by isotope dilution liquid chromatography–tandem mass spectrometry. Higher serum PFAS concentrations were associated with increased FSH and decreased AMH, estradiol, and progesterone. For example, each interquartile range (IQR) increase in ln-PFNA was associated with a 42.0% increase in ln-FSH (p = 0.01) and 32.2% lower ln-AMH (p < 0.001), 33.0% lower ln-estradiol (p = 0.004), and 40.9% lower ln-progesterone (p = 0.02). A PFAS exposure index was related to higher FSH and lower AMH, estradiol, and progesterone, with stronger effects in premenopausal women. Conclusions: PFAS exposure was linked to broad endocrine disruption in women, with consistent alterations across gonadotropins and sex steroids. These findings suggest that PFAS exposure was associated with hormonal patterns consistent with diminished ovarian reserve and potential changes in reproductive function, underscoring the need for longitudinal studies and regulatory actions to mitigate exposure.