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Biomedicines
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Beta Amyloid: Synaptic Regulation and Dysregulation
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Beta Amyloid: Synaptic Regulation and Dysregulation

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 10580

Special Issue Editors

Dr. Massimo Grilli

E-Mail Website
Guest Editor
Department of Pharmacy, University of Genova, 16148 Genoa, Italy
Interests: pharmacology; neuroscience
Special Issues, Collections and Topics in MDPI journals
Dr. Guendalina Olivero

E-Mail Website
Guest Editor
Department of Pharmacy, University of Genova, 16148 Genoa, Italy
Interests: neurobiology

Special Issue Information

Dear Colleagues,

The approval of Aducanumab and the confirmation of the anti-amyloid strategy against Alzheimer’s disease strongly support the need for new research focused on the role of beta-amyloid in central nervous system (CNS) homeostasis. Antibody-related treatment, alongside an efficacy dispute, provokes interesting side effects such as “amyloid-related imaging abnormalities” (ARIA) and vascular consequences. Other side effects occurring at the synaptic level could be masked by disease derangement. In our mind, all scientific reports (positive and negative results) in this field are fundamental to improve the efficacy and sustainability of this therapeutic approach. This Special Issue highlights the most recent research based on functional or pathological effects of beta-amyloid and/or neutralizing antibodies on CNS homeostasis.

Dr. Massimo Grilli
Dr. Guendalina Olivero
Guest Editors

Manuscript Submission Information

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Keywords

  • beta amyloid
  • aducanumab
  • amyloid neutralizing antibodies
  • ARIA
  • Alzheimer’s disease
  • synaptic modulation

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Published Papers (3 papers)

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Research

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12 pages, 2107 KiB  
Article
The Anti-Aggregative Peptide KLVFF Mimics Aβ1-40 in the Modulation of Nicotinic Receptors: Implications for Peptide-Based Therapy
by Hanna Trebesova, Guendalina Olivero, Mario Marchi and Massimo Grilli
Biomedicines 2022, 10(9), 2231; https://doi.org/10.3390/biomedicines10092231 - 8 Sep 2022
Cited by 3 | Viewed by 1786
Abstract
In recent years, the inhibition of beta-amyloid (Aβ) aggregation has emerged as a potential strategy for Alzheimer’s disease. KLVFF, a small peptide corresponding to the aminoacidic sequence 16-20 of Aβ, reduces Aβ fibrillation dose dependently. Therefore, the toxic and functional characterization of its [...] Read more.
In recent years, the inhibition of beta-amyloid (Aβ) aggregation has emerged as a potential strategy for Alzheimer’s disease. KLVFF, a small peptide corresponding to the aminoacidic sequence 16-20 of Aβ, reduces Aβ fibrillation dose dependently. Therefore, the toxic and functional characterization of its brain activity is fundamental for clarifying its potential therapeutic role. Accordingly, we studied the modulatory role of KLVFF on the cholinergic receptors regulating dopamine and noradrenaline release in rat synaptosomes. Nicotinic receptors on dopaminergic nerve terminals in the nucleus acccumbens are inhibited by KLVFF, which closely resembles full-length Aβ1-40. Moreover, KLVFF entrapped in synaptosomes does not modify the nicotinic receptor’s function, suggesting that external binding to the receptor is required for its activity. The cholinergic agent desformylflustrabromine counteracts the KLVFF effect. Remarkably, muscarinic receptors on dopaminergic terminals and nicotinic receptors regulating noradrenaline release in the hippocampus are completely insensitive to KLVFF. Based on our findings, KLVFF mimics Aβ1-40 as a negative modulator of specific nicotinic receptor subtypes affecting dopamine transmission in the rat brain. Therefore, new pharmacological strategies using the anti-aggregative properties of KLVFF need to be evaluated for potential interference with nicotinic receptor-mediated transmission. Full article
(This article belongs to the Special Issue Beta Amyloid: Synaptic Regulation and Dysregulation)
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Review

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12 pages, 643 KiB  
Review
The Fuzzy Border between the Functional and Dysfunctional Effects of Beta-Amyloid: A Synaptocentric View of Neuron–Glia Entanglement
by Francesca Fagiani, Tamas Fulop, Stefano Govoni and Cristina Lanni
Biomedicines 2023, 11(2), 484; https://doi.org/10.3390/biomedicines11020484 - 8 Feb 2023
Viewed by 2593
Abstract
Recent observations from clinical trials using monoclonal antibodies against Aβ seem to suggest that Aβ-targeting is modestly effective and not sufficiently based on an effective challenge of the role of Aβ from physiological to pathological. After an accelerated approval procedure for aducanumab, and [...] Read more.
Recent observations from clinical trials using monoclonal antibodies against Aβ seem to suggest that Aβ-targeting is modestly effective and not sufficiently based on an effective challenge of the role of Aβ from physiological to pathological. After an accelerated approval procedure for aducanumab, and more recently lecanemab, their efficacy and safety remain to be fully defined despite previous attempts with various monoclonal antibodies, and both academic institutions and pharmaceutical companies are actively searching for novel treatments. Aβ needs to be clarified further in a more complicated context, taking into account both its accumulation and its biological functions during the course of the disease. In this review, we discuss the border between activities affecting early, potentially reversible dysfunctions of the synapse and events trespassing the threshold of inflammatory, self-sustaining glial activation, leading to irreversible damage. We detail a clear understanding of the biological mechanisms underlying the derangement from function to dysfunction and the switch of the of Aβ role from physiological to pathological. A picture is emerging where the optimal therapeutic strategy against AD should involve a number of allied molecular processes, displaying efficacy not only in reducing the well-known AD pathogenesis players, such as Aβ or neuroinflammation, but also in preventing their adverse effects. Full article
(This article belongs to the Special Issue Beta Amyloid: Synaptic Regulation and Dysregulation)
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46 pages, 2833 KiB  
Review
Detecting Early Cognitive Decline in Alzheimer’s Disease with Brain Synaptic Structural and Functional Evaluation
by Samo Ribarič
Biomedicines 2023, 11(2), 355; https://doi.org/10.3390/biomedicines11020355 - 26 Jan 2023
Cited by 15 | Viewed by 5215
Abstract
Early cognitive decline in patients with Alzheimer’s (AD) is associated with quantifiable structural and functional connectivity changes in the brain. AD dysregulation of Aβ and tau metabolism progressively disrupt normal synaptic function, leading to loss of synapses, decreased hippocampal synaptic density and early [...] Read more.
Early cognitive decline in patients with Alzheimer’s (AD) is associated with quantifiable structural and functional connectivity changes in the brain. AD dysregulation of Aβ and tau metabolism progressively disrupt normal synaptic function, leading to loss of synapses, decreased hippocampal synaptic density and early hippocampal atrophy. Advances in brain imaging techniques in living patients have enabled the transition from clinical signs and symptoms-based AD diagnosis to biomarkers-based diagnosis, with functional brain imaging techniques, quantitative EEG, and body fluids sampling. The hippocampus has a central role in semantic and episodic memory processing. This cognitive function is critically dependent on normal intrahippocampal connections and normal hippocampal functional connectivity with many cortical regions, including the perirhinal and the entorhinal cortex, parahippocampal cortex, association regions in the temporal and parietal lobes, and prefrontal cortex. Therefore, decreased hippocampal synaptic density is reflected in the altered functional connectivity of intrinsic brain networks (aka large-scale networks), including the parietal memory, default mode, and salience networks. This narrative review discusses recent critical issues related to detecting AD-associated early cognitive decline with brain synaptic structural and functional markers in high-risk or neuropsychologically diagnosed patients with subjective cognitive impairment or mild cognitive impairment. Full article
(This article belongs to the Special Issue Beta Amyloid: Synaptic Regulation and Dysregulation)
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