Knock-in models related to Alzheimer’s disease: synaptic transmission, plaques and the role of microglia

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1750-1326

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Knock-in models related to Alzheimer’s disease: synaptic transmission, plaques and the role of microglia ; volume:16 ; number:1 ; day:15 ; month:7 ; year:2021 ; pages:1-20 ; date:12.2021
Molecular neurodegeneration ; 16, Heft 1 (15.7.2021), 1-20, 12.2021

Creator: Benitez, Diana P.
Jiang, Shenyi
Wood, Jack
Wang, Rui
Hall, Chloe M.
Peerboom, Carlijn
Wong, Natalie
Stringer, Katie M.
Vitanova, Karina S.
Smith, Victoria C.
Joshi, Dhaval
Saito, Takashi
Saido, Takaomi C.
Hardy, John
Hanrieder, Jörg
Strooper, Bart De
Salih, Dervis A.
Tripathi, Takshashila
Edwards, Frances A.
Cummings, Damian M.

Contributor: SpringerLink (Online service)

DOI: 10.1186/s13024-021-00457-0

URN: urn:nbn:de:101:1-2021110220392788668101

Rights: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 15.08.2025, 7:20 AM CEST

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Associated

Benitez, Diana P.
Jiang, Shenyi
Wood, Jack
Wang, Rui
Hall, Chloe M.
Peerboom, Carlijn
Wong, Natalie
Stringer, Katie M.
Vitanova, Karina S.
Smith, Victoria C.
Joshi, Dhaval
Saito, Takashi
Saido, Takaomi C.
Hardy, John
Hanrieder, Jörg
Strooper, Bart De
Salih, Dervis A.
Tripathi, Takshashila
Edwards, Frances A.
Cummings, Damian M.
SpringerLink (Online service)

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Knock-in models related to Alzheimer’s disease: synaptic transmission, plaques and the role of microglia

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Other Objects (12)

Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer’s Disease

Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein

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Microglia limit the expansion of β-amyloid plaques in a mouse model of Alzheimer’s disease

Protective effect of PDE4B subtype-specific inhibition in an App knock-in mouse model for Alzheimer’s disease

Brain region–specific lipid alterations in the PLB4 hBACE1 knock-in mouse model of Alzheimer’s disease

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Knock, Knock, Knockin’ on Tranformativeness’ Doors

Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models

Impact of hyperhomocysteinemia and different dietary interventions on cognitive performance in a knock-in mouse model for Alzheimer’s disease

Age-related changes in brain phospholipids and bioactive lipids in the APP knock-in mouse model of Alzheimer’s disease

Microglial-associated responses to comorbid amyloid pathology and hyperhomocysteinemia in an aged knock-in mouse model of Alzheimer’s disease

Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer’s Disease

Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein

Generation of App knock-in mice reveals deletion mutations protective against Alzheimer’s disease-like pathology

Microglia limit the expansion of β-amyloid plaques in a mouse model of Alzheimer’s disease

Protective effect of PDE4B subtype-specific inhibition in an App knock-in mouse model for Alzheimer’s disease

Brain region–specific lipid alterations in the PLB4 hBACE1 knock-in mouse model of Alzheimer’s disease

Neuritic Plaques — Gateways to Understanding Alzheimer’s Disease

Knock, Knock, Knockin’ on Tranformativeness’ Doors

Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models

Impact of hyperhomocysteinemia and different dietary interventions on cognitive performance in a knock-in mouse model for Alzheimer’s disease

Age-related changes in brain phospholipids and bioactive lipids in the APP knock-in mouse model of Alzheimer’s disease

Microglial-associated responses to comorbid amyloid pathology and hyperhomocysteinemia in an aged knock-in mouse model of Alzheimer’s disease

Homeostatic microglia initially seed and activated microglia later reshape amyloid plaques in Alzheimer’s Disease

Neuronal transcriptome, tau and synapse loss in Alzheimer’s knock-in mice require prion protein

Generation of App knock-in mice reveals deletion mutations protective against Alzheimer’s disease-like pathology

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Brain region–specific lipid alterations in the PLB4 hBACE1 knock-in mouse model of Alzheimer’s disease

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Microglial-associated responses to comorbid amyloid pathology and hyperhomocysteinemia in an aged knock-in mouse model of Alzheimer’s disease

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