Novel Therapeutic Strategies for Alzheimer’s Disease Treatment

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 May 2025 | Viewed by 1523

Special Issue Editor


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Guest Editor
Department of Internal Medicine, Endocrinology Diabetes and Metabolism, Diabetes and Cardiovascular Disease Center, University of Missouri School of Medicine, One Hospital Drive, Columbia, MO 65211, USA
Interests: ultrastructure; Alzheimer’s disease; cardiovascular disease; FOCM; hypertension; type 2 diabetes mellitus; metabolic syndrome; insulin and leptin resistance; neurovascular unit; endothelial cells; endothelial glycocalyx; reactive neuroglia; BBB; BCSF barrier; neuroinflammation; choroid plexus; perivascular spaces

Special Issue Information

Dear Colleagues,

Sporadic or late-onset Alzheimer’s disease (LOAD) is the most common multifactorial, progressive neurodegenerative disease that causes dementia globally. It is associated with aging (≥65 years of age) and increased morbidity and mortality. Currently, most therapies have utilized a single-target treatment protocol, and it is becoming more apparent that a multi-targeted approach or a combination approach may be necessary in order to attenuate, slow, or halt neurodegenerative disease progression as occurs in LOAD.

The primary goal of this Special Issue is to bring forth novel treatment strategies that may help to advance new paradigm treatments specifically for LOAD that may also have possible implications for other neurodegenerative diseases.

Reviews, case reports, or original research manuscripts will be considered.

Prof. Dr. Melvin Hayden
Guest Editor

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Keywords

  • Sporadic
  • late-onset Alzheimer’s disease (LOAD)
  • neurodegenerative diseases

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Published Papers (1 paper)

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Review

34 pages, 7313 KiB  
Review
Sodium Thiosulfate: An Innovative Multi-Target Repurposed Treatment Strategy for Late-Onset Alzheimer’s Disease
by Melvin R. Hayden and Neetu Tyagi
Pharmaceuticals 2024, 17(12), 1741; https://doi.org/10.3390/ph17121741 - 23 Dec 2024
Viewed by 1220
Abstract
Late-onset Alzheimer’s disease (LOAD) is a chronic, multifactorial, and progressive neurodegenerative disease that associates with aging and is highly prevalent in our older population (≥65 years of age). This hypothesis generating this narrative review will examine the important role for the use of [...] Read more.
Late-onset Alzheimer’s disease (LOAD) is a chronic, multifactorial, and progressive neurodegenerative disease that associates with aging and is highly prevalent in our older population (≥65 years of age). This hypothesis generating this narrative review will examine the important role for the use of sodium thiosulfate (STS) as a possible multi-targeting treatment option for LOAD. Sulfur is widely available in our environment and is responsible for forming organosulfur compounds that are known to be associated with a wide range of biological activities in the brain. STS is known to have (i) antioxidant and (ii) anti-inflammatory properties; (iii) chelation properties for calcium and the pro-oxidative cation metals such as iron and copper; (iv) donor properties for hydrogen sulfide production; (v) possible restorative properties for brain endothelial-cell-derived bioavailable nitric oxide. Thus, it becomes apparent that STS has the potential for neuroprotection and neuromodulation and may allow for an attenuation of the progressive nature of neurodegeneration and impaired cognition in LOAD. STS has been successfully used to prevent cisplatin oxidative-stress-induced ototoxicity in the treatment of head and neck and solid cancers, cyanide and arsenic poisoning, and fungal skin diseases. Most recently, intravenous STS has become part of the treatment plan for calciphylaxis globally due to vascular calcification and ischemia-induced skin necrosis and ulceration. Side effects have been minimal with reports of metabolic acidosis and increased anion gap; as with any drug treatment, there is also the possibility of allergic reactions, possible long-term osteoporosis from animal studies to date, and minor side-effects of nausea, headache, and rhinorrhea if infused too rapidly. While STS poorly penetrates the intact blood–brain barrier(s) (BBBs), it could readily penetrate BBBs that are dysfunctional and disrupted to deliver its neuroprotective and neuromodulating effects in addition to its ability to penetrate the blood–cerebrospinal fluid barrier of the choroid plexus. Novel strategies such as the future use of nano-technology may be helpful in allowing an increased entry of STS into the brain. Full article
(This article belongs to the Special Issue Novel Therapeutic Strategies for Alzheimer’s Disease Treatment)
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