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Article ; Online: Aβ-PET pathology accumulation index: Ready for the clinic?

Kerchner, Geoffrey A / Filippi, Massimo

2020 Volume 95, Issue 21, Page(s) 943–944

MeSH term(s)	Alzheimer Disease ; Amyloid beta-Peptides ; Humans ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000011060
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Book ; Thesis: Presynaptic kainate receptors in the spinal cord dorsal horn

Kerchner, Geoffrey Allen

2003

Author's details	Geoffrey Allen
Language	English
Size	XV, 172 S. : Ill., graph. Darst.
Publishing place	Seattle
Publishing country	United States
Document type	Book ; Thesis
Thesis / German Habilitation thesis	St. Louis, Mo., Washington Univ., Diss. 2003
HBZ-ID	HT014130225
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Multiple biomarkers improve diagnostic accuracy across Lewy body and Alzheimer's disease spectra.

Plastini, Melanie J / Abdelnour, Carla / Young, Christina B / Wilson, Edward N / Shahid-Besanti, Marian / Lamoureux, Jennifer / Andreasson, Katrin I / Kerchner, Geoffrey A / Montine, Thomas J / Henderson, Victor W / Poston, Kathleen L

Annals of clinical and translational neurology

2024

Abstract: Objective: More than half of neurodegenerative disease patients have multiple pathologies at autopsy; however, most receive one diagnosis during life. We used the α-synuclein seed amplification assay (αSyn-SAA) and CSF biomarkers for amyloidosis and ... ...

Abstract	Objective: More than half of neurodegenerative disease patients have multiple pathologies at autopsy; however, most receive one diagnosis during life. We used the α-synuclein seed amplification assay (αSyn-SAA) and CSF biomarkers for amyloidosis and Alzheimer's disease (AD) neuropathological change (ADNC) to determine the frequency of co-pathologies in participants clinically diagnosed with Lewy body (LB) disease or AD. Methods: Using receiver operating characteristic analyses on retrospective CSF samples from 150 participants determined αSyn-SAA accuracy, sensitivity, and specificity for identifying clinically defined LB disease and predicting future change in clinical diagnosis. CSF biomarkers helped determine the frequency of concomitant Lewy body pathology, ADNC, and/or amyloidosis in participants with LB disease and AD, across clinical spectra. Results: Following a decade-long follow-up, the clinically or autopsy-defined diagnosis changed for nine participants. αSyn-SAA demonstrated improved accuracy (91.3%), sensitivity (89.3%), and specificity (93.3%) for identifying LB disease compared to all non-LB disease, highlighting the limitations of clinical diagnosis alone. When examining biomarkers of co-pathology, amyloidosis was present in 18%, 48%, and 71% (χ Interpretation: Our study shows that using a combination of αSyn-SAA and AD biomarkers can identify people with αSyn, ADNC, and co-pathology better and earlier than traditional clinical diagnostic criteria alone.
Language	English
Publishing date	2024-03-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.52034
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Article ; Online: Evaluation of partial volume correction and analysis of longitudinal [

Sanabria Bohórquez, Sandra M / Baker, Suzanne / Manser, Paul T / Tonietto, Matteo / Galli, Christopher / Wildsmith, Kristin R / Zou, Yixuan / Kerchner, Geoffrey A / Weimer, Robby / Teng, Edmond

Frontiers in neuroimaging

2024 Volume 3, Page(s) 1355402

Abstract: Purpose: We evaluated the impact of partial volume correction (PVC) methods on the quantification of longitudinal [: Methods: We applied van Cittert iterative deconvolution (VC), 2-compartment, and 3-compartment, and the geometric transfer matrix ... ...

Abstract	Purpose: We evaluated the impact of partial volume correction (PVC) methods on the quantification of longitudinal [ Methods: We applied van Cittert iterative deconvolution (VC), 2-compartment, and 3-compartment, and the geometric transfer matrix plus region-based voxelwise methods to data acquired in an Alzheimer's disease natural history study over 18 months at a single imaging site. We determined the optimal PVC method by comparing the standardized uptake value ratio change (%ΔSUVR) between diagnostic and tau burden-level groups and the longitudinal repeatability derived from the LMEM. The performance of LMEM analysis for calculating %ΔSUVR was evaluated in a natural history study and in a multisite clinical trial of semorinemab in prodromal to mild Alzheimer's disease by comparing results to traditional per-visit estimates. Results: The VC, 2-compartment, and 3-compartment PVC methods had similar performance, whereas region-based voxelwise overcorrected regions with a higher tau burden. The lowest within-subject variability and acceptable group separation scores were observed without PVC. The LMEM-derived %ΔSUVR values were similar to the per-visit estimates with lower variability. Conclusion: The results indicate that the tested PVC methods do not offer a clear advantage or improvement over non-PVC images for the quantification of longitudinal [ Clinical trial registration: NCT02640092 and NCT03289143.
Language	English
Publishing date	2024-03-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	3123824-5
ISSN	2813-1193 ; 2813-1193
ISSN (online)	2813-1193
ISSN	2813-1193
DOI	10.3389/fnimg.2024.1355402
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Article ; Online: Ultra-high field 7T MRI: a new tool for studying Alzheimer's disease.

Kerchner, Geoffrey A

Journal of Alzheimer's disease : JAD

2011 Volume 26 Suppl 3, Page(s) 91–95

Abstract: Ultra-high field 7T MRI offers superior signal-to-noise and spatial resolution relative to any other noninvasive imaging technique. By revealing fine anatomical details of the living brain, 7T MRI allows neuroimaging researchers the opportunity to ... ...

Abstract	Ultra-high field 7T MRI offers superior signal-to-noise and spatial resolution relative to any other noninvasive imaging technique. By revealing fine anatomical details of the living brain, 7T MRI allows neuroimaging researchers the opportunity to observe in patients disease-related structural changes previously apparent only on postmortem tissue analysis. Alzheimer's disease (AD) is a natural subject for this technology, and I review here two AD-related applications of 7T MRI: direct visualization of cortical plaques, and high resolution hippocampal imaging. I also discuss limitations of this technology as well as expected advances that are likely to establish 7T MRI as an increasingly important tool for the diagnosis and tracking of AD.
MeSH term(s)	Alzheimer Disease/diagnosis ; Cerebral Cortex/pathology ; Hippocampus/pathology ; Humans ; Image Processing, Computer-Assisted/methods ; Magnetic Resonance Imaging/classification ; Magnetic Resonance Imaging/methods ; Plaque, Amyloid/pathology
Language	English
Publishing date	2011
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-2011-0023
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Article ; Online: Amyloid imaging for Alzheimer's disease.

Kerchner, Geoffrey A

Expert opinion on medical diagnostics

2011 Volume 5, Issue 6, Page(s) 527–538

Abstract: Introduction: Biomarkers for Alzheimer's disease (AD) may facilitate early and accurate diagnosis and offer a way to track the effectiveness of new therapies. Amyloid imaging offers an unrivaled ability to visualize the presence and anatomical ... ...

Abstract	Introduction: Biomarkers for Alzheimer's disease (AD) may facilitate early and accurate diagnosis and offer a way to track the effectiveness of new therapies. Amyloid imaging offers an unrivaled ability to visualize the presence and anatomical distribution of fibrillar beta-amyloid (Aβ) pathology non-invasively in living humans. New diagnostic criteria for AD incorporate the use of such biomarkers as amyloid imaging, highlighting the importance of this technology going forward. Areas covered: Here, the author reviews individual amyloid tracers, including the (11)C-labeled tracer Pittsburgh compound B and the (18)F-labeled tracers nearing FDA approval. While these tracers are reliable at detecting fibrillar Aβ pathology, there is a weaker connection with true AD pathology, reflecting the complex relationship between Aβ and AD. The author discusses apolipoprotein E genotyping and spinal fluid Aβ levels in relation to amyloid imaging, and considers the possible uses of amyloid imaging as a diagnostic instrument in the clinic, or as a clinical trials tool for selecting patients or monitoring outcomes. Selected literature retrieved by Medline searches for 'amyloid imaging' and related terms from 2001 to present is discussed. Expert opinion: Amyloid imaging accurately portrays the presence of fibrillar Aβ pathology in the brain. However, fundamental questions about the role of Aβ in AD must be answered before the full potential of amyloid imaging can be realized.
Language	English
Publishing date	2011-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2393880-8
ISSN	1753-0067 ; 1753-0059
ISSN (online)	1753-0067
ISSN	1753-0059
DOI	10.1517/17530059.2011.617365
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Article ; Online: Prasinezumab slows motor progression in rapidly progressing early-stage Parkinson's disease.

Pagano, Gennaro / Taylor, Kirsten I / Anzures Cabrera, Judith / Simuni, Tanya / Marek, Kenneth / Postuma, Ronald B / Pavese, Nicola / Stocchi, Fabrizio / Brockmann, Kathrin / Svoboda, Hanno / Trundell, Dylan / Monnet, Annabelle / Doody, Rachelle / Fontoura, Paulo / Kerchner, Geoffrey A / Brundin, Patrik / Nikolcheva, Tania / Bonni, Azad

Nature medicine

2024 Volume 30, Issue 4, Page(s) 1096–1103

Abstract: Prasinezumab, a monoclonal antibody that binds aggregated α-synuclein, is being investigated as a potential disease-modifying therapy in early-stage Parkinson's disease. Although in the PASADENA phase 2 study, the primary endpoint (Movement Disorder ... ...

Abstract	Prasinezumab, a monoclonal antibody that binds aggregated α-synuclein, is being investigated as a potential disease-modifying therapy in early-stage Parkinson's disease. Although in the PASADENA phase 2 study, the primary endpoint (Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) sum of Parts I + II + III) was not met, prasinezumab-treated individuals exhibited slower progression of motor signs than placebo-treated participants (MDS-UPDRS Part III). We report here an exploratory analysis assessing whether prasinezumab showed greater benefits on motor signs progression in prespecified subgroups with faster motor progression. Prasinezumab's potential effects on disease progression were assessed in four prespecified and six exploratory subpopulations of PASADENA: use of monoamine oxidase B inhibitors at baseline (yes versus no); Hoehn and Yahr stage (2 versus 1); rapid eye movement sleep behavior disorder (yes versus no); data-driven subphenotypes (diffuse malignant versus nondiffuse malignant); age at baseline (≥60 years versus <60 years); sex (male versus female); disease duration (>12 months versus <12 months); age at diagnosis (≥60 years versus <60 years); motor subphenotypes (akinetic-rigid versus tremor-dominant); and motor subphenotypes (postural instability gait dysfunction versus tremor-dominant). In these subpopulations, the effect of prasinezumab on slowing motor signs progression (MDS-UPDRS Part III) was greater in the rapidly progressing subpopulations (for example, participants who were diffuse malignant or taking monoamine oxidase B inhibitors at baseline). This exploratory analysis suggests that, in a trial of 1-year duration, prasinezumab might reduce motor progression to a greater extent in individuals with more rapidly progressing Parkinson's disease. However, because this was a post hoc analysis, additional randomized clinical trials are needed to validate these findings.
MeSH term(s)	Humans ; Male ; Female ; Middle Aged ; Parkinson Disease ; Tremor/drug therapy ; Antiparkinson Agents/therapeutic use ; Monoamine Oxidase/therapeutic use ; Disease Progression
Chemical Substances	Antiparkinson Agents ; Monoamine Oxidase (EC 1.4.3.4)
Language	English
Publishing date	2024-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-024-02886-y
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Article ; Online: Safety and Efficacy of Semorinemab in Individuals With Prodromal to Mild Alzheimer Disease: A Randomized Clinical Trial.

Teng, Edmond / Manser, Paul T / Pickthorn, Karen / Brunstein, Flavia / Blendstrup, Mira / Sanabria Bohorquez, Sandra / Wildsmith, Kristin R / Toth, Bali / Dolton, Michael / Ramakrishnan, Vidya / Bobbala, Ashwini / Sikkes, Sietske A M / Ward, Michael / Fuji, Reina N / Kerchner, Geoffrey A

JAMA neurology

2024 Volume 79, Issue 8, Page(s) 758–767

Abstract: Importance: Neurofibrillary tangles composed of aggregated tau protein are one of the neuropathological hallmarks of Alzheimer disease (AD) and correlate with clinical disease severity. Monoclonal antibodies targeting tau may have the potential to ... ...

Abstract	Importance: Neurofibrillary tangles composed of aggregated tau protein are one of the neuropathological hallmarks of Alzheimer disease (AD) and correlate with clinical disease severity. Monoclonal antibodies targeting tau may have the potential to ameliorate AD progression by slowing or stopping the spread and/or accumulation of pathological tau. Objective: To evaluate the safety and efficacy of the monoclonal anti-tau antibody semorinemab in prodromal to mild AD. Design, setting, and participants: This phase 2 randomized, double-blind, placebo-controlled, parallel-group clinical trial was conducted between October 18, 2017, and July 16, 2020, at 97 sites in North America, Europe, and Australia. Individuals aged 50 to 80 years (inclusive) with prodromal to mild AD, Mini-Mental State Examination scores between 20 and 30 (inclusive), and confirmed β-amyloid pathology (by positron emission tomography or cerebrospinal fluid) were included. Interventions: During the 73-week blinded study period, participants received intravenous infusions of placebo or semorinemab (1500 mg, 4500 mg, or 8100 mg) every 2 weeks for the first 3 infusions and every 4 weeks thereafter. Main outcomes and measures: The primary outcomes were change from baseline on the Clinical Dementia Rating-Sum of Boxes score from baseline to week 73 and assessments of the safety and tolerability for semorinemab compared with placebo. Results: In the modified intent-to-treat cohort (n = 422; mean [SD] age, 69.6 [7.0] years; 235 women [55.7%]), similar increases were seen on the Clinical Dementia Rating-Sum of Boxes score in the placebo (n = 126; Δ = 2.19 [95% CI, 1.74-2.63]) and semorinemab (1500 mg: n = 86; Δ = 2.36 [95% CI, 1.83-2.89]; 4500 mg: n = 126; Δ = 2.36 [95% CI, 1.92-2.79]; 8100 mg: n = 84; Δ = 2.41 [95% CI, 1.88-2.94]) arms. In the safety-evaluable cohort (n = 441), similar proportions of participants experienced adverse events in the placebo (130 [93.1%]) and semorinemab (1500 mg: 89 [88.8%]; 4500 mg: 132 [94.7%]; 8100 mg: 90 [92.2%]) arms. Conclusions and relevance: In participants with prodromal to mild AD in this randomized clinical trial, semorinemab did not slow clinical AD progression compared with placebo throughout the 73-week study period but did demonstrate an acceptable and well-tolerated safety profile. Additional studies of anti-tau antibodies may be needed to determine the clinical utility of this therapeutic approach. Trial registration: ClinicalTrials.gov Identifier: NCT03289143.
MeSH term(s)	Aged ; Alzheimer Disease/cerebrospinal fluid ; Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Antibodies, Monoclonal/therapeutic use ; Double-Blind Method ; Female ; Humans ; Male ; Treatment Outcome
Chemical Substances	Amyloid beta-Peptides ; Antibodies, Monoclonal
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2022.1375
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Article ; Online: Decision making in clinical trials: Interim analyses, innovative design, and biomarkers.

Welsh-Bohmer, Kathleen A / Kerchner, Geoffrey A / Dhadda, Shobha / Garcia, Miguel / Miller, David S / Natanegara, Fanni / Raket, Lars Lau / Robieson, Weining / Siemers, Eric R / Carrillo, Maria C / Weber, Christopher J

Alzheimer's & dementia (New York, N. Y.)

2023 Volume 9, Issue 4, Page(s) e12421

Abstract: The efficient and accurate execution of clinical trials testing novel treatments for Alzheimer's disease (AD) is a critical component of the field's collective efforts to develop effective disease-modifying treatments for AD. The lengthy and ... ...

Abstract	The efficient and accurate execution of clinical trials testing novel treatments for Alzheimer's disease (AD) is a critical component of the field's collective efforts to develop effective disease-modifying treatments for AD. The lengthy and heterogeneous nature of clinical progression in AD contributes to the challenges inherent in demonstrating a clinically meaningful benefit of any potential new AD therapy. The failure of many large and expensive clinical trials to date has prompted a focus on optimizing all aspects of decision making, to not only expedite the development of new treatments, but also maximize the value of the information that each clinical trial yields, so that all future clinical trials (including those that are negative) will contribute toward advancing the field. To address this important topic the Alzheimer's Association Research Roundtable convened December 1-2, 2020. The goals focused around identifying new directions and actionable steps to enhance clinical trial decision making in planned future studies.
Language	English
Publishing date	2023-10-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832891-7
ISSN	2352-8737 ; 2352-8737
ISSN (online)	2352-8737
ISSN	2352-8737
DOI	10.1002/trc2.12421
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Article ; Online: Comprehensive proteomics of CSF, plasma, and urine identify DDC and other biomarkers of early Parkinson's disease.

Acta neuropathologica

2024 Volume 147, Issue 1, Page(s) 52

Abstract: Parkinson's disease (PD) starts at the molecular and cellular level long before motor symptoms appear, yet there are no early-stage molecular biomarkers for diagnosis, prognosis prediction, or monitoring therapeutic response. This lack of biomarkers ... ...

Abstract	Parkinson's disease (PD) starts at the molecular and cellular level long before motor symptoms appear, yet there are no early-stage molecular biomarkers for diagnosis, prognosis prediction, or monitoring therapeutic response. This lack of biomarkers greatly impedes patient care and translational research-L-DOPA remains the standard of care more than 50 years after its introduction. Here, we performed a large-scale, multi-tissue, and multi-platform proteomics study to identify new biomarkers for early diagnosis and disease monitoring in PD. We analyzed 4877 cerebrospinal fluid, blood plasma, and urine samples from participants across seven cohorts using three orthogonal proteomics methods: Olink proximity extension assay, SomaScan aptamer precipitation assay, and liquid chromatography-mass spectrometry proteomics. We discovered that hundreds of proteins were upregulated in the CSF, blood, or urine of PD patients, prodromal PD patients with DAT deficit and REM sleep behavior disorder or anosmia, and non-manifesting genetic carriers of LRRK2 and GBA mutations. We nominate multiple novel hits across our analyses as promising markers of early PD, including DOPA decarboxylase (DDC), also known as L-aromatic acid decarboxylase (AADC), sulfatase-modifying factor 1 (SUMF1), dipeptidyl peptidase 2/7 (DPP7), glutamyl aminopeptidase (ENPEP), WAP four-disulfide core domain 2 (WFDC2), and others. DDC, which catalyzes the final step in dopamine synthesis, particularly stands out as a novel hit with a compelling mechanistic link to PD pathogenesis. DDC is consistently upregulated in the CSF and urine of treatment-naïve PD, prodromal PD, and GBA or LRRK2 carrier participants by all three proteomics methods. We show that CSF DDC levels correlate with clinical symptom severity in treatment-naïve PD patients and can be used to accurately diagnose PD and prodromal PD. This suggests that urine and CSF DDC could be a promising diagnostic and prognostic marker with utility in both clinical care and translational research.
MeSH term(s)	Humans ; Parkinson Disease/diagnosis ; Parkinson Disease/genetics ; Dopa Decarboxylase/genetics ; Proteomics ; Biomarkers/cerebrospinal fluid ; Plasma/metabolism ; Oxidoreductases Acting on Sulfur Group Donors ; Aromatic-L-Amino-Acid Decarboxylases
Chemical Substances	Dopa Decarboxylase (EC 4.1.1.-) ; Biomarkers ; SUMF1 protein, human (EC 3.1.6.-) ; Oxidoreductases Acting on Sulfur Group Donors (EC 1.8.-) ; DDC protein, human (EC 4.1.1.28) ; Aromatic-L-Amino-Acid Decarboxylases (EC 4.1.1.28)
Language	English
Publishing date	2024-03-11
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1079-0
ISSN	1432-0533 ; 0001-6322
ISSN (online)	1432-0533
ISSN	0001-6322
DOI	10.1007/s00401-024-02706-0
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