Publications by authors named "R Schlossberg"

Background: Triplication of the amyloid precursor protein in individuals with Down Syndrome (DS) produces an increased risk for the development of Alzheimer's disease (AD). Declining cholinergic integrity plays a role in the cognitive deficits observed in late-onset AD. In the present study, we assess the relationship between basal forebrain volume or [F]-FEOBV uptake and cognitive performance in adults with DS.

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Background: Adults with Down Syndrome (DS) have the highest risk of developing Alzheimer's disease (AD) worldwide. Triplication of the amyloid precursor protein gene on chromosome 21 results in early amyloid accumulation and Alzheimer's pathology. The cholinergic system is known to decline early in the development of AD and plays a fundamental role in observed cognitive deficits.

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Background: Adults with Down syndrome (DS) are at a high risk of developing Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein on chromosome 21. Despite the high incidence of AD within the DS population, there is less understanding of how AD progresses, although it may be reflected in an accelerated aging phenotype. Compared to typically developing populations, there is less understanding of the decline of cholinergic integrity with aging in adults with DS.

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Article Synopsis
  • - Adults with Down syndrome are genetically prone to developing Alzheimer's disease after 40, and their cholinergic system, crucial for cognitive function, shows a decline similar to Alzheimer's pathology.
  • - A study using PET imaging compared cholinergic terminals in 16 non-demented adults with Down syndrome to 20 neurotypically developed individuals, focusing on brain areas like the cerebellum and cortex.
  • - Results revealed that adults with Down syndrome had higher cholinergic terminal density in early adulthood, but experienced a faster decline with age compared to their neurotypical counterparts.
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B-cell maturation antigen (BCMA), a tumor necrosis factor receptor (TNFR) family member, is selectively expressed on terminally differentiated B-lymphocytes including multiple myeloma (MM) tumor cells. We sought to determine whether circulating (c)BCMA in MM serum interferes with antiBCMA antibody binding to MM cells. An enzyme-linked immunosorbent assay (ELISA) was used to determine serum (s) BCMA levels among 379 samples from patients with relapsed/refractory MM (RRMM).

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