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Dementia, including Alzheimer's disease (AD) and frontotemporal dementia (FTD), presents critical challenges for correctional systems, particularly as global populations age. AD, affecting 60-80% of dementia cases, primarily impairs memory and cognition in individuals over 65. In contrast, FTD, rarer than AD but not uncommon in those under 65, affects the frontal and temporal brain regions, leading to deficits in social behavior, language, and impulse control, often resulting in antisocial actions and legal consequences. Behavioral variant FTD is especially associated with socially inappropriate and impulsive behaviors due to frontal lobe degeneration. The prevalence of cognitive impairment in incarcerated populations is high, exacerbated by prison environments that compound distress and limited access to specialized healthcare. Studies indicate that up to 11% of United States state prison inmates over the age of 55 exhibit cognitive impairments, often undiagnosed, resulting in punitive rather than rehabilitative responses to symptoms like disinhibition and aggression. Ethical concerns around criminal responsibility for individuals with dementia are increasingly prominent, particularly regarding their ability to comprehend and engage in legal proceedings. The growing elderly prison population necessitates reform in correctional healthcare to include early cognitive assessment, targeted intervention, and tailored post-release programs. Addressing these needs is essential to ensure appropriate treatments, alleviate healthcare demands, and support reintegration for cognitively impaired inmates.
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http://dx.doi.org/10.3390/neurosci6010005 | DOI Listing |
Acta Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFJ Neural Transm (Vienna)
September 2025
Parkinson's Foundation Centre of Excellence, King's College Hospital, Denmark Hill, London, SE5 9RS, UK.
Parkinson's disease patients are at increased risk of road traffic and car accidents and those with excessive daytime sleepiness are specially susceptible. Abnormal scores on the Epworth Sleepiness Scale predicts risk for driving-related somnolence which may cause road traffic accidents in driving patients as many such patients declare dozing of while in a car. Our study estimates that over 40% of patients with daytime somnolence have risks of dozing off in a car.
View Article and Find Full Text PDFMol Psychiatry
September 2025
National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, 02130, USA.
Glial fibrillary acidic protein (GFAP) is an astrocytic marker that can be assessed in blood using single molecule array technology. Recent studies suggest that individuals with posttraumatic stress disorder (PTSD) have suppressed circulating levels of this CNS biomarker. This study examined the hypothesis that PTSD and plasma GFAP levels share common genetic and epigenetic pathways.
View Article and Find Full Text PDFNature
September 2025
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
As a key mitochondrial Ca transporter, NCLX regulates intracellular Ca signalling and vital mitochondrial processes. The importance of NCLX in cardiac and nervous-system physiology is reflected by acute heart failure and neurodegenerative disorders caused by its malfunction. Despite substantial advances in the field, the transport mechanisms of NCLX remain unclear.
View Article and Find Full Text PDFCytokine Growth Factor Rev
September 2025
Shandong University of Traditional Chinese Medicine, Jinan 250355, China; The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250001, China. Electronic address:
This review summarizes the biological properties of key myokines (Irisin, Apelin, CLCF1, and Myostatin) and osteokines (Osteocalcin, Sclerostin, FGF23 and the RANKL/OPG system). This work provides an in-depth analysis of the age-related network imbalance mechanism characterized by "downregulation of protective factors (Irisin, CLCF1, and uncarboxylated Osteocalcin) - upregulation of pro-degenerative factors (Myostatin, Sclerostin, and FGF23) - inflammation-driven amplification", and reveals the mechanism by which this network imbalance contributes to the comorbidity of sarcopenia, osteoporosis, and neurodegenerative diseases. Furthermore, the review evaluates the intersecting regulatory networks and molecular pathways through which myo-osteogenic factors modulate neurotrophic factors (BDNF, NGF and GDNF), and proposes intervention strategies based on these intersecting regulatory networks.
View Article and Find Full Text PDF