Molecular and Cellular Basis of Alzheimer's Disease

A special issue of NeuroSci (ISSN 2673-4087).

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 4106

Special Issue Editors


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1. Institut d'Investigació Sanitària Pere Virgili (IISPV), Reus, Spain
2. Carlos III Health Institute (Instituto de Salud Carlos III), Madrid, Spain
Interests: neurochemistry; proteinopathy; Alzheimer’s disease; vascular dementia; neurovascular unit; extracellular vesicles; proteomics
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1. IMDEA Food & Health Sciences Research Institute, +Pec Proteomics, Campus of International Excellence UAM+CSIC, Old Cantoblanco Hospital, 8 Crta. Canto Blanco, 28049 Madrid, Spain
2. Proteored-Instituto de Salud Carlos III (ISCIII), Madrid, Spain
Interests: proteomics; neurodegeneration; extracellular vesicles; protein post-translational modifications; degenerative protein modifications; metabolism; human diseases
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Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: inflammation; inflammasome; beta-amyloid; Tau; microglia; apoptosis; caspase; Alzheimer’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; frontotemporal dementia; traumatic brain injury; polyphenols; bioavailability; drug discovery
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Guest Editor
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Interests: Alzheimer’s Disease
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Special Issue Information

Dear colleagues,

Alzheimer’s disease (AD) is the main contributor to dementia worldwide, a cognitive syndrome that progressively and fatally impairs the ability of the affected individuals to perform essential everyday tasks. Dementia is also the major cause of disability among elderly people worldwide, and its derived social and economic costs are massive. Although the molecular and cellular basis of AD remains a matter of intense scientific investigation and has been partially uncovered, several crucial aspects related to the neuropathology of AD still require our attention and interest. These aspects, although not exhaustive, may involve the following actions: uncovering currently unknown idiopathic triggering factors, shedding light on the molecular mechanisms of neuropathology onset, understanding common neuropathological mechanisms that defy brain cell heterogeneity, identifying potential early-onset biological diagnostic and prognostic markers (neuropathology onset proposed as early as 20 years before clinical diagnosis). Thus, this Special Issue focuses on generating genuine and valuable scientific knowledge on the molecular and cellular basis of AD, with foresight on the apparition of novel diagnosis and therapeutic strategies for this fatal neurological disorder.

You may choose our Joint Special Issue in Biomolecules, or Joint Special Issue in Cells.

Dr. Xavier Gallart-Palau
Dr. Aida Serra
Prof. Dr. Giulio Pasinetti
Dr. Joyce Harary
Guest Editors

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Published Papers (1 paper)

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Research

13 pages, 5176 KiB  
Article
Sialic Acid Ameliorates Cognitive Deficits by Reducing Amyloid Deposition, Nerve Fiber Production, and Neuronal Apoptosis in a Mice Model of Alzheimer’s Disease
by Min Xiao, Chuangyu Yao, Fang Liu, Wei Xiang, Yao Zuo, Kejue Feng, Shuhuan Lu, Li Xiang, Muzi Li, Xiangyu Li and Xiubo Du
NeuroSci 2022, 3(1), 28-40; https://0-doi-org.brum.beds.ac.uk/10.3390/neurosci3010002 - 24 Dec 2021
Cited by 1 | Viewed by 3481
Abstract
(1) Background: As a natural carbohydrate, sialic acid (SA) is helpful for brain development, cognitive ability, and the nervous system, but there are few reports about the effect of SA on Alzheimer’s disease (AD). (2) Method: The present study evaluated the effect of [...] Read more.
(1) Background: As a natural carbohydrate, sialic acid (SA) is helpful for brain development, cognitive ability, and the nervous system, but there are few reports about the effect of SA on Alzheimer’s disease (AD). (2) Method: The present study evaluated the effect of SA on cognitive ability, neuronal activity, Aβ formation, and tau hyperphosphorylation in a double transgenic AD (2×Tg-AD) mice model. The 2×Tg-AD mice were randomly divided into four groups: the AD control group, 17 mg/kg SA-treated AD group, 84 mg/kg SA-treated AD group, and 420 mg/kg SA-treated AD group. Mice from all four groups were fed to 7 months of age for the behavioral test and to 9 months of age for the pathological factors investigation. (3) Results: In the Morris water maze, the escape latency significantly decreased on the fifth day in the SA-treated groups. The number of rearing and crossing times in the open field test also increased significantly, compared with the control group. SA treatment significantly reduced amyloid β-peptide (Aβ) and nerve fibers and increased the number of Nissl bodies in the brain of AD mice. (4) Conclusions: SA reduced the neuron damage by reducing Aβ and inhibited tau protein hyperphosphorylation, which improved the cognitive ability and mobility of AD mice. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Alzheimer's Disease)
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