Future climate change effects on US forest composition may offset benefits of reduced atmospheric deposition of N and S.

Climate change and atmospheric deposition of nitrogen (N) and sulfur (S) are important drivers of forest demography. Here we apply previously derived growth and survival responses for 94 tree species, representing >90% of the contiguous US forest basal area, to project how changes in mean annual temperature, precipitation, and N and S deposition from 20 different future scenarios may affect forest composition to 2100. We find that under the low climate change scenario (RCP 4.5), reductions in aboveground tree biomass from higher temperatures are roughly offset by increases in aboveground tree biomass from reductions in N and S deposition. However, under the higher climate change scenario (RCP 8.5) the decreases from climate change overwhelm increases from reductions in N and S deposition. These broad trends underlie wide variation among species. We found averaged across temperature scenarios the relative abundance of 60 species were projected to decrease more than 5% and 20 species were projected to increase more than 5%; and reductions of N and S deposition led to a decrease for 13 species and an increase for 40 species. This suggests large shifts in the composition of US forests in the future. Negative climate effects were mostly from elevated temperature and were not offset by scenarios with wetter conditions. We found that by 2100 an estimated 1 billion trees under the RCP 4.5 scenario and 20 billion trees under the RCP 8.5 scenario may be pushed outside the temperature record upon which these relationships were derived. These results may not fully capture future changes in forest composition as several other factors were not included. Overall efforts to reduce atmospheric deposition of N and S will likely be insufficient to overcome climate change impacts on forest demography across much of the United States unless we adhere to the low climate change scenario.

Projecting U.S. forest management, market, and carbon sequestration responses to a high-impact climate scenario.

The impact of climate change on forest ecosystems remains uncertain, with wide variation in potential climate impacts across different radiative forcing scenarios and global circulation models, as well as potential variation in forest productivity impacts across species and regions. This study uses an empirical forest composition model to estimate the impact of climate factors (temperature and precipitation) and other environmental parameters on forest productivity for 94 forest species across the conterminous United States. The composition model is linked to a dynamic optimization model of the U.S. forestry sector to quantify economic impacts of a high warming scenario (Representative Concentration Pathway 8.5) under six alternative climate projections and two socioeconomic scenarios. Results suggest that forest market impacts and consumer impacts could range from relatively large losses (-$2.6 billion) to moderate gain ($0.2 billion) per year across climate scenarios. Temperature-induced higher mortality and lower productivity for some forest types and scenarios, coupled with increasing economic demands for forest products, result in forest inventory losses by end of century relative to the current climate baseline (3%-23%). Lower inventories and reduced carbon sequestration capacity result in additional economic losses of up to approximately $4.1 billion per year. However, our results also highlight important adaptation mechanisms, such forest type changes and shifts in regional mill capacity that could reduce the impact of high impact climate scenarios.

Conditional vulnerability of plant diversity to atmospheric nitrogen deposition across the United States.

Atmospheric nitrogen (N) deposition has been shown to decrease plant species richness along regional deposition gradients in Europe and in experimental manipulations. However, the general response of species richness to N deposition across different vegetation types, soil conditions, and climates remains largely unknown even though responses may be contingent on these environmental factors. We assessed the effect of N deposition on herbaceous richness for 15,136 forest, woodland, shrubland, and grassland sites across the continental United States, to address how edaphic and climatic conditions altered vulnerability to this stressor. In our dataset, with N deposition ranging from 1 to 19 kg N⋅ha(-1)⋅y(-1), we found a unimodal relationship; richness increased at low deposition levels and decreased above 8.7 and 13.4 kg N⋅ha(-1)⋅y(-1) in open and closed-canopy vegetation, respectively. N deposition exceeded critical loads for loss of plant species richness in 24% of 15,136 sites examined nationwide. There were negative relationships between species richness and N deposition in 36% of 44 community gradients. Vulnerability to N deposition was consistently higher in more acidic soils whereas the moderating roles of temperature and precipitation varied across scales. We demonstrate here that negative relationships between N deposition and species richness are common, albeit not universal, and that fine-scale processes can moderate vegetation responses to N deposition. Our results highlight the importance of contingent factors when estimating ecosystem vulnerability to N deposition and suggest that N deposition is affecting species richness in forested and nonforested systems across much of the continental United States.

Atmospheric deposition and exceedances of critical loads from 1800-2025 for the conterminous United States.

Atmospheric deposition of nitrogen (N) and sulfur (S) has increased dramatically over pre-industrial levels, with many potential impacts on terrestrial and aquatic ecosystems. Quantitative thresholds, termed "critical loads" (CLs), have been developed to estimate the deposition rate above which damage is thought to occur. However, there remains no comprehensive comparison of when, where, and over what time periods individual CLs have been exceeded. We addressed this knowledge gap by combining several published data sources for historical and contemporary deposition, and overlaying these on six CL types from the National Critical Loads Database (NCLDv2.5; terrestrial acidification, aquatic acidification, lichen, nitrate leaching, plant community composition, and forest-tree health) to examine exceedances from 1800 to 2011. We expressed CLs as the minimum, 10th, and 50th percentiles within 12-km grid cells. Minimum CLs were relatively uniform across the country (200-400 eq·ha-1 ·yr-1 ), and have been exceeded for decades beginning in the early 20th century. The area exceeding minimum CLs peaked in the 1970s and 1980s, exposing 300,000 to 3 million km2 (depending on the CL type) to harmful levels of deposition, with a total area exceeded of 5.8 million km2 (~70% of the conterminous United States). Since then, deposition levels have dropped, especially for S, with modest reductions in exceedance by 2011 for all CL types, totaling 5.2 million km2 in exceedance. The 10th and 50th percentile CLs followed similar trends, but were not consistently available at the 12-km grid scale. We also examined near-term future deposition and exceedances in 2025 under current air quality regulations, and under various scenarios of climate change and additional nitrogen management controls. Current regulations were projected to reduce exceedances of any CL from 5.2 million km2 in 2011 to 4.8 million km2 in 2025. None of the additional N management or climate scenarios significantly affected areal exceedances, although exceedance severity declined. In total, it is clear that many CLs have been exceeded for decades, and are likely to remain so in the short term under current policies. Additionally, we suggest many areas for improvement to enhance our understanding of deposition and its effects to support informed decision making.

A conserved dopamine-cholecystokinin signaling pathway shapes context-dependent Caenorhabditis elegans behavior.

An organism's ability to thrive in changing environmental conditions requires the capacity for making flexible behavioral responses. Here we show that, in the nematode Caenorhabditis elegans, foraging responses to changes in food availability require nlp-12, a homolog of the mammalian neuropeptide cholecystokinin (CCK). nlp-12 expression is limited to a single interneuron (DVA) that is postsynaptic to dopaminergic neurons involved in food-sensing, and presynaptic to locomotory control neurons. NLP-12 release from DVA is regulated through the D1-like dopamine receptor DOP-1, and both nlp-12 and dop-1 are required for normal local food searching responses. nlp-12/CCK overexpression recapitulates characteristics of local food searching, and DVA ablation or mutations disrupting muscle acetylcholine receptor function attenuate these effects. Conversely, nlp-12 deletion reverses behavioral and functional changes associated with genetically enhanced muscle acetylcholine receptor activity. Thus, our data suggest that dopamine-mediated sensory information about food availability shapes foraging in a context-dependent manner through peptide modulation of locomotory output.

Monoaminergic orchestration of motor programs in a complex C. elegans behavior.

Monoamines provide chemical codes of behavioral states. However, the neural mechanisms of monoaminergic orchestration of behavior are poorly understood. Touch elicits an escape response in Caenorhabditis elegans where the animal moves backward and turns to change its direction of locomotion. We show that the tyramine receptor SER-2 acts through a Gαo pathway to inhibit neurotransmitter release from GABAergic motor neurons that synapse onto ventral body wall muscles. Extrasynaptic activation of SER-2 facilitates ventral body wall muscle contraction, contributing to the tight ventral turn that allows the animal to navigate away from a threatening stimulus. Tyramine temporally coordinates the different phases of the escape response through the synaptic activation of the fast-acting ionotropic receptor, LGC-55, and extrasynaptic activation of the slow-acting metabotropic receptor, SER-2. Our studies show, at the level of single cells, how a sensory input recruits the action of a monoamine to change neural circuit properties and orchestrate a compound motor sequence.

Neuronal regeneration in C. elegans requires subcellular calcium release by ryanodine receptor channels and can be enhanced by optogenetic stimulation.

Regulated calcium signals play conserved instructive roles in neuronal repair, but how localized calcium stores are differentially mobilized, or might be directly manipulated, to stimulate regeneration within native contexts is poorly understood. We find here that localized calcium release from the endoplasmic reticulum via ryanodine receptor (RyR) channels is critical in stimulating initial regeneration following traumatic cellular damage in vivo. Using laser axotomy of single neurons in Caenorhabditis elegans, we find that mutation of unc-68/RyR greatly impedes both outgrowth and guidance of the regenerating neuron. Performing extended in vivo calcium imaging, we measure subcellular calcium signals within the immediate vicinity of the regenerating axon end that are sustained for hours following axotomy and completely eliminated within unc-68/RyR mutants. Finally, using a novel optogenetic approach to periodically photo-stimulate the axotomized neuron, we can enhance its regeneration. The enhanced outgrowth depends on both amplitude and temporal pattern of excitation and can be blocked by disruption of UNC-68/RyR. This demonstrates the exciting potential of emerging optogenetic technology to beneficially manipulate cell physiology in the context of neuronal regeneration and indicates a link to the underlying cellular calcium signal. Taken as a whole, our findings define a specific localized calcium signal mediated by RyR channel activity that stimulates regenerative outgrowth, which may be dynamically manipulated for beneficial neurotherapeutic effects.

Allergic Fungal Rhinosinusitis and the Unified Airway: the Role of Antifungal Therapy in AFRS.

Allergic fungal sinusitis (AFS) or rhinosinusitis (AFRS) is a form of polypoid chronic rhinosinusitis that is believed to be due to hypersensitivity to fungal antigens. The disease is characterized by type 1 hypersensitivity to fungal allergens, dramatically elevated total serum IgE, accumulation of thick eosinophil-laden mucin with non-invasive fungal hyphae within the paranasal sinuses, nasal polyposis, and sinus bony remodeling. Because of many clinicopathologic similarities to allergic bronchopulmonary aspergillosis (ABPA), these conditions can be considered analogous examples of disease in the unified airway. However, these conditions rarely occur together and their treatment differs. The treatment of AFRS relies upon surgical removal of fungal hyphae in eosinophilic mucin, while antifungal therapy is used to clear fungi from the airways in ABPA. Several uncontrolled studies suggest there may be some benefit to antifungal agents in AFRS, but randomized trials of topical and systemic antifungal therapies have not shown beneficial results in chronic rhinosinusitis (CRS). Antifungal treatment within the sinonasal cavities does not appear to be an effective approach for most chronic sinusitis, and antifungal therapy for AFRS is unproven.

Loss of plant species after chronic low-level nitrogen deposition to prairie grasslands.

Rates of atmospheric deposition of biologically active nitrogen (N) are two to seven times the pre-industrial rates in many developed nations because of combustion of fossil fuels and agricultural fertilization. They are expected to increase similarly over the next 50 years in industrializing nations of Asia and South America. Although the environmental impacts of high rates of nitrogen addition have been well studied, this is not so for the lower, chronic rates that characterize much of the globe. Here we present results of the first multi-decadal experiment to examine the impacts of chronic, experimental nitrogen addition as low as 10 kg N ha(-1) yr(-1) above ambient atmospheric nitrogen deposition (6 kg N ha(-1) yr(-1) at our site). This total input rate is comparable to terrestrial nitrogen deposition in many industrialized nations. We found that this chronic low-level nitrogen addition rate reduced plant species numbers by 17% relative to controls receiving ambient N deposition. Moreover, species numbers were reduced more per unit of added nitrogen at lower addition rates, suggesting that chronic but low-level nitrogen deposition may have a greater impact on diversity than previously thought. A second experiment showed that a decade after cessation of nitrogen addition, relative plant species number, although not species abundances, had recovered, demonstrating that some effects of nitrogen addition are reversible.

Geographic variation in projected US forest aboveground carbon responses to climate change and atmospheric deposition.

Forest composition and ecosystem services are sensitive to anthropogenic pressures like climate change and atmospheric deposition of nitrogen (N) and sulfur (S). Here we extend recent forest projections for the current cohort of trees in the contiguous US, characterizing potential changes in aboveground tree carbon at the county level in response to varying mean annual temperature, precipitation, and N and S deposition. We found that relative to a scenario with N and S deposition reduction and no climate change, greater climate change led generally to decreasing aboveground carbon (mean -7.5% under RCP4.5, -16% under RCP8.5). Keeping climate constant, reduced N deposition tended to lessen aboveground carbon (mean -7%), whereas reduced S deposition tended to increase aboveground carbon (+3%) by 2100. Through mid-century (2050), deposition was more important for predicting carbon responses except under the extreme climate scenarios (RCP8.5); but, by 2100, climate drivers generally outweighed deposition. While more than 70% of counties showed reductions in aboveground carbon relative to the reference scenario, these were not evenly distributed across the US. Counties in the Northwest and Northern Great Plains, and the northern parts of New England and the Midwest, primarily showed positive responses, while counties in the Southeast showed negative responses. Counties with greater initial biomass showed less negative responses to climate change while those which exhibited the greatest change in composition (>15%) had a 95% chance of losing carbon relative to a no-climate change scenario. This analysis highlights that declines in forest growth and survival due to increases in mean temperature and reductions in atmospheric N deposition are likely to outweigh positive impacts of reduced S deposition and potential increases in precipitation. These effects vary at the regional and county level, however, so forest managers must consider local rather than national dynamics to maximize forest carbon sinks in the future.

Climate change could negate U.S. forest ecosystem service benefits gained through reductions in nitrogen and sulfur deposition.

Climate change and atmospheric deposition of nitrogen (N) and sulfur (S) impact the health and productivity of forests. Here, we explored the potential impacts of these environmental stressors on ecosystem services provided by future forests in the contiguous U.S. We found that all stand-level services benefitted (+ 2.6 to 8.1%) from reductions in N+S deposition, largely attributable to positive responses to reduced S that offset the net negative effects of lower N levels. Sawtimber responded positively (+ 0.5 to 0.6%) to some climate change, but negatively (- 2.4 to - 3.8%) to the most extreme scenarios. Aboveground carbon (C) sequestration and forest diversity were negatively impacted by all modelled changes in climate. Notably, the most extreme climate scenario eliminated gains in all three services achieved through reduced deposition. As individual tree species responded differently to climate change and atmospheric deposition, associated services unique to each species increased or decreased under future scenarios. Our results suggest that climate change should be considered when evaluating the benefits of N and S air pollution policies on the services provided by U.S. forests.

Estimated losses of plant biodiversity in the United States from historical N deposition (1985-2010).

Although nitrogen (N) deposition is a significant threat to herbaceous plant biodiversity worldwide, it is not a new stressor for many developed regions. Only recently has it become possible to estimate historical impacts nationally for the United States. We used 26 years (1985-2010) of deposition data, with ecosystem-specific functional responses from local field experiments and a national critical loads (CL) database, to generate scenario-based estimates of herbaceous species loss. Here we show that, in scenarios using the low end of the CL range, N deposition exceeded critical loads over 0.38, 6.5, 13.1, 88.6, and 222.1 million ha for the Mediterranean California, North American Desert, Northwestern Forested Mountains, Great Plains, and Eastern Forest ecoregions, respectively, with corresponding species losses ranging from < 1% to 30%. When we ran scenarios assuming ecosystems were less sensitive (using a common CL of 10 kg x ha(-1) x yr(-1), and the high end of the CL range) minimal losses were estimated. The large range in projected impacts among scenarios implies uncertainty as to whether current critical loads provide protection to terrestrial plant biodiversity nationally and urge greater research in refining critical loads for U.S. ecosystems.

Alzheimer's disease pattern of brain atrophy predicts cognitive decline in Parkinson's disease.

Research suggests overlap in brain regions undergoing neurodegeneration in Parkinson's and Alzheimer's disease. To assess the clinical significance of this, we applied a validated Alzheimer's disease-spatial pattern of brain atrophy to patients with Parkinson's disease with a range of cognitive abilities to determine its association with cognitive performance and decline. At baseline, 84 subjects received structural magnetic resonance imaging brain scans and completed the Dementia Rating Scale-2, and new robust and expanded Dementia Rating Scale-2 norms were applied to cognitively classify participants. Fifty-nine non-demented subjects were assessed annually with the Dementia Rating Scale-2 for two additional years. Magnetic resonance imaging scans were quantified using both a region of interest approach and voxel-based morphometry analysis, and a method for quantifying the presence of an Alzheimer's disease spatial pattern of brain atrophy was applied to each scan. In multivariate models, higher Alzheimer's disease pattern of atrophy score was associated with worse global cognitive performance (ß = -0.31, P = 0.007), including in non-demented patients (ß = -0.28, P = 0.05). In linear mixed model analyses, higher baseline Alzheimer's disease pattern of atrophy score predicted long-term global cognitive decline in non-demented patients [F(1, 110) = 9.72, P = 0.002], remarkably even in those with normal cognition at baseline [F(1, 80) = 4.71, P = 0.03]. In contrast, in cross-sectional and longitudinal analyses there was no association between region of interest brain volumes and cognitive performance in patients with Parkinson's disease with normal cognition. These findings support involvement of the hippocampus and parietal-temporal cortex with cognitive impairment and long-term decline in Parkinson's disease. In addition, an Alzheimer's disease pattern of brain atrophy may be a preclinical biomarker of cognitive decline in Parkinson's disease.

Modeling of pathological traits in Alzheimer's disease based on systemic extracellular signaling proteome.

The study of chronic brain diseases including Alzheimer's disease in patients is typically limited to brain imaging or psychometric testing. Given the epidemic rise and insufficient knowledge about pathological pathways in sporadic Alzheimer's disease, new tools are required to identify the molecular changes underlying this disease. We hypothesize that levels of specific secreted cellular signaling proteins in cerebrospinal fluid or plasma correlate with pathological changes in the Alzheimer's disease brain and can thus be used to discover signaling pathways altered in the disease. Here we measured 91 proteins of this subset of the cellular communication proteome in plasma or cerebrospinal fluid in patients with Alzheimer's disease and cognitively normal controls to mathematically model disease-specific molecular traits. We found small numbers of signaling proteins that were able to model key pathological markers of Alzheimer's disease, including levels of cerebrospinal fluid ß-amyloid and tau, and classify disease in independent samples. Several of these factors had previously been implicated in Alzheimer's disease supporting the validity of our approach. Our study also points to proteins which were previously unknown to be associated with Alzheimer's disease thereby implicating novel signaling pathways in this disorder.

Cognitive and functional resilience despite molecular evidence of Alzheimer's disease pathology.

BACKGROUND: The correlation between neuropathological lesions and cognition is modest. Some individuals remain cognitively intact despite the presence of significant Alzheimer's disease (AD) pathology, whereas others manifest cognitive symptoms and dementia in the same context. The aim of the present study was to examine cognitive and cerebral reserve factors associated with resilient functioning in the setting of AD pathology. METHODS: University of Pennsylvania Alzheimer's Disease Center research participants with biochemical biomarker evidence of AD pathology (cerebrospinal fluid amyloid-ß1-42 <192 pg/mL) and comparable medial temporal lobe atrophy were categorized by Clinical Dementia Rating Scale-Sum of Boxes (CDR-SOB) score as AD dementia (CDR-SOB >1) or AD resilient (CDR-SOB ≤0.5). Groups were compared for a variety of demographic, clinical, and neuroimaging variables to identify factors that are associated with resilience to AD pathology. RESULTS: A univariate model identified education and intracranial volume (ICV) as significant covariates. In a multivariate model with backward selection procedure, ICV was retained as a factor most significantly associated with resilience. The interaction term between ICV and education was not significant, suggesting that larger cranial vault size is associated with resilience even in the absence of more education. CONCLUSIONS: Premorbid brain volume, as measured through ICV, provided protection against clinical manifestations of dementia despite evidence of significant accumulations of AD pathology. This finding provides support for the brain reserve hypothesis of resilience to AD.

Amyloid imaging and cognitive decline in nondemented oldest-old: the 90+ Study.

BACKGROUND: The goal of this study was to examine cross-sectional and longitudinal associations between cognitive performance and beta amyloid (Aß) load determined by florbetapir F18 positron emission tomography (PET) in nondemented oldest-old. METHODS: Thirteen nondemented (normal or cognitively impaired nondemented) participants (median age, 94.2 years) from The 90+ Study underwent florbetapir-PET scanning within 3 months of baseline neuropsychological testing. Amyloid load was measured with a semi-automated quantitative analysis of average cortical-to-cerebellar standardized uptake value ratio (SUVr) and a visual interpretation (Aß- or Aß+). Neuropsychological testing was repeated every 6 months. RESULTS: At baseline, SUVr correlated significantly with tests of global cognition and memory. During follow-up (median, 1.5 years), the Aß+ group had steeper declines on most cognitive tests, particularly global cognitive measures. CONCLUSION: This preliminary study suggests that greater amyloid load is associated with poorer cognition and faster cognitive decline in nondemented oldest-old. Amyloid load may identify individuals at increased risk of developing Alzheimer's disease.

Florbetapir (F18-AV-45) PET to assess amyloid burden in Alzheimer's disease dementia, mild cognitive impairment, and normal aging.

OBJECTIVE: To evaluate the performance characteristics of florbetapir F18 positron emission tomography (PET) in patients with Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy control subjects (HCs). METHODS: Florbetapir PET was acquired in 184 subjects (45 AD patients, 60 MCI patients, and 79 HCs) within a multicenter phase 2 study. Amyloid burden was assessed visually and quantitatively, and was classified as positive or negative. RESULTS: Florbetapir PET was rated visually amyloid positive in 76% of AD patients, 38% of MCI patients, and 14% of HCs. Eighty-four percent of AD patients, 45% of MCI patients, and 23% of HCs were classified as amyloid positive using a quantitative threshold. Amyloid positivity and mean cortical amyloid burden were associated with age and apolipoprotein E ε4 carrier status. CONCLUSIONS: : The data are consistent with expected rates of amyloid positivity among individuals with clinical diagnoses of AD and MCI, and indicate the potential value of florbetapir F18 PET as an adjunct to clinical diagnosis.

Above-ground tree carbon storage in response to nitrogen deposition in the U.S. is heterogeneous and may have weakened.

Changes in nitrogen (N) availability affect the ability for forest ecosystems to store carbon (C). Here we extend an analysis of the growth and survival of 94 tree species and 1.2 million trees, to estimate the incremental effects of N deposition on changes in aboveground C (dC/dN) across the contiguous U.S. (CONUS). We find that although the average effect of N deposition on aboveground C is positive for the CONUS (dC/dN=+9 kg C per kg N), there is wide variation among species and regions. Furthermore, in the Northeastern U.S. where we may compare responses from 2000-2016 with those from the 1980s-90s, we find the recent estimate of dC/dN is weaker than from the 1980s-90s due to species-level changes in responses to N deposition. This suggests that the U.S. forest C-sink varies widely across forests and may be weakening overall, possibly necessitating more aggressive climate policies than originally thought.

Plasma epidermal growth factor levels predict cognitive decline in Parkinson disease.

OBJECTIVE: Most people with Parkinson disease (PD) eventually develop cognitive impairment (CI). However, neither the timing of onset nor the severity of cognitive symptoms can be accurately predicted. We sought plasma-based biomarkers for CI in PD. METHODS: A discovery cohort of 70 PD patients was recruited. Cognitive status was evaluated with the Mattis Dementia Rating Scale-2 (DRS) at baseline and on annual follow-up visits, and baseline plasma levels of 102 proteins were determined with a bead-based immunoassay. Using linear regression, we identified biomarkers of CI in PD, that is, proteins whose levels correlated with cognitive performance at baseline and/or cognitive decline at follow-up. We then replicated the association between cognitive performance and levels of the top biomarker, using a different technical platform, with a separate cohort of 113 PD patients. RESULTS: Eleven proteins exhibited plasma levels correlating with baseline cognitive performance in the discovery cohort. The best candidate was epidermal growth factor (EGF, p < 0.001); many of the other 10 analytes covaried with EGF across samples. Low levels of EGF not only correlated with poor cognitive test scores at baseline, but also predicted an 8-fold greater risk of cognitive decline to dementia-range DRS scores at follow-up for those with intact baseline cognition. A weaker, but still significant, relationship between plasma EGF levels and cognitive performance was found in an independent replication cohort of 113 PD patients. INTERPRETATION: Our data suggest that plasma EGF may be a biomarker for progression to CI in PD.

Amyloid imaging in Alzheimer's disease: comparison of florbetapir and Pittsburgh compound-B positron emission tomography.

BACKGROUND: Amyloid imaging provides in vivo detection of the fibrillar amyloid-ß (Aß) plaques of Alzheimer's disease (AD). The positron emission tomography (PET) ligand, Pittsburgh Compound-B (PiB-C11), is the most well studied amyloid imaging agent, but the short half-life of carbon-11 limits its clinical viability. Florbetapir-F18 recently demonstrated in vivo correlation with postmortem Aß histopathology, but has not been directly compared with PiB-C11. METHODS: Fourteen cognitively normal adults and 12 AD patients underwent PiB-C11 and florbetapir-F18 PET scans within a 28-day period. RESULTS: Both ligands displayed highly significant group discrimination and correlation of regional uptake. CONCLUSION: These data support the hypothesis that florbetapir-F18 provides comparable information with PiB-C11.