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Jan 16, 2025 | 
nature.com | Farwa Ali |Michelle M. Mielke |Clifford R. Jack |David S. Knopman |Prashanthi Vemuri |Ronald Petersen | +1 more
AbstractDeclining gait performance is seen in aging individuals, due to neural and systemic factors. Plasma biomarkers provide an accessible way to assess evolving brain changes; non-specific neurodegeneration (NfL, GFAP) or evolving Alzheimer’s disease (Aβ 42/40 ratio, P-Tau181). In a population-based cohort of older adults, we evaluate the hypothesis that plasma biomarkers of neurodegeneration and Alzheimer’s Disease pathology are associated with worse gait performance.
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Nov 1, 2024 | 
jamanetwork.com | Ronald Petersen |Elizabeth C. Mormino |Julie Schneider
Alzheimer Disease—What’s in a Name?
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Sep 20, 2024 | 
nature.com | Shannon L. Risacher |Paula J Bice |Jared Brosch |Kelley Faber |Martin R Farlow |Tatiana Foroud | +29 more
AbstractDetermining the genetic architecture of Alzheimer’s disease pathologies can enhance mechanistic understanding and inform precision medicine strategies. Here, we perform a genome-wide association study of cortical tau quantified by positron emission tomography in 3046 participants from 12 independent studies. The CYP1B1-RMDN2 locus is associated with tau deposition.
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Jun 24, 2024 | 00031-4/fulltext&sz=64)
mayoclinicproceedings.org | Wentao Li |Ronald Petersen |Alicia Algeciras-Schimnich
Abstract To evaluate the performance of Alzheimer disease (AD) cerebrospinal fluid (CSF) biomarkers in a tertiary neurology clinic setting with high frequency of non-AD cases, including normal pressure hydrocephalus (NPH). There were 534 patients who underwent AD CSF biomarkers (Roche Elecsys Aβ42, p-Tau181, total-Tau) from April 1, 2020, through April 23, 2021.
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Jun 20, 2024 | 
nature.com | Özkan İş |Xue Wang |Joseph S. Reddy |Yuhao Min |Elanur Yilmaz |Prabesh Bhattarai | +19 more
AbstractTo uncover molecular changes underlying blood-brain-barrier dysfunction in Alzheimer’s disease, we performed single nucleus RNA sequencing in 24 Alzheimer’s disease and control brains and focused on vascular and astrocyte clusters as main cell types of blood-brain-barrier gliovascular-unit. The majority of the vascular transcriptional changes were in pericytes.
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Feb 21, 2024 | 
medscape.com | Andrew Wilner |Ronald Petersen
This transcript has been edited for clarity. Andrew N. Wilner, MD: Welcome to Medscape. I'm Dr Andrew Wilner. Today I have a special guest: Dr Ron Petersen. Dr Petersen is the lead author of a paper recently published in JAMA Neurology, entitled, "A New Framework for Dementia Nomenclature." Welcome, Dr Petersen. Ronald C. Petersen, MD, PhD: Thanks, Dr Wilner, for having me. Wilner: Dr Petersen, you are a professor of neurology and an expert in the dementia field. Tell us about this paper.
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Oct 16, 2023 | 
jamanetwork.com | Ronald Petersen |Sandra Weintraub |Marwan Sabbagh
A New Framework for Dementia Nomenclature Abstract Importance Nomenclature in the field of neurodegenerative diseases presents a challenging problem. Inconsistent use of terms such as Alzheimer disease and dementia has compromised progress in clinical care, research, and development of therapeutics. Dementia-associated stigma further contributes to inconsistent and imprecise language.
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Sep 7, 2023 | 
nature.com | Juan Pablo Palavicini |Habil Zare |Peng Xu |Ronald Petersen |Tamara Tchkonia |James Kirkland | +3 more
Prince, M. J. et al. World Alzheimer Report 2015—The Global Impact of Dementia: An Analysis of Prevalence, Incidence, Cost and Trends (Alzheimer’s Disease International, 2015). Cummings, J., Ritter, A. & Zhong, K. Clinical trials for disease-modifying therapies in Alzheimer’s disease: a primer, lessons learned, and a blueprint for the future. J. Alzheimers Dis. 64, S3–S22 (2018). Article PubMed PubMed Central Google Scholar Aisen, P. S. et al. The future of anti-amyloid trials. J. Prev. Alzheimers Dis.
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May 29, 2023 | 
nature.com | Emily S. Lundt |Christopher Schwarz |Matthew L. Senjem |Robert Reid |David S. Knopman |Prashanthi Vemuri | +3 more
In this work, we used an AFT model to study the association of individual adjustments in timing of AD and CVD biomarker progression. These findings are important in informing the proposed relationships between AD (defined as an accumulation of pathological aggregated amyloid and tau proteins) and small vessel cerebrovascular disease. The individual adjustments of AD biomarkers (amyloid and tau PET) and established CVD biomarkers (WMH and FA GCC) showed weak to no association.
