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Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research

EMBO molecular medicine, 2023-11, Vol.15 (11), p.e18479-e18479

D'Adamio, Luciano

2023

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Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation

eLife, 2020-02, Vol.9

2020

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Initial assessment of the spatial learning, reversal, and sequencing task capabilities of knock-in rats with humanizing mutations in the Aβ-coding region of App

PloS one, 2022-05, Vol.17 (5), p.e0263546-e0263546

2022

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LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

eLife, 2017-07, Vol.6

2017

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Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade

Journal of Alzheimer's disease, 2018-01, Vol.64 (s1), p.S611-S631

2018

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Beyond amyloid: altered gene function in neurodegenerative diseases

Aging (Albany, NY.), 2023-09, Vol.15 (18), p.9235-9237

2023

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Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP

Aging cell, 2019-12, Vol.18 (6), p.e13033-n/a

2019

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APP is cleaved by Bace1 in pre-synaptic vesicles and establishes a pre-synaptic interactome, via its intracellular domain, with molecular complexes that regulate pre-synaptic vesicles functions

PloS one, 2014-09, Vol.9 (9), p.e108576-e108576

2014

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APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses

eLife, 2015-11, Vol.4, p.e09743

2015

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Mitochondrial Rhomboid PARL Regulates Cytochrome c Release during Apoptosis via OPA1-Dependent Cristae Remodeling

Cell, 2006-07, Vol.126 (1), p.163-175

2006

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Intracellular accumulation of tau oligomers in astrocytes and their synaptotoxic action rely on Amyloid Precursor Protein Intracellular Domain-dependent expression of Glypican-4

Progress in neurobiology, 2023-08, Vol.227, p.102482-102482, Article 102482

2023

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Reply to Johansson ‘Treatment with BRICHOS domain helps to clarify issues with Alzheimer mouse models’

EMBO molecular medicine, 2024-04, Vol.16 (4), p.717-719

D’Adamio, Luciano

2024

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Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels

eLife, 2020-06, Vol.9

2020

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Rescue of Learning and Memory Deficits in the Human Nonsyndromic Intellectual Disability Cereblon Knock-Out Mouse Model by Targeting the AMP-Activated Protein Kinase-mTORC1 Translational Pathway

The Journal of neuroscience, 2018-03, Vol.38 (11), p.2780-2795

2018

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Tau is not necessary for amyloid-β-induced synaptic and memory impairments

The Journal of clinical investigation, 2020-09, Vol.130 (9), p.4831-4844

2020

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Late-long-term potentiation magnitude, but not Aβ levels and amyloid pathology, is associated with behavioral performance in a rat knock-in model of Alzheimer disease

Frontiers in aging neuroscience, 2022-11, Vol.14, p.1040576-1040576

2022

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APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant

The EMBO journal, 2011-06, Vol.30 (12), p.2501-2509

2011

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Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits

Proceedings of the National Academy of Sciences - PNAS, 2010-11, Vol.107 (48), p.20822-20827

2010

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The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains

Molecular neurodegeneration, 2009-07, Vol.4 (1), p.28-28, Article 28

2009

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BRI3 Inhibits Amyloid Precursor Protein Processing in a Mechanistically Distinct Manner from Its Homologue Dementia Gene BRI2

The Journal of biological chemistry, 2009-06, Vol.284 (23), p.15815-15825

2009

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Role of Amyloid-β and Tau Proteins in Alzheimer’s Disease: Confuting the Amyloid Cascade

Journal of Alzheimer's disease, 2019-01, Vol.68 (1), p.415-415

2019

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A role for tau in learning, memory and synaptic plasticity

Scientific reports, 2018-02, Vol.8 (1), p.3184-13, Article 3184

2018

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Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP

Neuron (Cambridge, Mass.), 2005-05, Vol.46 (4), p.541-554

2005

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Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer’s and related dementias

EMBO reports, 2024-03, Vol.25 (3), p.1326-1360

2024

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Increased AβPP processing in familial Danish dementia patients

Journal of Alzheimer's disease, 2011-01, Vol.27 (2), p.385-391

2011

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Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research

Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation

Initial assessment of the spatial learning, reversal, and sequencing task capabilities of knock-in rats with humanizing mutations in the Aβ-coding region of App

LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade

Beyond amyloid: altered gene function in neurodegenerative diseases

Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP

APP is cleaved by Bace1 in pre-synaptic vesicles and establishes a pre-synaptic interactome, via its intracellular domain, with molecular complexes that regulate pre-synaptic vesicles functions

APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses

Mitochondrial Rhomboid PARL Regulates Cytochrome c Release during Apoptosis via OPA1-Dependent Cristae Remodeling

Intracellular accumulation of tau oligomers in astrocytes and their synaptotoxic action rely on Amyloid Precursor Protein Intracellular Domain-dependent expression of Glypican-4

Reply to Johansson ‘Treatment with BRICHOS domain helps to clarify issues with Alzheimer mouse models’

Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels

Rescue of Learning and Memory Deficits in the Human Nonsyndromic Intellectual Disability Cereblon Knock-Out Mouse Model by Targeting the AMP-Activated Protein Kinase-mTORC1 Translational Pathway

Tau is not necessary for amyloid-β-induced synaptic and memory impairments

Late-long-term potentiation magnitude, but not Aβ levels and amyloid pathology, is associated with behavioral performance in a rat knock-in model of Alzheimer disease

APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits

The interactome of the amyloid beta precursor protein family members is shaped by phosphorylation of their intracellular domains

BRI3 Inhibits Amyloid Precursor Protein Processing in a Mechanistically Distinct Manner from Its Homologue Dementia Gene BRI2

Role of Amyloid-β and Tau Proteins in Alzheimer’s Disease: Confuting the Amyloid Cascade

A role for tau in learning, memory and synaptic plasticity

Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP

Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer’s and related dementias

Increased AβPP processing in familial Danish dementia patients

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