Skip to main content

previous disabled Page of 2
and
  1. Article

    Open Access

    Astrocytic accumulation of tau fibrils isolated from Alzheimer’s disease brains induces inflammation, cell-to-cell propagation and neuronal impairment

    Accumulating evidence highlights the involvement of astrocytes in Alzheimer’s disease (AD) progression. We have previously demonstrated that human iPSC-derived astrocytes ingest and modify synthetic tau fibril...

    Khalid Eltom, Tobias Mothes, Sylwia Libard in Acta Neuropathologica Communications (2024)

  2. Article

    Open Access

    Altered amyloid-β structure markedly reduces gliosis in the brain of mice harboring the Uppsala APP deletion

    Deposition of amyloid beta (Aβ) into plaques is a major hallmark of Alzheimer’s disease (AD). Different amyloid precursor protein (APP) mutations cause early-onset AD by altering the production or aggregation pro...

    María Pagnon de la Vega, Stina Syvänen in Acta Neuropathologica Communications (2024)

  3. Article

    Open Access

    Cryo-EM of Aβ fibrils from mouse models find tg-APPArcSwe fibrils resemble those found in patients with sporadic Alzheimer’s disease

    The use of transgenic mice displaying amyloid-β (Aβ) brain pathology has been essential for the preclinical assessment of new treatment strategies for Alzheimer’s disease. However, the properties of Aβ in such...

    Mara Zielinski, Fernanda S. Peralta Reyes, Lothar Gremer in Nature Neuroscience (2023)

  4. Article

    Open Access

    Levels of inflammatory cytokines MCP-1, CCL4, and PD-L1 in CSF differentiate idiopathic normal pressure hydrocephalus from neurodegenerative diseases

    Neuroinflammatory processes have been suggested to play a role in the pathophysiology of neurodegenerative diseases and post-hemorrhagic hydrocephalus, but have rarely been investigated in patients with idiopa...

    Madelene Braun, Gustaf Boström, Martin Ingelsson in Fluids and Barriers of the CNS (2023)

  5. Article

    Open Access

    Altered Distribution of SNARE Proteins in Primary Neurons Exposed to Different Alpha-Synuclein Proteoforms

    Growing evidence indicates that the pathological alpha-synuclein (α-syn) aggregation in Parkinson’s disease (PD) and dementia with Lewy bodies (DLB) starts at the synapses. Physiologic α-syn is involved in reg...

    Emma Brolin, Martin Ingelsson, Joakim Bergström in Cellular and Molecular Neurobiology (2023)

  6. Article

    Open Access

    Astrocytic uptake of neuronal corpses promotes cell-to-cell spreading of tau pathology

    Tau deposits in astrocytes are frequently found in Alzheimer’s disease (AD) and other tauopathies. Since astrocytes do not express tau, the inclusions have been suggested to be of neuronal origin. However, the...

    Tobias Mothes, Benjamin Portal in Acta Neuropathologica Communications (2023)

  7. Article

    Open Access

    The G51D SNCA mutation generates a slowly progressive α-synuclein strain in early-onset Parkinson’s disease

    Unique strains of α-synuclein aggregates have been postulated to underlie the spectrum of clinical and pathological presentations seen across the synucleinopathies. Whereas multiple system atrophy (MSA) is ass...

    Heather H. C. Lau, Ivan Martinez-Valbuena in Acta Neuropathologica Communications (2023)

  8. Article

    Open Access

    Genome-wide meta-analysis for Alzheimer’s disease cerebrospinal fluid biomarkers

    Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer’s disease (AD) more directly than clinical diagnosis. Initiated b...

    Iris E. Jansen, Sven J. van der Lee, Duber Gomez-Fonseca in Acta Neuropathologica (2022)

  9. Article

    Open Access

    Challenges at the APOE locus: a robust quality control approach for accurate APOE genoty**

    Genetic variants within the APOE locus may modulate Alzheimer’s disease (AD) risk independently or in conjunction with APOE*2/3/4 genotypes. Identifying such variants and mechanisms would importantly advance our ...

    Michael E. Belloy, Sarah J. Eger, Yann Le Guen in Alzheimer's Research & Therapy (2022)

  10. No Access

    Article

    Lack of fibrillar amyloid plaques but hypometabolism and astrogliosis in autosomal dominant variant AßPParc Alzheimer’s disease

    Laetitia Lemoine, Per-Göran Gillberg, Nenad Bogdanovic in Molecular Psychiatry (2021)

  11. Article

    Open Access

    Astroglial tracer BU99008 detects multiple binding sites in Alzheimer’s disease brain

    With reactive astrogliosis being established as one of the hallmarks of Alzheimer’s disease (AD), there is high interest in develo** novel positron emission tomography (PET) tracers to detect early astrocyte...

    Amit Kumar, Niina A. Koistinen, Mona-Lisa Malarte, Inger Nennesmo in Molecular Psychiatry (2021)

  12. Article

    Open Access

    Amyloid, tau, and astrocyte pathology in autosomal-dominant Alzheimer’s disease variants: AβPParc and PSEN1DE9

    Autosomal-dominant Alzheimer’s disease (ADAD) may be associated with atypical amyloid beta deposits in the brain. In vivo amyloid imaging using 11C-Pittsburgh compound B (PiB) tracer has shown differences in bind...

    Laetitia Lemoine, Per-Göran Gillberg, Nenad Bogdanovic in Molecular Psychiatry (2021)

  13. No Access

    Article

    The existence of Aβ strains and their potential for driving phenotypic heterogeneity in Alzheimer’s disease

    Reminiscent of the human prion diseases, there is considerable clinical and pathological variability in Alzheimer’s disease, the most common human neurodegenerative condition. As in prion disorders, protein mi...

    Heather H. C. Lau, Martin Ingelsson, Joel C. Watts in Acta Neuropathologica (2021)

  14. Article

    Open Access

    Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates

    Alzheimer’s disease (AD) and Parkinson’s disease (PD) are characterized by brain accumulation of aggregated amyloid-beta (Aβ) and alpha-synuclein (αSYN), respectively. In order to develop effective therapies, ...

    **ar Rostami, Tobias Mothes, Mahshad Kolahdouzan in Journal of Neuroinflammation (2021)

  15. Article

    Open Access

    Accumulation of alpha-synuclein within the liver, potential role in the clearance of brain pathology associated with Parkinson’s disease

    Alpha-synuclein (α-syn) aggregation is the hallmark pathological lesion in brains of patients with Parkinson’s disease (PD) and related neurological disorders characterized as synucleinopathies. Accumulating e...

    Juan F. Reyes, Sara Ekmark-Léwen, Marina Perdiki in Acta Neuropathologica Communications (2021)

  16. Article

    Open Access

    Altered levels of CSF proteins in patients with FTD, presymptomatic mutation carriers and non-carriers

    The clinical presentations of frontotemporal dementia (FTD) are diverse and overlap with other neurological disorders. There are, as of today, no biomarkers in clinical practice for diagnosing the disorders. H...

    Julia Remnestål, Linn Öijerstedt, Abbe Ullgren in Translational Neurodegeneration (2020)

  17. No Access

    Article

    α-Synuclein strains target distinct brain regions and cell types

    The clinical and pathological differences between synucleinopathies such as Parkinson’s disease and multiple system atrophy have been postulated to stem from unique strains of α-synuclein aggregates, akin to w...

    Angus Lau, Raphaella W. L. So, Heather H. C. Lau, Jason C. Sang in Nature Neuroscience (2020)

  18. Article

    Open Access

    Binding of α-synuclein oligomers to Cx32 facilitates protein uptake and transfer in neurons and oligodendrocytes

    The intercellular transfer of alpha-synuclein (α-syn) has been implicated in the progression of Parkinson’s disease (PD) and multiple system atrophy (MSA). The cellular mechanisms underlying this process are n...

    Juan F. Reyes, Christopher Sackmann, Alana Hoffmann in Acta Neuropathologica (2019)

  19. Article

    Open Access

    Transethnic meta-analysis of rare coding variants in PLCG2, ABI3, and TREM2 supports their general contribution to Alzheimer’s disease

    Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer’s disease (AD) in Caucasians. Frequencies and AD-associated effects of variants differ across ethniciti...

    Maria Carolina Dalmasso, Luis Ignacio Brusco, Natividad Olivar in Translational Psychiatry (2019)

  20. Article

    Open Access

    Secretion and Uptake of α-Synuclein Via Extracellular Vesicles in Cultured Cells

    In Parkinson’s disease and other Lewy body disorders, the propagation of pathology has been accredited to the spreading of extracellular α-synuclein (α-syn). Although the pathogenic mechanisms are not fully un...

    Gabriel Gustafsson, Camilla Lööv, Emma Persson in Cellular and Molecular Neurobiology (2018)

previous disabled Page of 2