Are Older Americans Getting the Long-Term Services and Supports They Need?

Issue: Older adults' needs have evolved and are no longer met by the Medicare program. With the recent passage of the Bipartisan Budget Act of 2018 (BBA), Medicare Advantage (MA) plans can now provide beneficiaries with nonmedical benefits, such as long-term services and supports (LTSS), which Medicare does not cover. Goal: To examine the use of LTSS among Medicare beneficiaries age 65 and older living in the community and explore differences by age, income, and other variables. Methods: Descriptive analyses of the National Health and Aging Trends Study (NHATS), 2015. Findings and Conclusions: Two-thirds of older adults living in the community use some degree of LTSS. Reliance on assistive devices and environmental modifications is high; however many adults, particularly dual-eligible beneficiaries, experience adverse consequences of not receiving care. Although the recent policy change allowing MA plans to offer LTSS benefits is an important step toward meeting the medical and nonmedical needs of Medicare beneficiaries, only the one-third of Medicare beneficiaries enrolled in MA plans stand to benefit. Accountable care organizations operating in traditional Medicare also should have the increased flexibility to provide nonmedical services.

Spatial relation between microbleeds and amyloid deposits in amyloid angiopathy.

Advanced cerebrovascular ß-amyloid deposition (cerebral amyloid angiopathy, CAA) is associated with cerebral microbleeds, but the precise relationship between CAA burden and microbleeds is undefined. We used T2*-weighted magnetic resonance imaging (MRI) and noninvasive amyloid imaging with Pittsburgh Compound B (PiB) to analyze the spatial relationship between CAA and microbleeds. On coregistered positron emission tomography (PET) and MRI images, PiB retention was increased at microbleed sites compared to simulated control lesions (p = 0.002) and declined with increasing distance from the microbleed (p < 0.0001). These findings indicate that microbleeds occur preferentially in local regions of concentrated amyloid and support therapeutic strategies aimed at reducing vascular amyloid deposition.

Cerebrospinal fluid amyloid beta(40) is decreased in cerebral amyloid angiopathy.

Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature. In analogy to previous observations in Alzheimer disease, we hypothesized that analysis of amyloid beta(40) and beta(42) proteins in the cerebrospinal fluid might serve as a molecular biomarker. We observed strongly decreased cerebrospinal fluid amyloid beta(40) (p < 0.01 vs controls or Alzheimer disease) and amyloid beta(42) concentrations (p < 0.001 vs controls and p < 0.05 vs Alzheimer disease) in cerebral amyloid angiopathy patients. The combination of amyloid beta(42) and total tau discriminated cerebral amyloid angiopathy from controls, with an area under the receiver operator curve of 0.98. Our data are consistent with neuropathological evidence that amyloid beta(40) as well as amyloid beta(42) protein are selectively trapped in the cerebral vasculature from interstitial fluid drainage pathways that otherwise transport amyloid beta proteins toward the cerebrospinal fluid.

Detection of isolated cerebrovascular beta-amyloid with Pittsburgh compound B.

Imaging of cerebrovascular beta-amyloid (cerebral amyloid angiopathy) is complicated by the nearly universal overlap of this pathology with Alzheimer's pathology. We performed positron emission tomographic imaging with Pittsburgh Compound B on 42-year-old man with early manifestations of Iowa-type hereditary cerebral amyloid angiopathy, a form of the disorder with little or no plaque deposits of fibrillar beta-amyloid. The results demonstrated increased Pittsburgh Compound B retention selectively in occipital cortex, sparing regions typically labeled in Alzheimer's disease. These results offer compelling evidence that Pittsburgh Compound B positron emission tomography can noninvasively detect isolated cerebral amyloid angiopathy before overt signs of tissue damage such as hemorrhage or white matter lesions.