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Background: Atlantoaxial rotatory fixation (AARF) is extremely rare in adults, and there is no consensus on the ideal treatment of adult AARF because of its rarity. We presented a case series of three adult AARFs and reviewed the literature on adult AARFs. We suggest treatment guidelines for the injury based on the literature review.
Methods: We compiled a series of three adult AARFs seen in our hospital. We also utilized the NCBI library to retrieve literature on adult AARF from 2000 to 2021. We included articles on adult AARF, which described the number of days from injury to diagnosis, Fielding classification, occurrence of associated cervical injuries, and details of treatment and the results.
Results: Thirty adult AARFs reports fulfilled the criteria and 32 patients were analyzed. Eighteen patients had Fielding Type 1 AARF and were diagnosed within 1 month of injury. Among them, 13 cases healed with conservative treatment. Patients with acute AARF of Fielding Type 1 who underwent manual reduction healed successfully. All patients that required more than 1 month from injury to diagnosis underwent surgery. All cases with AARF Fielding Types 2, 3, and 4 failed conservative treatment.
Conclusion: The case series and literature review suggest that early diagnosis of adult AARF is essential for successful closed reduction, and the Fielding classification may help determine treatment strategy. Furthermore, this study showed that not only traction but also manual reduction may be a useful treatment for early diagnosed AARF Fielding Type 1 without complications. .
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Alzheimers Dement
September 2025
Department of Clinical and Health Psychology, University of Florida, Gainesville, Florida, USA.
Introduction: Glial fibrillary acidic protein (GFAP) may contribute to Alzheimer's pathology at early disease stages. GFAP moderation of Alzheimer's disease (AD)-related neurodegeneration and cognition is unclear.
Methods: We examined plasma GFAP moderation of AD biomarkers (amyloid beta [Aβ]-positron emission tomography [PET][A]; plasma phosphorylated tau-181 [p-tau181][T]), neurodegeneration (plasma NfL[N]; structural magnetic resonance imaging [MRI][N]), and cognition (Cog; Cog) in two cohorts: University of California San Francisco (UCSF) (N = 212, 91.
Acta Neuropathol
July 2025
Department of Biochemistry, Emory University, Atlanta, GA, 30322, USA.
Extracellular amyloid plaques, the pathognomonic hallmark of Alzheimer's disease (AD), are also observed in cognitively unimpaired subjects in the preclinical stages. Progressive accumulation of fibrillar amyloid-β (Aβ) as plaques and perivascular deposits occur two decades before clinical onset, making Aβ a long-lived peptide. To characterize the amyloid plaques biochemically, both the Aβ-load as well the post-translational modifications (PTMs) could serve as markers for distinguishing the pre-clinical stage compared to later prodromal and clinical stages of AD.
View Article and Find Full Text PDFExp Physiol
July 2025
Bruno Balke Biodynamics Laboratory, Department of Kinesiology, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Cerebral pulsatility is a potential marker of cerebrovascular health, yet little is understood about sex differences in cerebral pulsatility with age, especially within different cerebral arteries. Additionally, cerebral damping can blunt cerebral pulsatility and might decline with age. Therefore, we aimed to identify sex differences in cerebral pulsatility and damping across the adult lifespan.
View Article and Find Full Text PDFNat Neurosci
August 2025
Clinical Memory Research Unit, Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden.
Tau positron emission tomography (PET) imaging allows in vivo detection of tau proteinopathy in Alzheimer's disease, which is associated with neurodegeneration and cognitive decline. Understanding how demographic, clinical and genetic factors relate to tau PET positivity will facilitate its use for clinical practice and research. Here we conducted an analysis of 42 cohorts worldwide (N = 12,048), including 7,394 cognitively unimpaired (CU) participants, 2,177 participants with mild cognitive impairment (MCI) and 2,477 participants with dementia.
View Article and Find Full Text PDFAlzheimers Dement
July 2025
Department of Imaging and Pathology, Laboratory of Neuropathology, KU Leuven, Leuven, Belgium.
Introduction: In neurodegenerative dementias, the co-occurrence and interaction of amyloid β peptide (Aβ), tau pathology, and other pathological lesions confound their individual contributions to neurodegeneration and their modulation by risk factors.
Methods: We analyzed 480 post mortem human brains (ages 50-99) using regression and structural equation models to assess the relationships among Aβ, tau, limbic-predominant age-related TDP-43 encephalopathy neuropathological changes (LATE-NC), α-synuclein, other age-related lesions, and apolipoprotein E (APOE) ε4, as well as their effects on CA1 neuronal density, brain weight, and cognitive status.
Results: Aβ, tau, LATE-NC, and amygdala-predominant α-synuclein pathology were mutually interdependent.