Correction to: Regional [F]flortaucipir PET is more closely associated with disease severity than CSF p-tau in Alzheimer's disease.

The authors regret to inform readers that the following error was detected in the original article. The values for entorhinal, limbic and neortical SUVr were switched between SCD Aβ + and Aβ- in Table 1 and have now been corrected. Unnecessary symbols in Table 2 have been removed.

Repeatability of parametric methods for [F]florbetapir imaging in Alzheimer's disease and healthy controls: A test-retest study.

Accumulation of amyloid beta (Aβ) is one of the pathological hallmarks of Alzheimer's disease (AD), which can be visualized using [F]florbetapir positron emission tomography (PET). The aim of this study was to evaluate various parametric methods and to assess their test-retest (TRT) reliability. Two 90 min dynamic [F]florbetapir PET scans, including arterial sampling, were acquired ( = 8 AD patient,  = 8 controls).

Regional [F]flortaucipir PET is more closely associated with disease severity than CSF p-tau in Alzheimer's disease.

Purpose: In vivo Alzheimer's disease (AD) biomarkers for tau pathology are cerebrospinal fluid (CSF) phosphorylated tau (p-tau) and [F]flortaucipir positron emission tomography (PET). Our aim was to assess associations between CSF p-tau with [F]flortaucipir PET and the associations of both tau biomarkers with cognition and atrophy.

Methods: We included 78 amyloid positive cognitively impaired patients (clinical diagnoses mild cognitive impairment (MCI, n = 8) and AD dementia (n = 45) and 25 cognitively normal subjects with subjective cognitive decline (SCD) (40% amyloid-positive)).

PLCG2 protective variant p.P522R modulates tau pathology and disease progression in patients with mild cognitive impairment.

A rare coding variant (rs72824905, p.P522R) conferring protection against Alzheimer's disease (AD) was identified in the gene encoding the enzyme phospholipase-C-γ2 (PLCG2) that is highly expressed in microglia. To explore the protective nature of this variant, we employed latent process linear mixed models to examine the association of p.

A Suboptimal Diet is Associated with Poorer Cognition: The NUDAD Project.

Nutrition is one of the modifiable risk factors for cognitive decline and Alzheimer's disease (AD) dementia, and is therefore highly relevant in the context of prevention. However, knowledge of dietary quality in clinical populations on the spectrum of AD dementia is lacking, therefore we studied the association between dietary quality and cognitive impairment in Alzheimer's disease (AD) dementia, mild cognitive impairment (MCI) and controls. We included 357 participants from the NUDAD project (134 AD dementia, 90 MCI, 133 controls).

The Association Between Biomarkers and Neuropsychiatric Symptoms Across the Alzheimer's Disease Spectrum.

Objective: To investigate the relationship between Alzheimer's disease biomarkers and neuropsychiatric symptoms.

Methods: Data from two large cohort studies, the Dutch Parelsnoer Institute - Neurodegenerative Diseases and the Alzheimer's Disease Neuroimaging Initiative was used, including subjects with subjective cognitive decline (N = 650), mild cognitive impairment (N = 887), and Alzheimer's disease dementia (N = 626). Cerebrospinal fluid (CSF) levels of Aβ, t-tau, p-tau, and hippocampal volume were associated with neuropsychiatric symptoms (measured with the Neuropsychiatric Inventory) using multiple logistic regression analyses.

Plasma amyloid is associated with the rate of cognitive decline in cognitively normal elderly: the SCIENCe project.

Plasma biomarkers are promising prognostic tools in individuals with subjective cognitive decline (SCD). We aimed to investigate the relationships of baseline plasma amyloid beta (Aβ)42/Aβ40 and total Tau (tTau) with rate of cognitive decline, in comparison to relationships of baseline cerebrospinal fluid (CSF) Aβ42, tTau, and phosphorylated tau181 (pTau181) with rate of cognitive decline. We included 241 subjects with SCD (age = 61 ± 9, 40% female, Mini-Mental State Examination = 28 ± 2) with follow-up (average: 2 ± 2 years, median visits: 3 [range: 1-11]) for re-evaluation of neuropsychological test performance (attention, memory, language, and executive functioning domains).

Prodromal Dementia With Lewy Bodies: Clinical Characterization and Predictors of Progression.

Objective: The objective of this study was to examine clinical characteristics, cognitive decline, and predictors for time to dementia in prodromal dementia with Lewy bodies with mild cognitive impairment (MCI-LB) compared with prodromal Alzheimer's disease (MCI-AD).

Methods: We included 73 MCI-LB patients (12% female; 68 ± 6 years; Mini Mental State Examination, 27 ± 2) and 124 MCI-AD patients (48% female; 68 ± 7 years; Mini Mental State Examination, 27 ± 2) from the Amsterdam Dementia Cohort. Follow-up was available for 61 MCI-LB patients and all MCI-AD patients (3 ± 2 years).

Author Correction: Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer's disease risk.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Specific Nutritional Biomarker Profiles in Mild Cognitive Impairment and Subjective Cognitive Decline Are Associated With Clinical Progression: The NUDAD Project.

Objectives: Nutritional insufficiencies have been associated with cognitive impairment. Understanding whether nutritional biomarker levels are associated with clinical progression could help to design dietary intervention trials. This longitudinal study examined a panel of nutritional biomarkers in relation to clinical progression in patients with subjective cognitive decline (SCD) or mild cognitive impairment (MCI).

Clinicians' communication with patients receiving a MCI diagnosis: The ABIDE project.

Background: We aimed to explore clinicians' communication, including the discussion of diagnosis, cause, prognosis and care planning, in routine post-diagnostic testing consultations with patients with Mild Cognitive Impairment (MCI).

Methods: Thematic content analysis was used to analyze audiotaped consultations in which 10 clinicians (eight neurologists and two geriatricians) from 7 memory clinics, disclosed diagnostic information to 13 MCI patients and their care partners. We assessed clinician-patient communication regarding diagnostic label, cause, prognosis and care planning to identify core findings.

CCL23: A Chemokine Associated with Progression from Mild Cognitive Impairment to Alzheimer's Disease.

CCL23 is a chemokine implicated in inflammation and host defense responses. It has been recently associated with acquired brain damage and stroke outcomes. In this study, we reported the role of CCL23 in Alzheimer's disease (AD).

Correction to: A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity.

The IPDGC (The International Parkinson Disease Genomics Consortium) and EADB (Alzheimer Disease European DNA biobank) are listed correctly as an author to the article, however, they were incorrectly listed more than once.

Selection of memory clinic patients for CSF biomarker assessment can be restricted to a quarter of cases by using computerized decision support, without compromising diagnostic accuracy.

Introduction: An accurate and timely diagnosis for Alzheimer's disease (AD) is important, both for care and research. The current diagnostic criteria allow the use of CSF biomarkers to provide pathophysiological support for the diagnosis of AD. How these criteria should be operationalized by clinicians is unclear.

Methylphenidate and galantamine in patients with vascular cognitive impairment-the proof-of-principle study STREAM-VCI.

Background: To date, no symptomatic treatment is available for patients with vascular cognitive impairment (VCI). In the proof-of-principle study Symptomatic Treatment of Vascular Cognitive Impairment (STREAM-VCI), we investigated whether a single dose of a monoaminergic drug (methylphenidate) improves executive functioning and whether a single dose of a cholinergic drug (galantamine) improves memory in VCI patients.

Methods: STREAM-VCI is a single-center, double-blind, three-way crossover trial.

Hippocampal [F]flortaucipir BP corrected for possible spill-in of the choroid plexus retains strong clinico-pathological relationships.

Background: Off-target [F]flortaucipir (tau) PET binding in the choroid plexus causes spill-in into the nearby hippocampus, which may influence the correlation between [F]flortaucipir binding and measures of cognition. Previously, we showed that partial volume correction (combination of Van Cittert iterative deconvolution and HYPR denoising; PVC HDH) and manually eroding the hippocampus resulted in a significant decrease of the choroid plexus spill-in. In this study, we compared three different approaches for the quantification of hippocampal [F]flortaucipir signal using a semi-automated technique, and assessed correlations with cognitive performance across methods.

PET and CSF amyloid-β status are differently predicted by patient features: information from discordant cases.

Background: Amyloid-β PET and CSF Aβ yield discordant results in 10-20% of memory clinic patients, possibly providing unique information. Although the predictive power of demographic, clinical, genetic, and imaging features for amyloid positivity has previously been investigated, it is unknown whether these features differentially predict amyloid-β status based on PET or CSF or whether this differs by disease stage.

Methods: We included 768 patients (subjective cognitive decline (SCD, n = 194), mild cognitive impairment (MCI, n = 127), dementia (AD and non-AD, n = 447) with amyloid-β PET and CSF Aβ measurement within 1 year.

Why Is Amyloid-β PET Requested After Performing CSF Biomarkers?

Background: Amyloid-β positron emission tomography (PET) and cerebrospinal fluid (CSF) Aβ42 are considered interchangeable for clinical diagnosis of Alzheimer's disease.

Objective: To explore the clinical reasoning for requesting additional amyloid-β PET after performing CSF biomarkers.

Methods: We retrospectively identified 72 memory clinic patients who underwent amyloid-β PET after CSF biomarkers analysis for clinical diagnostic evaluation between 2011 and 2019.

Comorbid amyloid-β pathology affects clinical and imaging features in VCD.

Introduction: To date, the clinical relevance of comorbid amyloid-β (Aβ) pathology in patients with vascular cognitive disorders (VCD) is largely unknown.

Methods: We included 218 VCD patients with available cerebrospinal fluid Aβ levels. Patients were divided into Aβ+ mild-VCD (n = 84), Aβ- mild-VCD (n = 68), Aβ+ major-VCD (n = 31), and Aβ- major-VCD (n = 35).

Performance of five automated white matter hyperintensity segmentation methods in a multicenter dataset.

White matter hyperintensities (WMHs) are a common manifestation of cerebral small vessel disease, that is increasingly studied with large, pooled multicenter datasets. This data pooling increases statistical power, but poses challenges for automated WMH segmentation. Although there is extensive literature on the evaluation of automated WMH segmentation methods, such evaluations in a multicenter setting are lacking.

Frequent Cognitive Impairment in Patients With Disorders Along the Heart-Brain Axis.

Background and Purpose- Patients with cardiovascular disease are at increased risk for cognitive decline. We studied the occurrence and profile of cognitive impairment in 3 patient groups as exemplar conditions of hemodynamic disturbances at different levels of the heart-brain axis, including patients with heart failure (HF), carotid occlusive disease (COD), and patients with cognitive complaints and vascular brain injury on magnetic resonance imaging (possible vascular cognitive impairment [VCI]). Methods- In 555 participants (160 HF, 107 COD, 160 possible VCI, 128 reference participants; 68±9 years; 36% F; Mini-Mental State Examination 28±2), we assessed cognitive functioning with a comprehensive test battery.

Exploring effects of Souvenaid on cerebral glucose metabolism in Alzheimer's disease.

Introduction: Alzheimer's disease (AD) is associated with synapse loss. Souvenaid, containing the specific nutrient combination Fortasyn Connect, was designed to improve synapse formation and function. The NL-ENIGMA study explored the effect of Souvenaid on synapse function in early AD by assessing cerebral glucose metabolism (CMRglc) with F-fluorodeoxyglucose ([F]FDG) positron emission tomography (PET).