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Article ; Online: Lessons from Down syndrome and autosomal dominant Alzheimer's disease.

Fortea, Juan / Quiroz, Yakeel T / Ryan, Natalie S

2022 Volume 22, Issue 1, Page(s) 5–6

MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Down Syndrome/genetics ; Amyloid beta-Peptides ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2022-11-02
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2081241-3
ISSN	1474-4465 ; 1474-4422
ISSN (online)	1474-4465
ISSN	1474-4422
DOI	10.1016/S1474-4422(22)00437-9
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Article ; Online: Clinical considerations in early-onset cerebral amyloid angiopathy.

Banerjee, Gargi / Collinge, John / Fox, Nick C / Lashley, Tammaryn / Mead, Simon / Schott, Jonathan M / Werring, David J / Ryan, Natalie S

Brain : a journal of neurology

2023 Volume 146, Issue 10, Page(s) 3991–4014

Abstract: Cerebral amyloid angiopathy (CAA) is an important cerebral small vessel disease associated with brain haemorrhage and cognitive change. The commonest form, sporadic amyloid-β CAA, usually affects people in mid- to later life. However, early-onset forms, ... ...

Abstract	Cerebral amyloid angiopathy (CAA) is an important cerebral small vessel disease associated with brain haemorrhage and cognitive change. The commonest form, sporadic amyloid-β CAA, usually affects people in mid- to later life. However, early-onset forms, though uncommon, are increasingly recognized and may result from genetic or iatrogenic causes that warrant specific and focused investigation and management. In this review, we firstly describe the causes of early-onset CAA, including monogenic causes of amyloid-β CAA (APP missense mutations and copy number variants; mutations of PSEN1 and PSEN2) and non-amyloid-β CAA (associated with ITM2B, CST3, GSN, PRNP and TTR mutations), and other unusual sporadic and acquired causes including the newly-recognized iatrogenic subtype. We then provide a structured approach for investigating early-onset CAA, and highlight important management considerations. Improving awareness of these unusual forms of CAA amongst healthcare professionals is essential for facilitating their prompt diagnosis, and an understanding of their underlying pathophysiology may have implications for more common, late-onset, forms of the disease.
MeSH term(s)	Humans ; Cerebral Amyloid Angiopathy/genetics ; Cerebral Amyloid Angiopathy/complications ; Amyloid beta-Peptides/genetics ; Mutation ; Mutation, Missense ; Iatrogenic Disease ; Alzheimer Disease/genetics
Chemical Substances	Amyloid beta-Peptides
Language	English
Publishing date	2023-06-06
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awad193
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Article ; Online: Iatrogenic Alzheimer's disease in recipients of cadaveric pituitary-derived growth hormone.

Banerjee, Gargi / Farmer, Simon F / Hyare, Harpreet / Jaunmuktane, Zane / Mead, Simon / Ryan, Natalie S / Schott, Jonathan M / Werring, David J / Rudge, Peter / Collinge, John

Nature medicine

2024 Volume 30, Issue 2, Page(s) 394–402

Abstract: Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau. Compelling genetic and ... ...

Abstract	Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau. Compelling genetic and biomarker evidence supports Aβ as the root cause of AD. We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt-Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds. This raised the possibility that c-hGH recipients who did not die from iCJD may eventually develop AD. Here we describe recipients who developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms. Although iatrogenic AD may be rare, and there is no suggestion that Aβ can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures. As propagating Aβ assemblies may exhibit structural diversity akin to conventional prions, it is possible that therapeutic strategies targeting disease-related assemblies may lead to selection of minor components and development of resistance.
MeSH term(s)	Young Adult ; Humans ; Child ; Alzheimer Disease/pathology ; Growth Hormone ; Amyloid beta-Peptides/metabolism ; Creutzfeldt-Jakob Syndrome/genetics ; Creutzfeldt-Jakob Syndrome/pathology ; Cerebral Amyloid Angiopathy ; Brain/pathology ; Prions/metabolism ; Cadaver ; Iatrogenic Disease ; Biomarkers
Chemical Substances	Growth Hormone (9002-72-6) ; Amyloid beta-Peptides ; Prions ; Biomarkers
Language	English
Publishing date	2024-01-29
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/s41591-023-02729-2
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease.

Willumsen, Nanet / Poole, Teresa / Nicholas, Jennifer M / Fox, Nick C / Ryan, Natalie S / Lashley, Tammaryn

Brain pathology (Zurich, Switzerland)

2021 Volume 32, Issue 3, Page(s) e13009

Abstract: Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. Here we investigate variability in clinical data and the type and ... ...

Abstract	Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. Here we investigate variability in clinical data and the type and distribution of Aβ pathologies throughout the cortical layers of different FAD mutation cases. Brain tissue from 20 FAD cases [PSEN1 pre-codon 200 (n = 10), PSEN1 post-codon 200 (n = 6), APP (n = 4)] were investigated. Frontal cortex sections were stained immunohistochemically for Aβ, and Nissl to define the cortical layers. The frequency of different amyloid-beta plaque types was graded for each cortical layer and the severity of cerebral amyloid angiopathy (CAA) was determined in cortical and leptomeningeal blood vessels. Comparisons were made between FAD mutations and APOE4 status, with associations between pathology, clinical and genetic data investigated. In this cohort, possession of an APOE4 allele was associated with increased disease duration but not with age at onset, after adjusting for mutation sub-group and sex. We found Aβ pathology to be heterogeneous between cases although Aβ load was highest in cortical layer 3 for all mutation groups and a higher Aβ load was associated with APOE4. The PSEN1 post-codon 200 group had a higher Aβ load in lower cortical layers, with a small number of this group having increased cotton wool plaque pathology in lower layers. Cotton wool plaque frequency was positively associated with the severity of CAA in the whole cohort and in the PSEN1 post-codon 200 group. Carriers of the same PSEN1 mutation can have differing patterns of Aβ deposition, potentially because of differences in risk factors. Our results highlight possible influences of APOE4 genotype, and PSEN1 mutation type on Aβ deposition, which may have effects on the clinical heterogeneity of FAD.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/genetics ; Apolipoprotein E4/genetics ; Cerebral Amyloid Angiopathy/genetics ; Cerebral Amyloid Angiopathy/pathology ; Codon ; Mutation ; Plaque, Amyloid/pathology ; Presenilin-1/genetics
Chemical Substances	Amyloid beta-Peptides ; Apolipoprotein E4 ; Codon ; Presenilin-1
Language	English
Publishing date	2021-07-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.13009
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Article ; Online: Reply: Implications of presymptomatic change in thalamus and caudate in Alzheimer's disease.

Ryan, Natalie S / Fox, Nick C

Brain : a journal of neurology

2013 Volume 136, Issue Pt 11, Page(s) e259

MeSH term(s)	Alzheimer Disease/diagnosis ; Asymptomatic Diseases/epidemiology ; Caudate Nucleus/pathology ; Female ; Humans ; Male ; Thalamus/pathology
Language	English
Publishing date	2013-07-03
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awt168
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Article ; Online: The PSEN1 E280G mutation leads to increased amyloid-β43 production in induced pluripotent stem cell neurons and deposition in brain tissue.

Willumsen, Nanet / Arber, Charles / Lovejoy, Christopher / Toombs, Jamie / Alatza, Argyro / Weston, Philip S J / Chávez-Gutiérrez, Lucia / Hardy, John / Zetterberg, Henrik / Fox, Nick C / Ryan, Natalie S / Lashley, Tammaryn / Wray, Selina

Brain communications

2022 Volume 5, Issue 1, Page(s) fcac321

Abstract: Mutations in the presenilin 1 gene, ...

Abstract	Mutations in the presenilin 1 gene,
Language	English
Publishing date	2022-12-07
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcac321
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Article ; Online: Chemical traits of cerebral amyloid angiopathy in familial British-, Danish-, and non-Alzheimer's dementias.

Michno, Wojciech / Koutarapu, Srinivas / Camacho, Rafael / Toomey, Christina / Stringer, Katie / Minta, Karolina / Ge, Junyue / Jha, Durga / Fernandez-Rodriguez, Julia / Brinkmalm, Gunnar / Zetterberg, Henrik / Blennow, Kaj / Ryan, Natalie S / Lashley, Tammaryn / Hanrieder, Jörg

Journal of neurochemistry

2022 Volume 163, Issue 3, Page(s) 233–246

Abstract: Familial British dementia (FBD) and familial Danish dementia (FDD) are autosomal dominant forms of dementia caused by mutations in the integral membrane protein 2B (ITM2B, also known as BRI2) gene. Secretase processing of mutant BRI2 leads to secretion ... ...

Abstract	Familial British dementia (FBD) and familial Danish dementia (FDD) are autosomal dominant forms of dementia caused by mutations in the integral membrane protein 2B (ITM2B, also known as BRI2) gene. Secretase processing of mutant BRI2 leads to secretion and deposition of BRI2-derived amyloidogenic peptides, ABri and ADan that resemble APP/β-amyloid (Aβ) pathology, which is characteristic of Alzheimer's disease (AD). Amyloid pathology in FBD/FDD manifests itself predominantly in the microvasculature by ABri/ADan containing cerebral amyloid angiopathy (CAA). While ABri and ADan peptide sequences differ only in a few C-terminal amino acids, CAA in FDD is characterized by co-aggregation of ADan with Aβ, while in contrast no Aβ deposition is observed in FBD. The fact that FDD patients display an earlier and more severe disease onset than FBD suggests a potential role of ADan and Aβ co-aggregation that promotes a more rapid disease progression in FDD compared to FBD. It is therefore critical to delineate the chemical signatures of amyloid aggregation in these two vascular dementias. This in turn will increase the knowledge on the pathophysiology of these diseases and the pathogenic role of heterogenous amyloid peptide interactions and deposition, respectively. Herein, we used matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) in combination with hyperspectral, confocal microscopy based on luminescent conjugated oligothiophene probes (LCO) to delineate the structural traits and associated amyloid peptide patterns of single CAA in postmortem brain tissue of patients with FBD, FDD as well as sporadic CAA without AD (CAA+) that show pronounced CAA without parenchymal plaques. The results show that CAA in both FBD and FDD consist of N-terminally truncated- and pyroglutamate-modified amyloid peptide species (ADan and ABri), but that ADan peptides in FDD are also extensively C-terminally truncated as compared to ABri in FBD, which contributes to hydrophobicity of ADan species. Further, CAA in FDD showed co-deposition with Aβ x-42 and Aβ x-40 species. CAA+ vessels were structurally more mature than FDD/FBD CAA and contained significant amounts of pyroglutamated Aβ. When compared with FDD, Aβ in CAA+ showed more C-terminal and less N-terminally truncations. In FDD, ADan showed spatial co-localization with Aβ3pE-40 and Aβ3-40 but not with Aβx-42 species. This suggests an increased aggregation propensity of Aβ in FDD that promotes co-aggregation of both Aβ and ADan. Further, CAA maturity appears to be mainly governed by Aβ content based on the significantly higher 500/580 patterns observed in CAA+ than in FDD and FBD, respectively. Together this is the first study of its kind on comprehensive delineation of Bri2 and APP-derived amyloid peptides in single vascular plaques in both FDD/FBD and sporadic CAA that provides new insight in non-AD-related vascular amyloid pathology. Cover Image for this issue: https://doi.org/10.1111/jnc.15424.
MeSH term(s)	Humans ; Adaptor Proteins, Signal Transducing/metabolism ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid Neuropathies, Familial ; Cerebral Amyloid Angiopathy/genetics ; Dementia/pathology ; Denmark ; Membrane Glycoproteins/metabolism ; Plaque, Amyloid ; England
Chemical Substances	Adaptor Proteins, Signal Transducing ; Amyloid ; Amyloid beta-Peptides ; Membrane Glycoproteins
Language	English
Publishing date	2022-09-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15694
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Article ; Online: Aβ profiles generated by Alzheimer's disease causing PSEN1 variants determine the pathogenicity of the mutation and predict age at disease onset.

Petit, Dieter / Fernández, Sara Gutiérrez / Zoltowska, Katarzyna Marta / Enzlein, Thomas / Ryan, Natalie S / O'Connor, Antoinette / Szaruga, Maria / Hill, Elizabeth / Vandenberghe, Rik / Fox, Nick C / Chávez-Gutiérrez, Lucía

Molecular psychiatry

2022 Volume 27, Issue 6, Page(s) 2821–2832

Abstract: Familial Alzheimer's disease (FAD), caused by mutations in Presenilin (PSEN1/2) and Amyloid Precursor Protein (APP) genes, is associated with an early age at onset (AAO) of symptoms. AAO is relatively consistent within families and between carriers of ... ...

Abstract	Familial Alzheimer's disease (FAD), caused by mutations in Presenilin (PSEN1/2) and Amyloid Precursor Protein (APP) genes, is associated with an early age at onset (AAO) of symptoms. AAO is relatively consistent within families and between carriers of the same mutations, but differs markedly between individuals carrying different mutations. Gaining a mechanistic understanding of why certain mutations manifest several decades earlier than others is extremely important in elucidating the foundations of pathogenesis and AAO. Pathogenic mutations affect the protease (PSEN/γ-secretase) and the substrate (APP) that generate amyloid β (Aβ) peptides. Altered Aβ metabolism has long been associated with AD pathogenesis, with absolute or relative increases in Aβ42 levels most commonly implicated in the disease development. However, analyses addressing the relationships between these Aβ42 increments and AAO are inconsistent. Here, we investigated this central aspect of AD pathophysiology via comprehensive analysis of 25 FAD-linked Aβ profiles. Hypothesis- and data-driven approaches demonstrate linear correlations between mutation-driven alterations in Aβ profiles and AAO. In addition, our studies show that the Aβ (37 + 38 + 40) / (42 + 43) ratio offers predictive value in the assessment of 'unclear' PSEN1 variants. Of note, the analysis of PSEN1 variants presenting additionally with spastic paraparesis, indicates that a different mechanism underlies the aetiology of this distinct clinical phenotype. This study thus delivers valuable assays for fundamental, clinical and genetic research as well as supports therapeutic interventions aimed at shifting Aβ profiles towards shorter Aβ peptides.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Mutation/genetics ; Presenilin-1/genetics ; Presenilin-1/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Presenilin-1 ; PSEN1 protein, human
Language	English
Publishing date	2022-04-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-022-01518-6
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Article ; Online: Alzheimer's disease in the 100 years since Alzheimer's death.

Ryan, Natalie S / Rossor, Martin N / Fox, Nick C

Brain : a journal of neurology

2015 Volume 138, Issue Pt 12, Page(s) 3816–3821

MeSH term(s)	Alzheimer Disease/history ; History, 20th Century ; History, 21st Century ; Humans
Language	English
Publishing date	2015-12
Publishing country	England
Document type	Historical Article ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awv316
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Article: Disease duration in autosomal dominant familial Alzheimer disease: A survival analysis.

Pavisic, Ivanna M / Nicholas, Jennifer M / O'Connor, Antoinette / Rice, Helen / Lu, Kirsty / Fox, Nick C / Ryan, Natalie S

Neurology. Genetics

2020 Volume 6, Issue 5, Page(s) e507

Abstract: Objective: To use survival modeling to estimate disease duration in autosomal dominant familial Alzheimer disease (ADAD) and ascertain whether factors influencing age at onset also affect survival.: Methods: Symptomatic mutation carriers (201 ... ...

Abstract	Objective: To use survival modeling to estimate disease duration in autosomal dominant familial Alzheimer disease (ADAD) and ascertain whether factors influencing age at onset also affect survival. Methods: Symptomatic mutation carriers (201 presenilin 1 [ Results: Estimated mean survival was 11.6 (10.4-12.9) years and was similar for Conclusions: Survival is influenced by mutation to a much lesser extent than age at onset. Survival time has increased over time and is longer in atypical presentations. These insights may inform the interpretation of disease-modifying therapy trials in ADAD.
Language	English
Publishing date	2020-08-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2818607-2
ISSN	2376-7839
ISSN	2376-7839
DOI	10.1212/NXG.0000000000000507
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