Introduction: Postmortem studies suggest that fibrillar brain amyloid places people at higher risk for hazardous driving in the preclinical stage of Alzheimer's disease (AD).
Methods: We administered driving questionnaires to 104 older drivers (19 AD, 24 mild cognitive impairment, and 61 cognitive normal) who had a recent F-florbetapir positron emission tomography scan. We examined associations of amyloid standardized uptake value ratios with driving behaviors: traffic violations or accidents in the past 3 years.
Results: The frequency of violations or accidents was curvilinear with respect to standardized uptake value ratios, peaking around a value of 1.1 (model = 0.10, = .002); moreover, this relationship was evident for the cognitively normal participants.
Discussion: We found that driving risk is strongly related to accumulating amyloid on positron emission tomography, and that this trend is evident in the preclinical stage of AD. Brain amyloid burden may in part explain the increased crash risk reported in older adults.
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http://dx.doi.org/10.1016/j.dadm.2016.10.008 | DOI Listing |
J Vis Exp
January 2025
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, Harvard Medical School;
A method to quantitate the stabilization of Mitochondria-Associated endoplasmic reticulum Membranes (MAMs) in a 3-dimensional (3D) neural model of Alzheimer's disease (AD) is presented here. To begin, fresh human neuro progenitor ReN cells expressing β-amyloid precursor protein (APP) containing familial Alzheimer's disease (FAD) or naïve ReN cells are grown in thin (1:100) Matrigel-coated tissue culture plates. After the cells reach confluency, these are electroporated with expression plasmids encoding red fluorescence protein (RFP)-conjugated mitochondria-binding sequence of AKAP1(34-63) (Mito-RFP) that detects mitochondria or constitutive MAM stabilizers MAM 1X or MAM 9X that stabilize tight (6 nm ± 1 nm gap width) or loose (24 nm ± 3 nm gap width) MAMs, respectively.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Unitat de Trastorns Cognitius, Cognition and Behavior Study Group, Hospital Universitari Santa Maria Universitat de Lleida, Lleida, Spain.
Introduction: Changes in sleep physiology can predate cognitive symptoms by decades in persons with Alzheimer's disease (AD), but it remains unclear which sleep characteristics predict cognitive and neurodegenerative changes after AD onset.
Methods: Using data from a prospective cohort of mild to moderate AD (n = 60), we analyzed non-rapid eye movement sleep spindles and slow oscillations (SOs) at baseline and their associations with baseline amyloid beta (Aβ) and tau and with cognition from baseline to 3-year follow-up.
Results: Higher spindle and SO activity predicted significant changes in Aβ and tau at baseline, lower Alzheimer's Disease Assessment Scale Cognitive Subscale (better cognitive performance) score, and higher Mini-Mental State Examination score from baseline to 36 months.
Curr Alzheimer Res
January 2025
Metabolic Syndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Extracellular vesicles (EVs) are nano-sized membranous particles that are secreted by various cell types and play a critical role in intercellular communication. Their unique properties and remarkable ability to deliver bioactive cargo to target cells have made them promising tools in the treatment of various diseases, including Alzheimer's disease (AD). AD is a devastating neurodegenerative disease characterized by progressive cognitive decline and neuropathological hallmarks, such as amyloid-beta plaques and neurofibrillary tangles.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
Introduction: Plasma phosphorylated tau (p-tau) biomarkers have improved Alzheimer's disease (AD) diagnosis, but data from diverse Asian populations are limited. This study evaluated plasma p-tau217 and p-tau181 levels in Korean and Taiwanese populations.
Methods: All participants (n = 270) underwent amyloid positron emission tomography (PET) and blood tests.
Background: Although Amyloid-beta and Tau are the hallmarks of Alzheimer's Disease (AD), other protein pathways such as endothelial dysfunction may be involved and may precede cognitive symptoms. Our objective was to characterize the cerebrospinal fluid (CSF) proteomic profiles focusing on cardiometabolic-related protein pathways in individuals on the AD spectrum.
Methods: We performed CSF and plasma-targeted proteomics (276 proteins) from 354 participants of the Brain Stress Hypertension and Aging Program (BSHARP), of which 8% had preclinical AD, and 24% had MCI due to AD.
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