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The mechanism and consequences of amyloid-β modulating thiamine pyrophosphokinase-1 expression in microglia

https://doi.org/10.1101/2024.09.18.613405

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Reduced Activities of Thiamine-Dependent Enzymes in the Brains and Peripheral Tissues of Patients With Alzheimer's Disease

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Association of Amyloid and Tau With Cognition in Preclinical Alzheimer Disease

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P2Y12receptor‐mediated integrin‐β1 activation regulates microglial process extension induced by ATP

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Microglia-Mediated Neuroprotection, TREM2, and Alzheimer’s Disease: Evidence From Optical Imaging

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A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease

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TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease

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Microglia Biology: One Century of Evolving Concepts

inferredcites →https://doi.org/10.1016/j.expneurol.2016.04.018openalex-snapshot

Amyloid-β plaques disrupt axon initial segments

inferredcites →https://doi.org/10.1016/j.neuron.2009.07.003openalex-snapshot

Amyloid Deposition Is Associated with Impaired Default Network Function in Older Persons without Dementia

inferredcites →https://doi.org/10.1016/j.neuron.2015.11.013openalex-snapshot

Purification and Characterization of Progenitor and Mature Human Astrocytes Reveals Transcriptional and Functional Differences with Mouse

inferredcites →https://doi.org/10.1016/j.neuron.2016.09.016openalex-snapshot

TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy

inferredcites →https://doi.org/10.1016/j.pneurobio.2013.06.004openalex-snapshot

Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: Implications for diagnostic and therapeutic strategies

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APP Processing and Synaptic Function

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Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers

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Plasma neurofilament light chain in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional and longitudinal cohort study

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APOE and Alzheimer's disease: advances in genetics, pathophysiology, and therapeutic approaches

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Thiamin Function, Metabolism, Uptake, and Transport

inferredcites →https://doi.org/10.1038/349704a0openalex-snapshot

Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease

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Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene

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A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline

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Microglia constitute a barrier that prevents neurotoxic protofibrillar Aβ42 hotspots around plaques

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Amyloid-β plaques enhance Alzheimer's brain tau-seeded pathologies by facilitating neuritic plaque tau aggregation

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A robust and high-throughput Cre reporting and characterization system for the whole mouse brain

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ATP mediates rapid microglial response to local brain injury in vivo

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CSF1R inhibitors induce a sex-specific resilient microglial phenotype and functional rescue in a tauopathy mouse model

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The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics

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A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease

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Single-cell transcriptomic analysis of Alzheimer’s disease

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PLD3 affects axonal spheroids and network defects in Alzheimer’s disease

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Microglia in neurodegeneration

inferredcites →https://doi.org/10.1038/s41593-019-0566-1openalex-snapshot

Lipid-droplet-accumulating microglia represent a dysfunctional and proinflammatory state in the aging brain

inferredcites →https://doi.org/10.1038/s42255-022-00643-4openalex-snapshot

Microglial hexokinase 2 deficiency increases ATP generation through lipid metabolism leading to β-amyloid clearance

inferredcites →https://doi.org/10.1093/brain/awy059openalex-snapshot

Longitudinal tau PET in ageing and Alzheimer’s disease

inferredcites →https://doi.org/10.1126/science.1072994openalex-snapshot

The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

inferredcites →https://doi.org/10.1126/science.1566067openalex-snapshot

Alzheimer's Disease: The Amyloid Cascade Hypothesis

inferredcites →https://doi.org/10.1126/scitranslmed.abn9380openalex-snapshot

Synaptogenic effect of APP -Swedish mutation in familial Alzheimer’s disease

inferredcites →https://doi.org/10.1146/annurev.biochem.78.072407.102340openalex-snapshot

The Structural and Biochemical Foundations of Thiamin Biosynthesis

inferredcites →https://doi.org/10.1177/193229680800200619openalex-snapshot

Alzheimer's Disease is Type 3 Diabetes—Evidence Reviewed

inferredcites →https://doi.org/10.1212/wnl.0000000000006075openalex-snapshot

Influence of tau PET, amyloid PET, and hippocampal volume on cognition in Alzheimer disease

inferredcites →https://doi.org/10.1523/jneurosci.2531-15.2016openalex-snapshot

Attenuation of β-Amyloid Deposition and Neurotoxicity by Chemogenetic Modulation of Neural Activity

inferredcites →https://doi.org/10.1523/jneurosci.4970-06.2007openalex-snapshot

Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway

inferredcites →https://doi.org/10.3233/jad-220808openalex-snapshot

High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer’s Disease-Causing Mutations

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.1101/2025.01.16.633468openalex-snapshot

Apolipoprotein E ε4 exacerbates microglia-mediated complement-dependent synapse loss caused by neuronal Tpk deficiency

inferred← citeshttps://doi.org/10.3390/ijms27115022openalex-snapshot

Hippocampal, Microglial, Morphological, and Amyloid Profiles Following Thiamine Pyrophosphate Treatment in 3xTg-AD Mice

Editorial review for independent work. ICSAC — the Institute for Complexity Science and Advanced Computing — runs a structured editorial panel for researchers publishing outside journals, and publishes on CiteStamp rails. Submission is free and goes through ORCID: icsacinstitute.org/submit.