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http://dx.doi.org/10.1111/jgs.14219 | DOI Listing |
Alzheimer's disease (AD) is a form of dementia in which memory and cognitive decline is thought to arise from underlying neurodegeneration. These cognitive impairments, however, are transient when they first appear and can fluctuate across disease progression. Here, we investigate the neural mechanisms underlying fluctuations of performance in amnestic mice.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Rush University Medical Center, Chicago, Illinois, USA.
Limbic predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is highly prevalent in late life and a common co-pathology with Alzheimer's disease neuropathologic change (ADNC). LATE-NC is a slowly progressive, amnestic clinical syndrome. Alternatively, when present with ADNC, LATE-NC is associated with a more rapid course.
View Article and Find Full Text PDFAlzheimers Res Ther
October 2024
German Centre for Neurodegenerative Diseases (DZNE), Leipziger Str. 44, Magdeburg, 39120, Germany.
Background: Perivascular space (PVS) enlargement in ageing and Alzheimer's disease (AD) and the drivers of such a structural change in humans require longitudinal investigation. Elucidating the effects of demographic factors, hypertension, cerebrovascular dysfunction, and AD pathology on PVS dynamics could inform the role of PVS in brain health function as well as the complex pathophysiology of AD.
Methods: We studied PVS in centrum semiovale (CSO) and basal ganglia (BG) computationally over three to four annual visits in 503 participants (255 females; mean = 70.
Alzheimers Res Ther
September 2024
Department of Diagnostic Radiology, Clinical Sciences, Lund University, Klinikgatan 13B, Lund, SE-22242, Sweden.
bioRxiv
May 2024
Department of Diagnostic Radiology, Clinical Sciences, Lund University, 22242 Lund, Sweden.
Background: The medial temporal lobe (MTL) is hypothesized to be relatively spared in early-onset Alzheimer's disease (EOAD). Yet, detailed examination of MTL subfield volumes and drivers of atrophy in amnestic EOAD is lacking.
Methods: BioFINDER-2 participants with memory impairment, abnormal amyloid-β status and tau-PET were included.
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