ArticleActa neuropathologica communications2015
Intracellular amyloid β oligomers impair organelle transport and induce dendritic spine loss in primary neurons.
Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- A Clinical Trial of Transcranial Electromagnetic Treatment in Alzheimer's Disease: Cognitive Enhancement and Associated Changes in Cerebrospinal Fluid, Blood, and Brain Imaging.Journal of Alzheimer's disease : JAD · 2019Trial
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Neuronal Microtubules and Radiofrequency Waves: The Quantum Core of Human Consciousness, Memory, and Pathway to Memory Enhancement/Recovery.International journal of molecular sciences · 2026Review
- Endogenously generated Dutch-type Aβ non-fibrillar aggregates dysregulate presynaptic neurotransmission in the absence of detectable inflammation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Amyloid-β "Co-assembles" with Coatomer Subunit Delta (δ-COP).The journal of physical chemistry letters · 2026Article
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology.Molecular neurodegeneration · 2026Article
- Organelle perturbation in Alzheimer's disease: do intracellular amyloid-ß and the fragmented Golgi mediate early intracellular neurotoxicity?Frontiers in cell and developmental biology · 2025Review
- Comprehensive Investigation of Natural Ligands as Inhibitors of β Secretase to Identify Alzheimer's Disease Therapeutics.Current Alzheimer research · 2024Article
- The effects of enhancing angiotensin converting enzyme in myelomonocytes on ameliorating Alzheimer's-related disease and preserving cognition.Frontiers in physiology · 2023Review
- IncreasediScience · 2022Article
- Synthetic PPAR Agonist DTMB Alleviates Alzheimer's Disease Pathology by Inhibition of Chronic Microglial Inflammation in 5xFAD Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Transcranial Electromagnetic Treatment Stops Alzheimer's Disease Cognitive Decline over a 2½-Year Period: A Pilot Study.Medicines (Basel, Switzerland) · 2022Article
- The role of astrocytes in prion-like mechanisms of neurodegeneration.Brain : a journal of neurology · 2022Review
- Lipid flippase dysfunction as a therapeutic target for endosomal anomalies in Alzheimer's disease.iScience · 2022Article
- Amyloid Pathology in the Central Auditory Pathway of 5XFAD Mice Appears First in Auditory Cortex.Journal of Alzheimer's disease : JAD · 2022Article
- Role of Receptors in Relation to Plaques and Tangles in Alzheimer's Disease Pathology.International journal of molecular sciences · 2021Review
- Accumulation of cellular prion protein within β-amyloid oligomer plaques in aged human brains.Brain pathology (Zurich, Switzerland) · 2021Article
- Beneficial Effects of Cyclic Ether 2-Butoxytetrahydrofuran from Sea CucumberMolecules (Basel, Switzerland) · 2021Article
- Neuropathological and Biomarker Findings in Parkinson's Disease and Alzheimer's Disease: From Protein Aggregates to Synaptic Dysfunction.Journal of Parkinson's disease · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSynaptic dysfunction and intracellular transport defects are early events in Alzheimer's disease (AD). Extracellular amyloid β (Aβ) oligomers cause spine alterations and impede the transport of proteins and organelles such as brain-derived neurotrophic factor (BDNF) and mitochondria that are required for synaptic function. Meanwhile, intraneuronal accumulation of Aβ precedes its extracellular deposition and is also associated with synaptic dysfunction in AD. However, the links between intracellular Aβ, spine alteration, and mechanisms that support synaptic maintenance such as organelle trafficking are poorly understood.
resultsWe compared the effects of wild-type and Osaka (E693Δ)-mutant amyloid precursor proteins: the former secretes Aβ into extracellular space and the latter accumulates Aβ oligomers within cells. First we investigated the effects of intracellular Aβ oligomers on dendritic spines in primary neurons and their tau-dependency using tau knockout neurons. We found that intracellular Aβ oligomers caused a reduction in mushroom, or mature spines, independently of tau. We also found that intracellular Aβ oligomers significantly impaired the intracellular transport of BDNF, mitochondria, and recycling endosomes: cargoes essential for synaptic maintenance. A reduction in BDNF transport by intracellular Aβ oligomers was also observed in tau knockout neurons.
conclusionsOur findings indicate that intracellular Aβ oligomers likely contribute to early synaptic pathology in AD and argue against the consensus that Aβ-induced spine loss and transport defects require tau.
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