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Neurodegenerative Diseases: New Insights into Mechanisms, Prevention, Markers, and Therapeutic Targets

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (29 September 2024) | Viewed by 1221

Special Issue Editor

Dr. Katarzyna Kaczyńska

E-Mail Website
Guest Editor
Department of Respiration Physiology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Pawińskiego 5, 02-106 Warsaw, Poland
Interests: neurodegenerative disorders; breathing control; neurotransmitters; hypoxia; therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues，

The most common neurodegenerative diseases associated with aging are Alzheimer's disease with its dominant dementia and Parkinson's disease featured by motor disorders. The incidence of both diseases has increased significantly in recent years and forecasts for future years indicate a further escalation in the morbidity rate. They are mainly the consequence of abnormalities in the processes of certain proteins that cause them to accumulate in or near neurons, reducing or destroying their functions. Despite growing knowledge of neurodegenerative diseases, progress in their treatment has not been satisfactory, and they are still treated mainly symptomatically.
The intent of this special issue is to harvest the latest information on both diseases, including new insights into molecular mechanisms, prevention strategies, markers, new targets. disease modeling and treatments that can help expand our knowledge and forge new potential therapeutic pathways. Original research, mini- and full reviews, short communications, and perspectives on any aspect related to Alzheimer's or Parkinson's disease are welcome.

Dr. Katarzyna Kaczyńska
Guest Editor

Manuscript Submission Information

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Keywords

  • Alzheimer’s disease
  • Parkinson’s disease
  • molecular targets
  • biomarkers
  • disease modeling
  • therapeutic strategies
  • prevention
  • drug design

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Published Papers (2 papers)

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16 pages, 2519 KiB  
Article
A Novel Tetrahydroacridine Derivative with Potent Acetylcholinesterase Inhibitory Properties and Dissociative Capability against Aβ42 Fibrils Confirmed by In Vitro Studies
by Ilona Mojzych, Anna Zawadzka, Kryspin Andrzejewski, Monika Jampolska, Zuzana Bednarikova, Miroslav Gancar, Zuzana Gazova, Maciej Mazur and Katarzyna Kaczyńska
Int. J. Mol. Sci. 2024, 25(18), 10072; https://doi.org/10.3390/ijms251810072 - 19 Sep 2024
Viewed by 394
Abstract
Alzheimer’s disease (AD) is one of the most common causes of dementia, accounting for more than 60% of all cases. It is a neurodegenerative disease in which symptoms such as a decline in memory, thinking, learning, and organizing skills develop gradually over many [...] Read more.
Alzheimer’s disease (AD) is one of the most common causes of dementia, accounting for more than 60% of all cases. It is a neurodegenerative disease in which symptoms such as a decline in memory, thinking, learning, and organizing skills develop gradually over many years and eventually become more severe. To date, there is no effective treatment for the cause of Alzheimer’s disease, and the existing pharmacological options primarily help manage symptoms. Treatment is mainly based on acetylcholinesterase (AChE) inhibitors such as donepezil, rivastigmine, and galantamine, which exhibit numerous adverse cardiovascular and gastrointestinal effects due to excessive stimulation of peripheral cholinergic activity involving muscarinic receptors. Therefore, in addition to the obvious drugs that act on the cause of the disease, new drugs based on AChE inhibition that show the fewest side effects are needed. One potential drug could be a new compound under study, tetrahydroacridine derivative (CHDA), which showed significant potential to inhibit the AChE enzyme in previous in vitro studies. The present study shows that while having very potent AChE inhibitory properties, CHDA is a compound with low toxicity to nerve cell culture and living organisms. In addition, it exhibits dissociative activity against amyloid β fibrils, which is extremely important for applications in Alzheimer’s disease therapy. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: New Insights into Mechanisms, Prevention, Markers, and Therapeutic Targets)
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9 pages, 5825 KiB  
Hypothesis
Alzheimer’s Disease as a Membrane Dysfunction Tauopathy? New Insights into the Amyloid Cascade Hypothesis
by Tomas Olejar, Nikol Jankovska and Radoslav Matej
Int. J. Mol. Sci. 2024, 25(17), 9689; https://doi.org/10.3390/ijms25179689 - 7 Sep 2024
Viewed by 484
Abstract
The amyloid cascade hypothesis postulates that extracellular deposits of amyloid β (Aβ) are the primary and initial cause leading to the full development of Alzheimer’s disease (AD) with intracellular neurofibrillary tangles; however, the details of this mechanism have not been fully described until [...] Read more.
The amyloid cascade hypothesis postulates that extracellular deposits of amyloid β (Aβ) are the primary and initial cause leading to the full development of Alzheimer’s disease (AD) with intracellular neurofibrillary tangles; however, the details of this mechanism have not been fully described until now. Our preliminary data, coming from our day-to-day neuropathology practice, show that the primary location of the hyperphosphorylated tau protein is in the vicinity of the cell membrane of dystrophic neurites. This observation inspired us to formulate a hypothesis that presumes an interaction between low-density lipoprotein receptor-related protein 1 (LRP1) and fibrillar aggregates of, particularly, Aβ42 anchored at the periphery of neuritic plaques, making internalization of the LRP1-Aβ42 complex infeasible and, thus, causing membrane dysfunction, leading to the tauopathy characterized by intracellular accumulation and hyperphosphorylation of the tau protein. Understanding AD as a membrane dysfunction tauopathy may draw attention to new treatment approaches not only targeting Aβ42 production but also, perhaps paradoxically, preventing the formation of LRP1-Aβ42. Full article
(This article belongs to the Special Issue Neurodegenerative Diseases: New Insights into Mechanisms, Prevention, Markers, and Therapeutic Targets)
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