Research on the Amyloid in Alzheimer’s Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 1100

Special Issue Editor


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Guest Editor
Institute of Molecular Medicine, Feinstein Institutes for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA
Interests: Alzheimer’s disease-associated neuroinflammation and neurodegeneration; tau hyperphosphorylation; neurotoxic astrocytes; brain injury; ischemic stroke; microglial dysfunction

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is a globally prevalent progressive and neurodegenerative brain disorder, characterized by amyloid plaques and tau tangles leading to cognitive decline. Recent research on the amyloid in AD, including the “amyloid clock” biomarker, has made significant strides. While there is still no cure for AD, the recent FDA-approved anti-amyloid drugs aducanumab and lecanemab reduce its symptoms. However, there is a need to understand the interaction between neurons and non-neurons, which contributes to an imbalance between the production and clearance of the amyloid in AD, better. AD-patient-derived inducible pluripotent stem cells (iPSCs) can differentiate into various types of neurons, non-neurons, and brain organoids in vitro and in in vivo models, recapitulating the AD pathology in relevant cells.

This Special Issue will examine novel amyloid-associated mechanisms and improved biomarkers for AD; the amyloid’s effect on the AD brain network; AD patient iPSC-derived neurons, non-neurons, and brain organoids; and in vivo models investigating the role of the amyloid in AD.

Yours faithfully,

Dr. Archna Sharma
Guest Editor

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Keywords

  • amyloid
  • Alzheimer’s disease
  • amyloid biomarkers
  • brain network
  • anti-amyloid immunotherapy
  • inducible pluripotent stem cells
  • neuron and non-neuron differentiation
  • brain organoids
  • amyloidopathy animal models

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Published Papers (1 paper)

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Research

13 pages, 2383 KiB  
Article
Glutamate Transporter 1 as a Novel Negative Regulator of Amyloid β
by Priyanka Sinha, Yuliia Turchyna, Shane Patrick Clancy Mitchell, Michael Sadek, Gokce Armagan, Florian Perrin, Masato Maesako and Oksana Berezovska
Cells 2024, 13(19), 1600; https://doi.org/10.3390/cells13191600 - 24 Sep 2024
Viewed by 902
Abstract
Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer’s disease (AD) progression. Early stages of AD are often marked by hyperactivity and increased epileptiform activity preceding cognitive decline. Previously, we identified a direct interaction between GLT-1 and Presenilin 1 (PS1) in the [...] Read more.
Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer’s disease (AD) progression. Early stages of AD are often marked by hyperactivity and increased epileptiform activity preceding cognitive decline. Previously, we identified a direct interaction between GLT-1 and Presenilin 1 (PS1) in the brain, highlighting GLT-1 as a promising target in AD research. This study reports the significance of this interaction and uncovers a novel role of GLT-1 in modulating amyloid-beta (Aβ) production. Overexpression of GLT-1 in cells reduces the levels of Aβ40 and Aβ42 by decreasing γ-secretase activity pertinent to APP processing and induces a more “open” PS1 conformation, resulting in decreased Aβ42/40 ratio. Inhibition of the GLT-1/PS1 interaction using cell-permeable peptides produced an opposing effect on Aβ, highlighting the pivotal role of this interaction in regulating Aβ levels. These findings emphasize the potential of targeting the GLT-1/PS1 interaction as a novel therapeutic strategy for AD. Full article
(This article belongs to the Special Issue Research on the Amyloid in Alzheimer’s Disease)
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