Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

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Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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2017年學術文章

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Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

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Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

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Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

@en

Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

@nl

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Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

@en

Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis.

@nl

P1476

Trans-Synaptic Spread of Amyloid-β in Alzheimer's Disease: Paths to β-Amyloidosis

@en

P2093

Silvia Middei

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Creative Commons Attribution 4.0 International

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Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer's disease

Alzheimer amyloid protein precursor in the rat hippocampus: transport and processing through the perforant path

Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ ) deposition

Regional aerobic glycolysis in the human brain

Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle

Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

Evolving the lock to fit the key to create a family of G protein-coupled receptors potently activated by an inert ligand

The brain's default network: anatomy, function, and relevance to disease

Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host

Trafficking and proteolytic processing of APP

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5281829

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scholarly article

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10.1155/2017/5281829

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2017

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Annabella Pignataro

Silvia Middei

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2017-12-24T00:00:00Z

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