Publications by authors named "A Paganini-Hill"

Background: Subjective Memory Complaints (SMC) are defined as the perception of one's own memory. In several studies SMC are associated with Alzheimer's disease (AD) neuropathologic changes, and only one study has analyzed and found an association of SMC with other neurodegenerative, but not vascular, neuropathologic changes. Yet, the evidence on the association of SMC with non-AD neuropathologic changes is insufficient.

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Objectives: Exploration of medical histories and medications associated with Alzheimer disease neuropathologic change (ADNC) absence and potential resistance may identify protective factors against ADNC. This was a retrospective examination of data from participants age ≥90 years who enrolled in , a longitudinal study based in California. Participants underwent neuropathologic analysis for the presence of neuritic amyloid plaques (NPs) (any), beta amyloid plaques (Thal phase > 0), and neurofibrillary tangles (>2).

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Objectives: Periodic imaging follow-up for patients with unruptured intracranial aneurysms (UIA) is crucial, as studies indicate higher rupture risk with aneurysm growth. However, few studies address patient adherence to follow-up recommendations. This study aims to identify compliance rates and factors influencing follow-up adherence.

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Introduction: We investigated the association between sleep duration and neuropathologic changes 19 to 40 years later in oldest-old (age 90+) participants of The 90+ Study.

Methods: Participants self-reported sleep duration and underwent neuropathologic evaluation. We categorized sleep duration as < 7, 7 to 8 = reference, > 8 hours and dichotomized neuropathologic changes as present/absent.

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Article Synopsis
  • Cerebellar amyloid-β (Aβ) plaques play a crucial role in diagnosing Alzheimer disease (AD) and were studied for their characteristics in 73 cases with specific A3 scores in the ABC criteria.
  • Over 85% of these cases showed significant parenchymal Aβ-42 staining, particularly in those classified as Braak stage V-VI/B3, indicating a strong correlation between Aβ deposits and disease severity.
  • The study also found that the presence of Aβ-42 in the Purkinje cell layer was linked to neuronal damage, with varying morphologies of the plaques noted, and a significant occurrence of cerebral amyloid angiopathy (CAA) in both parenchymal and leptomeningeal
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