Pathological Mechanisms and Therapeutic Strategies of Alzheimer’s Disease

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

Deadline for manuscript submissions: 20 August 2026 | Viewed by 339

Special Issue Editors


E-Mail Website
Guest Editor
Department of Pharmacology and Neuroscience, School of Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA
Interests: Alzheimer’s disease; clinical trials; dementia; pharmacology; translational neuroscience

E-Mail Website
Guest Editor
Department of Mathematics and Statistics, Texas Tech University, 2500 Broadway, Lubbock, TX 79409, USA
Interests: translational mathematical modeling; scientific machine learning; neurodegenerative disorders; metabolic disorders

E-Mail Website
Guest Editor
Neurobiology of Nutrition Laboratory, Department of Nutritional Sciences, College of Health & Human Sciences, Texas Tech University, 2500 Broadway, Lubbock, TX 79409, USA
Interests: brain metabolism; diabetes; metabolic disorders; neurodegenerative disorders; nutrition

Special Issue Information

Dear Colleagues,

Despite the approval of the first disease-modifying therapies by many international regulatory agencies, Alzheimer’s disease (AD) remains incurable while its incidence continuously increases. The amyloid cascade hypothesis has been extensively investigated in the past three decades, but the therapeutic interventions derived from these investigations have yielded modest results. Therefore, there is an urgent need to explore in-depth other existing and novel pathological mechanisms and therapeutic strategies to finally reach a point where cognitive decline and the underlying neuropathology stop, or reverse, in patients affected by this progressive neurodegenerative disease. For the present Special Issue of the journal Cells, we invite scientists from all over the world to submit manuscripts, including reviews, focused on Alzheimer’s pathological mechanisms and (novel) therapeutic strategies in the broad sense, both in human and pre-clinical models of AD. Articles on pathologies can report on amyloid and non-amyloid topics, including the emerging role of the gut–brain axis disturbances, underlying inflammatory conditions, neurotransmitter imbalances, or any other abnormal condition that could be involved in the neuropathogenesis or progression of AD. Articles on the modeling of Alzheimer’s pathology are also welcome. Reports on therapeutic interventions can describe pre-clinical and observational clinical studies or clinical trials using drugs, devices (ex. deep brain stimulation, transcranial ultrasound, magnetic, electrical stimulation),  with or without combination of biomarker assessments, provided there is a focus on cellular mechanisms.

All articles submitted to this Special Issue will be assessed by our team of Guest Editors and, if fitting the topics of interest, peer-reviewed by specialists in the corresponding field of research.

Dr. Boris DeCourt
Dr. Travis Thompson
Dr. Andrew C. Shin
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Alzheimer’s disease
  • amyloid beta
  • biomarkers
  • gut-brain axis
  • mechanisms
  • neurotransmitter imbalance
  • pathology
  • tau
  • treatments

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

25 pages, 1839 KB  
Review
Mitochondrial Dysfunction in Alzheimer’s Disease and Mitochondria-Targeted Therapeutics
by Jasbir Bisht, Priyanka Rawat, Andrew C. Shin and Vijay Hegde
Cells 2026, 15(11), 990; https://doi.org/10.3390/cells15110990 - 28 May 2026
Abstract
Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by progressive cognitive decline due to the loss of neurons. The accumulation of extracellular senile plaques (Aβ) and intracellular tau neurofibrillary tangles (NFTs) is a key pathological feature of AD. [...] Read more.
Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by progressive cognitive decline due to the loss of neurons. The accumulation of extracellular senile plaques (Aβ) and intracellular tau neurofibrillary tangles (NFTs) is a key pathological feature of AD. Mitochondrial dysfunction is implicated in all key AD pathologies, whether as a cause or a consequence of disease progression. Growing evidence indicates that mitochondrial impairment plays a central role in AD pathogenesis by disrupting cellular homeostasis, promoting oxidative stress, and contributing to progressive neuronal death. Therefore, targeting mitochondria may offer promising insights into the development of disease-modifying therapies. In this review, we summarize current evidence on the role of mitochondrial dysfunction in the pathophysiology of AD and on its therapeutic potential. Full article
Show Figures

Figure 1

Back to TopTop