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  • American Association for the Advancement of Science (AAAS)  (3)
  • 2015-2019  (3)
  • 1
    Online Resource
    Online Resource
    Tau and Aβ imaging, CSF measures, and cognition in Alzheimer’s disease
    American Association for the Advancement of Science (AAAS) ; 2016
    In:  Science Translational Medicine Vol. 8, No. 338 ( 2016-05-11)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 8, No. 338 ( 2016-05-11)
    Abstract: Alzheimer’s disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. Until recently, only Aβ could be studied in humans using positron emission tomography (PET) imaging owing to a lack of tau PET imaging agents. Clinical pathological studies have linked tau pathology closely to the onset and progression of cognitive symptoms in patients with AD. We report PET imaging of tau and Aβ in a cohort of cognitively normal older adults and those with mild AD. Multivariate analyses identified unique disease-related stereotypical spatial patterns (topographies) for deposition of tau and Aβ. These PET imaging tau and Aβ topographies were spatially distinct but correlated with disease progression. Cerebrospinal fluid measures of tau, often used to stage preclinical AD, correlated with tau deposition in the temporal lobe. Tau deposition in the temporal lobe more closely tracked dementia status and was a better predictor of cognitive performance than Aβ deposition in any region of the brain. These data support models of AD where tau pathology closely tracks changes in brain function that are responsible for the onset of early symptoms in AD.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.aaf2362
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2016
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Reduced non–rapid eye movement sleep is associated with tau pathology in early Alzheimer’s disease
    American Association for the Advancement of Science (AAAS) ; 2019
    In:  Science Translational Medicine Vol. 11, No. 474 ( 2019-01-09)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 11, No. 474 ( 2019-01-09)
    Abstract: In Alzheimer’s disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. By the time even the earliest clinical symptoms are detectable, Aβ accumulation is close to reaching its peak and neocortical tau pathology is frequently already present. The period in which AD pathology is accumulating in the absence of cognitive symptoms represents a clinically relevant time window for therapeutic intervention. Sleep is increasingly recognized as a potential marker for AD pathology and future risk of cognitive impairment. Previous studies in animal models and humans have associated decreased non–rapid eye movement (NREM) sleep slow wave activity (SWA) with Aβ deposition. In this study, we analyzed cognitive performance, brain imaging, and cerebrospinal fluid (CSF) AD biomarkers in participants enrolled in longitudinal studies of aging. In addition, we monitored their sleep using a single-channel electroencephalography (EEG) device worn on the forehead. After adjusting for multiple covariates such as age and sex, we found that NREM SWA showed an inverse relationship with AD pathology, particularly tauopathy, and that this association was most evident at the lowest frequencies of NREM SWA. Given that our study participants were predominantly cognitively normal, this suggested that changes in NREM SWA, especially at 1 to 2 Hz, might be able to discriminate tau pathology and cognitive impairment either before or at the earliest stages of symptomatic AD.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.aau6550
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2019
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Early changes in CSF sTREM2 in dominantly inherited Alzheimer’s disease occur after amyloid deposition and neuronal injury
    American Association for the Advancement of Science (AAAS) ; 2016
    In:  Science Translational Medicine Vol. 8, No. 369 ( 2016-12-14)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 8, No. 369 ( 2016-12-14)
    Abstract: Emerging evidence supports a role for innate immunity and microglia in Alzheimer’s disease (AD) pathophysiology. However, no marker related to microglia has been included in the temporal evolution models of AD. TREM2 is a transmembrane protein involved in innate immunity and is selectively expressed by microglia and genetically linked to AD and other neurodegenerative disorders. Its ectodomain is released by proteolysis as a soluble variant (sTREM2) and can be detected in the cerebrospinal fluid (CSF). In patients with autosomal dominant AD, we tested how many years before the expected symptom onset did CSF sTREM2 increase in mutation carriers (MCs) compared to noncarriers (NCs). We also determined the temporal sequence of changes in CSF sTREM2 and markers for amyloid deposition and neurodegeneration as well as cognitive performance. We included 218 participants consisting of 127 MC and 91 NC siblings from the Dominantly Inherited Alzheimer Network. We observed that CSF sTREM2 increased in MCs compared to NCs 5 years before the expected symptom onset and this difference remained significant until 5 years after the expected symptom onset. Changes in CSF sTREM2 occurred after alterations were observed in markers for brain amyloidosis and neuronal injury. We propose that microglial activation occurs several years before the expected symptom onset, but after amyloidosis and neuronal injury have already occurred.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.aag1767
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2016
    Location Call Number Limitation Availability
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    Online Resource
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