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Article: Practice effects in cognitive assessments three years later in non-carriers but not in symptom-free mutation carriers of autosomal-dominant Alzheimer's disease: Exemplifying procedural learning and memory?

Almkvist, Ove / Graff, Caroline

2022 Volume 14, Page(s) 905329

Abstract: Practice effects (PEs) defined as an improvement of performance in cognition due to repeated assessments between sessions are well known in unimpaired individuals, while less is known about impaired cognition and particularly in latent brain disease as ... ...

Abstract	Practice effects (PEs) defined as an improvement of performance in cognition due to repeated assessments between sessions are well known in unimpaired individuals, while less is known about impaired cognition and particularly in latent brain disease as autosomal-dominant Alzheimer's disease. The purpose was to evaluate the general (across tests/domains) and domain-specific PE calculated as the annual rate of change (ARC) in relation to years to the estimated disease onset (YECO) and in four groups of AD: asymptomatic mutation carriers (aAD,
Language	English
Publishing date	2022-10-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2022.905329
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Article ; Online: Cortical microstructural imaging from diffusion MRI: towards sensitive biomarkers for clinical trials.

Rodriguez-Vieitez, Elena / Vannini, Patrizia / Montal, Victor / Graff, Caroline

Brain : a journal of neurology

2024 Volume 147, Issue 3, Page(s) 746–748

MeSH term(s)	Humans ; Alzheimer Disease ; Diffusion Magnetic Resonance Imaging/methods ; Diffusion Tensor Imaging/methods ; Biomarkers
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-02-26
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awae054
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Article ; Online: Odor Identification Across Time in Mutation Carriers and Non-Carriers in Autosomal-Dominant Alzheimer's Disease.

Almkvist, Ove / Larsson, Maria / Graff, Caroline

Journal of Alzheimer's disease : JAD

2023 Volume 97, Issue 2, Page(s) 587–598

Abstract: Background: Impaired odor identification is a characteristic of sporadic Alzheimer'sdisease(AD), but its presence in autosomal-dominantAD (adAD) remains uncertain.: Objective: To investigate odor identification ability in mutation carriers (MC) and ... ...

Abstract	Background: Impaired odor identification is a characteristic of sporadic Alzheimer'sdisease(AD), but its presence in autosomal-dominantAD (adAD) remains uncertain. Objective: To investigate odor identification ability in mutation carriers (MC) and non-carriers (NC) of adAD in relation to years to estimated clinical onset clinical onset (YECO) of disease. Methods: Participants from six families with autosomal-dominant mutations (APP Swedish, APP Arctic, and PSEN1 mutations) included 20 MC and 20 NC. The groups were comparable in age, gender, education, number of APOE ɛ4 alleles, and YECO, but differed in global cognition (Mini-Mental State Examination). The MC group included individuals in asymptomatic, symptomatic cognitively unimpaired, mild cognitive impairment, and dementia stages of disease, spanning approximately 40 years of the AD continuum. All NC were asymptomatic. Olfactory function was assessed by means of free and cued identification of common odors summarized as total identification. Results: MC performed poorer than NC in free and total identification. Four MC and none of the NC were anosmic. Olfactory functions in MC and NC were significantly and inversely related to time course (YECO) for both free and total identification. The decline in free identification began approximately 10 years prior to the estimated clinical onset of AD in MC. Odor identification proficiency was associated with episodic memory and executive function in MC and NC. Conclusions: Impaired odor identification is present well before the clinical diagnosis of AD in MC and is associated with disease progression. Odor identification ability may be a useful early biomarker for adAD.
MeSH term(s)	Humans ; Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Odorants ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/complications ; Cognition ; Mutation/genetics ; Presenilin-1/genetics
Chemical Substances	Presenilin-1
Language	English
Publishing date	2023-12-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230618
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Article ; Online: The

Almkvist, Ove / Graff, Caroline

Genes

2021 Volume 12, Issue 12

Abstract: Mounting evidence shows that ... ...

Abstract	Mounting evidence shows that the
MeSH term(s)	Adult ; Aging ; Alleles ; Alzheimer Disease/physiopathology ; Amyloid beta-Protein Precursor/genetics ; Apolipoprotein E4/genetics ; Case-Control Studies ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/pathology ; Female ; Humans ; Male ; Middle Aged ; Mutation ; Presenilin-1/genetics
Chemical Substances	APP protein, human ; Amyloid beta-Protein Precursor ; Apolipoprotein E4 ; PSEN1 protein, human ; Presenilin-1
Language	English
Publishing date	2021-12-07
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12121954
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Article: The APOE 4 Allele Affects Cognitive Functions Differently in Carriers of APP Mutations Compared to Carriers of PSEN1 Mutations in Autosomal-Dominant Alzheimer’s Disease

Almkvist, Ove / Graff, Caroline

Genes. 2021 Dec. 07, v. 12, no. 12

2021

Abstract: Mounting evidence shows that the APOE 4 allele interferes with cognition in sporadic Alzheimer’s disease. Less is known about APOE in autosomal-dominant Alzheimer’s disease (adAD). The present study explored the effects on cognition associated with the ... ...

Abstract	Mounting evidence shows that the APOE 4 allele interferes with cognition in sporadic Alzheimer’s disease. Less is known about APOE in autosomal-dominant Alzheimer’s disease (adAD). The present study explored the effects on cognition associated with the gene–gene interactions between the APOE gene and the APP and PSEN1 genes in adAD. This study includes mutation carriers (MC) and non-carriers (NC) from adAD families with mutations in APP (n = 28 and n = 25; MC and NC, respectively) and PSEN1 (n = 12 and n = 15; MC and NC, respectively) that represent the complete spectrum of disease: AD dementia (n = 8) and mild cognitive impairment (MCI, n = 15 and presymptomatic AD, n = 17). NC represented unimpaired normal aging. There was no significant difference in the distribution of APOE 4 (absence vs. presence) between the APP vs. PSEN1 adAD genes and mutation status (MC vs. NC). However, episodic memory was significantly affected by the interaction between APOE and the APP vs. PSEN1 genes in MC. This was explained by favorable performance in the absence of APOE 4 in PSEN1 compared to APP MC. Similar trends were seen in other cognitive functions. No significant associations between APOE 4 and cognitive performance were obtained in NC. In conclusion, cognitive effects of APOE–adAD gene interaction were differentiated between the PSEN1 and APP mutation carriers, indicating epistasis.
Keywords	alleles ; cognition ; cognitive disorders ; epistasis ; memory ; mutation
Language	English
Dates of publication	2021-1207
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12121954
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Article ; Online: Correction: Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer's disease.

George, Sonia / Rönnbäck, Annica / Gouras, Gunnar K / Petit, Géraldine H / Grueninger, Fiona / Winblad, Bengt / Graff, Caroline / Brundin, Patrik

Acta neuropathologica communications

2024 Volume 12, Issue 1, Page(s) 26

Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Published Erratum
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-023-01712-9
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Article ; Online: Findings from the Swedish Study on Familial Alzheimer's Disease Including the APP Swedish Double Mutation.

Thordardottir, Steinunn / Graff, Caroline

Journal of Alzheimer's disease : JAD

2018 Volume 64, Issue s1, Page(s) S491–S496

Abstract: This is a brief summary of the findings from the Swedish study on familial Alzheimer's disease (FAD). Similar to other FAD studies, it includes prospective assessments of cognitive function, tissue sampling, and technical analyses such as MRI and PET. ... ...

Abstract	This is a brief summary of the findings from the Swedish study on familial Alzheimer's disease (FAD). Similar to other FAD studies, it includes prospective assessments of cognitive function, tissue sampling, and technical analyses such as MRI and PET. This 24-year-old study involves 69 individuals with a 50% risk of inheriting a disease-causing mutation in presenilin 1 (PSEN1 H163Y or I143T), or amyloid precursor protein (the Swedish APP or the arctic APP mutation) who have made a total of 169 visits. Our results show the extraordinary power in this study design to unravel the earliest changes in preclinical AD. The Swedish FAD study will continue and future research will focus on disentangling the order of pathological change using longitudinal data as well as modeling the changes in patient derived cell systems.
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Alzheimer Disease/psychology ; Amyloid beta-Protein Precursor/genetics ; Biomarkers/cerebrospinal fluid ; Brain/diagnostic imaging ; Disease Progression ; Humans ; Mutation ; Presenilin-1/genetics ; Sweden
Chemical Substances	APP protein, human ; Amyloid beta-Protein Precursor ; Biomarkers ; PSEN1 protein, human ; Presenilin-1
Language	English
Publishing date	2018-03-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-179922
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Article ; Online: APOE ε4 influences cognitive decline positively in APP and negatively in PSEN1 mutation carriers with autosomal-dominant Alzheimer's disease.

Almkvist, Ove / Johansson, Charlotte / Laffita-Mesa, Jose / Thordardottir, Steinunn / Graff, Caroline

European journal of neurology

2022 Volume 29, Issue 12, Page(s) 3580–3589

Abstract: Background and purpose: The aim was to investigate the effect of APOE ε4 allele on cognitive decline in adAD. Presence of the APOE ε4 allele reduces age of symptom onset, increases disease progression, and lowers cognitive performance in sporadic ... ...

Abstract	Background and purpose: The aim was to investigate the effect of APOE ε4 allele on cognitive decline in adAD. Presence of the APOE ε4 allele reduces age of symptom onset, increases disease progression, and lowers cognitive performance in sporadic Alzheimer's disease (AD), while the impact of the APOE ε4 allele in autosomal-dominant AD (adAD) is incompletely known. Methods: Mutation carriers (MCs; n = 39) and non-carriers (NCs; n = 40) from six adAD families harbouring a mutation in the APP (28 MCs and 25 NCs) or the PSEN1 genes (11 MCs and 15 NCs) underwent repeated cognitive assessments. A timeline of disease course was defined as years to expected age of clinical onset (YECO) based on history of disease onset in each family. The MC and NC groups were comparable with regard to demographics and prevalence of the APOE ε4 allele. The relationship between cognitive decline and YECO, YECO Results: The trajectory of cognitive decline was significantly predicted by linear and quadratic YECO and education in MCs and was determined by age and education in NCs. Adding APOE ε4 allele (presence/absence) as a predictor did not change the results in the MC and NC groups. The outcome also remained the same for MCs and NCs after adding the APOE-by-YECO interaction as a predictor. Analyses of APP and PSEN1 MCs separately showed favourable APOE-by-YECO interaction in APP (less steep decline) and unfavourable interaction in PSEN1 (steeper decline), linked to the APOE ε4 allele. Conclusion: The APOE ε4 allele influences cognitive decline positively in APP and negatively in PSEN1 mutation carriers with adAD, indicating a possible antagonistic pleiotropy.
MeSH term(s)	Humans ; Alzheimer Disease/epidemiology ; Apolipoprotein E4/genetics ; Cognitive Dysfunction/diagnosis ; Disease Progression ; Mutation ; Presenilin-1/genetics
Chemical Substances	Apolipoprotein E4 ; Presenilin-1 ; PSEN1 protein, human
Language	English
Publishing date	2022-09-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1280785-0
ISSN	1468-1331 ; 1351-5101 ; 1471-0552
ISSN (online)	1468-1331
ISSN	1351-5101 ; 1471-0552
DOI	10.1111/ene.15536
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Article ; Online: Tracking reactive astrogliosis in autosomal dominant and sporadic Alzheimer's disease with multi-modal PET and plasma GFAP.

Chiotis, Konstantinos / Johansson, Charlotte / Rodriguez-Vieitez, Elena / Ashton, Nicholas J / Blennow, Kaj / Zetterberg, Henrik / Graff, Caroline / Nordberg, Agneta

Molecular neurodegeneration

2023 Volume 18, Issue 1, Page(s) 60

Abstract: Background: Plasma assays for the detection of Alzheimer's disease neuropathological changes are receiving ever increasing interest. The concentration of plasma glial fibrillary acidic protein (GFAP) has been suggested as a potential marker of ... ...

Abstract	Background: Plasma assays for the detection of Alzheimer's disease neuropathological changes are receiving ever increasing interest. The concentration of plasma glial fibrillary acidic protein (GFAP) has been suggested as a potential marker of astrocytes or recently, amyloid-β burden, although this hypothesis remains unproven. We compared plasma GFAP levels with the astrocyte tracer Methods: Twenty-four individuals from families with known Autosomal Dominant Alzheimer's Disease mutations (mutation carriers = 10; non-carriers = 14) and fifteen patients with sporadic Alzheimer's disease were included. The individuals underwent PET imaging with Results: In mutation carriers, plasma GFAP levels and Conclusions: Plasma GFAP concentration and astrocyte
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Amyloid beta-Peptides ; Fluorodeoxyglucose F18 ; Glial Fibrillary Acidic Protein ; Gliosis ; Inflammation
Chemical Substances	Amyloid beta-Peptides ; Fluorodeoxyglucose F18 (0Z5B2CJX4D) ; Glial Fibrillary Acidic Protein
Language	English
Publishing date	2023-09-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-023-00647-y
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Article ; Online: Plasma biomarker profiles in autosomal dominant Alzheimer's disease.

Johansson, Charlotte / Thordardottir, Steinunn / Laffita-Mesa, José / Rodriguez-Vieitez, Elena / Zetterberg, Henrik / Blennow, Kaj / Graff, Caroline

Brain : a journal of neurology

2023 Volume 146, Issue 3, Page(s) 1132–1140

Abstract: Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. ...

Abstract	Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. It is, however, unclear which pathological processes in the CNS can be adequately detected by peripheral measurements and whether plasma biomarkers are equally applicable in both clinical and preclinical phases. Here we aimed to explore the timing and performance of plasma biomarkers in mutation carriers compared to non-carriers in autosomal dominant Alzheimer's disease. Samples (n = 164) from mutation carriers (n = 33) and non-carriers (n = 42) in a Swedish cohort of autosomal dominant Alzheimer's disease (APP p.KM670/671NL, APP p.E693G and PSEN1 p.H163Y) were included in explorative longitudinal analyses. Plasma phosphorylated tau (P-tau181), total tau (T-tau), neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) concentrations were measured with a single-molecule array method as previously described. Plasma biomarkers were additionally correlated to Alzheimer's disease core biomarkers in the CSF. Results from the longitudinal analyses confirmed that plasma P-tau181, NfL and GFAP concentrations were higher in mutation carriers compared to non-carriers. This change was observed in the presymptomatic phase and detectable first as an increase in GFAP approximately 10 years before estimated symptom onset, followed by increased levels of P-tau181 and NfL closer to expected onset. Plasma P-tau181 levels were correlated to levels of P-tau181 and T-tau in the CSF. Altogether, plasma P-tau181, GFAP and NfL seem to be feasible biomarkers to detect different Alzheimer's disease-related pathologies already in presymptomatic individuals. Interestingly, changes in plasma GFAP concentrations were detected prior to P-tau181 and NfL. Our results suggest that plasma GFAP might reflect Alzheimer's disease pathology upstream to accumulation of tangles and neurodegeneration. The implications of these findings need additional validation, in particular because of the limited sample size.
MeSH term(s)	Humans ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides ; Biomarkers ; tau Proteins ; Genes, Dominant
Chemical Substances	Amyloid beta-Peptides ; Biomarkers ; tau Proteins
Language	English
Publishing date	2023-02-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac399
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