[Anonymous]

A Jyoti

A Sydow

A Tanghe

AC McKee

Amar Jyoti

Andrea Plano

Andy Welch

Aneli Utan

B Bediou

B Cvetkovic

B De Strooper

B Dogdas

B Horwitz

B Platt

B Zhang

BD Drever

Benjamin Drever

Bettina Platt

C Holmes

C Janus

C Kuntner

C Stenh

C Vale

CR Figley

D Morgan

D Tampellini

David Koss

DL Bliwise

DR Borchelt

DS Woodruff-Pak

Duncan Ryan

Emanuele Porcu

F Luo

G Hale

G Rauchs

G Riedel

Georgina Merrick

Gernot Riedel

H Oakley

Hong Wan

Huaibin Cai

IR Olson

J Backhaus

J Brankack

J Dukart

J Jeong

J Magrane

J Micheau

JC Dodart

JC O'Leary

JP Wisor

K Duff

K Ghosal

KL Youmans

LM Billings

Louise Scrocchi

LS Prichep

M Mayford

MA Gama Sosa

MA Meraz-Rios

Marco Mingarelli

N Sahara

P Fries

R Craig-Schapiro

R Epis

RD Terry

RH Takahashi

RM Nicholson

RP Kessels

S Deiana

S Oddo

S Palva

S Stoppelkamp

Sandra Stoppelkamp

T Tomiyama

V Echeverria

Valeria Melis

W Klimesch

Y Li

PLoS ONE

English

PubMed

Platt, Bettina

Drever, Benjamin

Koss, David

Stoppelkamp, Sandra

Jyoti, Amar

Plano, Andrea

Utan, Aneli

Merrick, Georgina

Ryan, Duncan

Melis, Valeria

Wan, Hong

Mingarelli, Marco

Porcu, Emanuele

Scrocchi, Louise

Welch, Andy

Riedel, Gernot

Aberdeen University Research

A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer’s disease.

A beta peptide vaccination prevents memory loss in an animal model of Alzheimer’s disease.

A mouse model of amyloid beta oligomers: Their contribution to synaptic alteration, abnormal tau phosphorylation, glial activation, and neuronal loss in vivo.

Alzheimer’s disease-like pathological features in transgenic mice expressing the APP intracellular domain.

Amyloid-beta oligomers are inefficiently measured by enzyme-linked immunosorbent assay.

Amyloidbeta42 alters apolipoprotein E solubility in brains of mice with five familial AD mutations.

Animal models of Alzheimer’s disease: Therapeutic implications.

Animal transgenesis: An overview.

Assembly of two distinct dimers and higher-order oligomers from full-length tau.

Biomarkers of Alzheimer’s disease.

Characterization of 7- and 19-month-old Tg2576 mice using multimodal in vivo imaging: Limitations as a translatable model of Alzheimer’s disease. Neurobiol Aging

Characterization of pathology in transgenic mice over-expressing human genomic and cDNA tau transgenes.

Differential effects of global and cerebellar normalization on detection and differentiation of dementia in FDG-PET studies.

EEG dynamics in patients with Alzheimer’s disease.

EEG, activity, and sleep architecture in a transgenic AbetaPPswe/PSEN1A246E Alzheimer’s disease mouse.

GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer’s disease.

Heat shock protein 70 participates in the neuroprotective response to intracellularly expressed betaamyloid in neurons.

Immunization reverses memory deficits without reducing brain abeta burden in Alzheimer’s disease model.

Impaired rapid eye movement sleep in the Tg2576 APP murine model of Alzheimer’s disease with injury to pedunculopontine cholinergic neurons.

Impaired social cognition in mild Alzheimer disease.

In vitro modelling of Alzheimer’s disease: Degeneration and cell death induced by viral delivery of amyloid and tau. Exp Neurol.

Intraneuronal abeta causes the onset of early Alzheimer’s disease-related cognitive deficits in transgenic mice.

Intraneuronal betaamyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer’s disease mutations: Potential factors in amyloid plaque formation.

Limitations of small animal PET imaging with [18F]FDDNP and FDG for quantitative studies in a transgenic mouse model of Alzheimer’s disease.

Longterm effects of Abeta42 immunisation in Alzheimer’s disease: Follow-up of a randomised, placebo-controlled phase I trial.

Memantine acts as a cholinergic stimulant in the mouse hippocampus.

Midlife decline in declarative memory consolidation is correlated with a decline in slow wave sleep.

NerveCenter: Phase III Alzheimer trial halted: Search for therapeutic biomarkers continues.

Neuritic pathology and dementia in Alzheimer’s disease.

New vistas for alpha-frequency band oscillations.

Olde Rikkert MG (2010) Spatial working memory in aging and mild cognitive impairment: Effects of task load and contextual cueing.

Oligomerization of Alzheimer’s beta-amyloid within processes and synapses of cultured neurons and brain.

Oscillatory mechanisms of process binding in memory.

Phenothiazine-mediated rescue of cognition in tau transgenic mice requires neuroprotection and reduced soluble tau burden.

Physical basis of cognitive alterations in Alzheimer’s disease: Synapse loss is the major correlate of cognitive impairment.

Profile for amyloid-beta and tau expression in primary cortical cultures from 3xTg-AD mice.

Proteases and proteolysis in Alzheimer disease: A multifactorial view on the disease process.

Quantitative EEG and electromagnetic brain imaging in aging and in the evolution of dementia.

Rat transgenic models with a phenotype of intracellular abeta accumulation in hippocampus and cortex.

Regional cerebral glucose uptake in the 3xTG model of Alzheimer’s disease highlights common regional vulnerability across AD mouse models.

Reversible hippocampal inactivation partially dissociates how and where to search in the water maze.

Reversible neural inactivation reveals hippocampal participation in several memory processes.

Scopolamine-induced deficits in social memory in mice: Reversal by donepezil. Behav Brain Res

Searching for new animal models of Alzheimer’s disease.

Sleep and circadian abnormalities in a transgenic mouse model of Alzheimer’s disease: A role for cholinergic transmission.

Sleep and hippocampus: Do we search for the right things?

Sleep disorders in Alzheimer’s disease and other dementias.

Some surprising findings on the involvement of the parietal lobe in human memory.

Synapses, synaptic activity and intraneuronal abeta in Alzheimer’s disease.

Tau oligomers and aggregation in Alzheimer’s disease.

Tauinduced defects in synaptic plasticity, learning, and memory are reversible in transgenic mice after switching off the toxic tau mutant.

The cholinergic system, EEG and sleep.

The elusive concept of brain connectivity.

The relationships between memory systems and sleep stages.

Tripletransgenic model of Alzheimer’s disease with plaques and tangles: Intracellular abeta and synaptic dysfunction.

Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1

Platt Bettina

Drever Benjamin

Koss David

Stoppelkamp Sandra

Jyoti Amar

Plano Andrea

Utan Aneli

Merrick Georgina

Ryan Duncan

Melis Valeria

Wan Hong

Mingarelli Marco

Porcu Emanuele

Scrocchi Louise

Welch Andy

Riedel Gernot

Public Library of Science (PLOS)

Abnormal Cognition, Sleep, EEG and Brain Metabolism in a Novel Knock-In Alzheimer Mouse, PLB1

Late-stage neuropathological hallmarks of Alzheimer's disease (AD) are β-amyloid (βA) and hyperphosphorylated tau peptides, aggregated into plaques and tangles, respectively. Corresponding phenotypes have been mimicked in existing transgenic mice, however, the translational value of aggressive over-expression has recently been questioned. As controlled gene expression may offer animal models with better predictive validity, we set out to design a transgenic mouse model that circumvents complications arising from pronuclear injection and massive over-expression, by targeted insertion of human mutated amyloid and tau transgenes, under the forebrain- and neurone-specific CaMKIIα promoter, termed PLB1(Double). Crossing with an existing presenilin 1 line resulted in PLB1(Triple) mice. PLB1(Triple) mice presented with stable gene expression and age-related pathology of intra-neuronal amyloid and hyperphosphorylated tau in hippocampus and cortex from 6 months onwards. At this early stage, pre-clinical (18)FDG PET/CT imaging revealed cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain. Quantitative EEG analyses yielded heightened delta power during wakefulness and REM sleep, and time in wakefulness was already reliably enhanced at 6 months of age. These anomalies were paralleled by impairments in long-term and short-term hippocampal plasticity and preceded cognitive deficits in recognition memory, spatial learning, and sleep fragmentation all emerging at ∼12 months. These data suggest that prodromal AD phenotypes can be successfully modelled in transgenic mice devoid of fibrillary plaque or tangle development. PLB1(Triple) mice progress from a mild (MCI-like) state to a more comprehensive AD-relevant phenotype, which are accessible using translational tools such as wireless EEG and microPET/CT

Directory of Open Access Journals

Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1.

Late-stage neuropathological hallmarks of Alzheimer's disease (AD) are β-amyloid (βA) and hyperphosphorylated tau peptides, aggregated into plaques and tangles, respectively. Corresponding phenotypes have been mimicked in existing transgenic mice, however, the translational value of aggressive over-expression has recently been questioned. As controlled gene expression may offer animal models with better predictive validity, we set out to design a transgenic mouse model that circumvents complications arising from pronuclear injection and massive over-expression, by targeted insertion of human mutated amyloid and tau transgenes, under the forebrain- and neurone-specific CaMKIIα promoter, termed PLB1 Double. Crossing with an existing presenilin 1 line resulted in PLB1 Triple mice. PLB1 Triple mice presented with stable gene expression and age-related pathology of intra-neuronal amyloid and hyperphosphorylated tau in hippocampus and cortex from 6 months onwards. At this early stage, pre-clinical 18FDG PET/CT imaging revealed cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain. Quantitative EEG analyses yielded heightened delta power during wakefulness and REM sleep, and time in wakefulness was already reliably enhanced at 6 months of age. These anomalies were paralleled by impairments in long-term and short-term hippocampal plasticity and preceded cognitive deficits in recognition memory, spatial learning, and sleep fragmentation all emerging at ~12 months. These data suggest that prodromal AD phenotypes can be successfully modelled in transgenic mice devoid of fibrillary plaque or tangle development. PLB1 Triple mice progress from a mild (MCI-like) state to a more comprehensive AD-relevant phenotype, which are accessible using translational tools such as wireless EEG and microPET/CT.</p

Discovery Research Portal

Abnormal cognition, sleep, eeg and brain metabolism in a novel knock-in alzheimer mouse, plb1

Crossref

https://discovery.dundee.ac.uk/files/115134792/file.pdf

Abnormal cognition, sleep, EEG and brain metabolism in a novel knock-in Alzheimer mouse, PLB1

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Aberdeen University Research

Public Library of Science (PLOS)

Directory of Open Access Journals

Discovery Research Portal

Public Library of Science (PLOS)

Crossref

Discovery Research Portal

Discovery Research Portal