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Research in Alzheimer’s Disease: Advances and Perspectives
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Research in Alzheimer’s Disease: Advances and Perspectives

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2026 | Viewed by 4228

Special Issue Editor

Dr. Silvia Boschi

E-Mail Website
Guest Editor
Aging Brain and Memory Clinic, Department of Neuroscience, “Rita Levi Montalcini”, Memory Clinic, University of Torino, Via Cherasco 15, 10126 Turin, Italy
Interests: Alzheimer’s disease; dementia; neurodegeneration; neuronal biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Contemporary research into Alzheimer’s disease (AD) is increasingly focusing on elucidating its molecular intricacies. At the molecular level, AD is distinguished by the aggregation of amyloid-beta peptides and hyperphosphorylated tau proteins, resulting in the formation of insoluble plaques and neurofibrillary tangles, respectively. This pathological hallmark disrupts neuronal function, synaptic transmission, and, ultimately, cognitive abilities. Molecular investigations aim to elucidate the precise mechanisms governing the synthesis, clearance, and cytotoxicity of these proteins, as well as their interactions with cellular processes such as inflammation, oxidative stress, and mitochondrial dysfunction. Moreover, genetic studies have pinpointed risk variants associated with AD, shedding light on the molecular pathways implicated in disease pathogenesis. By leveraging advanced molecular techniques, including genome editing, proteomics, and high-resolution imaging, researchers strive to decipher the molecular underpinnings of AD progression. Insights derived from these efforts hold promise for the development of targeted therapies aimed at arresting or reversing molecular aberrations, thus offering prospects for efficacious interventions in the battle against AD.

Dr. Silvia Boschi
Guest Editor

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Keywords

  • neuroinflammation
  • synaptic dysfunction
  • oxidative stress
  • neurofibrillary tangles
  • mitochondrial dysfunction
  • biomarkers

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Published Papers (4 papers)

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Research

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12 pages, 2126 KB  
Article
Early Molecular Biomarkers in an Amyloid-β-Induced Rat Model of Alzheimer’s Disease: Effects of Kelulut Honey
by Ammara Shaikh, Fairus Ahmad, Jayakumar Murthy, Seong Lin Teoh and Mohamad Fairuz Yahaya
Int. J. Mol. Sci. 2026, 27(2), 1059; https://doi.org/10.3390/ijms27021059 - 21 Jan 2026
Viewed by 126
Abstract
Alzheimer’s disease (AD) is the leading cause of dementia worldwide, characterized by progressive neurodegeneration and cognitive decline. Early diagnosis remains critical for enabling timely intervention. However, detecting the earliest pathological changes is challenging due to the limited availability of reliable biomarkers that reflect [...] Read more.
Alzheimer’s disease (AD) is the leading cause of dementia worldwide, characterized by progressive neurodegeneration and cognitive decline. Early diagnosis remains critical for enabling timely intervention. However, detecting the earliest pathological changes is challenging due to the limited availability of reliable biomarkers that reflect early disease pathology in experimental models. This study evaluated molecular markers associated with AD-related processes in a rat model inoculated with human amyloid β (Aβ)1-42 peptides. We assessed the levels of biomarkers: Aβ1-42, Aβ42, phosphorylated tau, monocyte chemoattractant protein-1 (MCP-1), nuclear factor kappa B (NF-κB p65) and superoxide dismutase 1 (SOD1) in hippocampal tissue and serum using enzyme-linked immunosorbent assay. A treatment group receiving Kelulut honey was included to evaluate biomarker responsiveness. Results showed significant elevation in hippocampal Aβ1-42 and phosphorylated tau in diseased rats, with changes in inflammatory markers MCP-1 and NF-κB p65, whereas no significant change was observed in oxidative stress marker SOD1. Serum levels of Aβ1-42 and MCP-1 did not differ significantly between groups, indicating limited peripheral sensitivity after a month of disease induction. These findings suggest that amyloid-, tau-, and inflammation-related markers in hippocampal tissue may be informative for early pathological changes in this acute model, while serum markers showed limited sensitivity. Full article
(This article belongs to the Special Issue Research in Alzheimer’s Disease: Advances and Perspectives)
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16 pages, 2274 KB  
Article
Plasma Protein Panel for Assessing the Risk of Alzheimer’s Disease by MRM-MS Analysis: The Study of Two Independent Clinical Cohorts
by Polina A. Strelnikova, Alexey S. Kononikhin, Natalia V. Zakharova, Anna E. Bugrova, Maria I. Indeykina, Yana B. Fedorova, Igor V. Kolykhalov, Anna Y. Morozova, Alisa V. Andryushchenko, Elena D. Fedoseeva, Marina A. Emelyanova, Dmitry A. Gryadunov, Svetlana I. Gavrilova, Vladimir A. Mitkevich, George P. Kostyuk, Yulia A. Chaika, Alexander A. Makarov and Evgeny N. Nikolaev
Int. J. Mol. Sci. 2026, 27(1), 15; https://doi.org/10.3390/ijms27010015 - 19 Dec 2025
Viewed by 743
Abstract
Early recognition of a risk of Alzheimer’s disease (AD) remains a global challenge, and blood proteomic markers are of particular interest for wide-scale diagnostic use. Quantitative multiple reaction monitoring (MRM) approach demonstrates good reproducibility in the characteristic changes in the levels of reported [...] Read more.
Early recognition of a risk of Alzheimer’s disease (AD) remains a global challenge, and blood proteomic markers are of particular interest for wide-scale diagnostic use. Quantitative multiple reaction monitoring (MRM) approach demonstrates good reproducibility in the characteristic changes in the levels of reported candidate biomarkers (CBs) in different cohorts in AD. Following up on our previous study, we performed a joint analysis of 331 blood plasma samples from two different clinical cohorts of participants, comprising a total of 95 samples from patients with AD, 136 samples from patients with mild cognitive impairment (MCI), and 100 samples from controls. The obtained results confirm the significance of 37 CBs. A logistic regression-based algorithm was used to build protein classifiers, and a total of 21 important proteins were selected, 13 of which (ORM1, APOA4, LBP, HP, FN1, BCHE, APOE, PZP, A1BG, TF, SERPINA7, TTR, and F12) formed a universal panel that demonstrated strong classification performance in distinguishing AD patients from controls (ROC-AUC = 0.90) and in separating stable and progressing patients with MCI (ROC-AUC = 0.81). Overall, the analysis confirms the high potential of the MRM method for validating CBs in independent cohorts. Full article
(This article belongs to the Special Issue Research in Alzheimer’s Disease: Advances and Perspectives)
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18 pages, 2990 KB  
Article
Early Dysregulation of RNA Splicing and Translation Processes Are Key Markers from Mild Cognitive Impairment to Alzheimer’s Disease: An In Silico Transcriptomic Analysis
by Simone D’Angiolini, Agnese Gugliandolo, Gabriella Calì and Luigi Chiricosta
Int. J. Mol. Sci. 2025, 26(15), 7303; https://doi.org/10.3390/ijms26157303 - 28 Jul 2025
Viewed by 1214
Abstract
About one billion people worldwide are affected by neurologic disorders. Among the various neurologic disorders, one of the most common is Alzheimer’s disease (AD). AD is a neurodegenerative disorder that progressively affects cognitive functions, disrupting the daily lives of millions of individuals. Mild [...] Read more.
About one billion people worldwide are affected by neurologic disorders. Among the various neurologic disorders, one of the most common is Alzheimer’s disease (AD). AD is a neurodegenerative disorder that progressively affects cognitive functions, disrupting the daily lives of millions of individuals. Mild cognitive impairment (MCI) is often considered a prodromal stage of Alzheimer’s disease. In this article, we retrieved data from the online available dataset GSE63060, which includes transcriptomic data of 329 blood samples, of which there are 104 cognitively normal controls, 80 MCI patients, and 145 AD patients. We used transcriptomic data related to all three groups to perform an over-representation analysis of the gene ontologies followed by a network analysis. The aim of our study is to pinpoint alterations, detectable through a non-invasive method, in biological processes affected in MCI that persist during AD. Our goal is to uncover transcriptomic changes that could support earlier diagnosis and the development of more effective therapeutic strategies, starting from the early stages of the disease, to slow down or mitigate its progression. Our work provides a consistent picture of the transcriptomic unbalance of many genes strongly involved in ribosomal formation and biogenesis and splicing processes both in patients with MCI and with AD. Full article
(This article belongs to the Special Issue Research in Alzheimer’s Disease: Advances and Perspectives)
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Review

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20 pages, 1094 KB  
Review
UCH-L1 in Alzheimer’s Disease: A Crucial Player in Dementia-Associated Mechanisms
by Elisa Porchietto, Giulia Morello, Giulia Cicilese, Innocenzo Rainero, Elisa Rubino, Elena Tamagno, Silvia Boschi and Michela Guglielmotto
Int. J. Mol. Sci. 2025, 26(18), 9012; https://doi.org/10.3390/ijms26189012 - 16 Sep 2025
Cited by 1 | Viewed by 1688
Abstract
Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) is a critical deubiquitinating enzyme that is highly expressed in the central nervous system, where it participates in protein degradation and turnover as part of the ubiquitin–proteasome system (UPS). Convincing evidence supports the role of UCH-L1 dysfunction in [...] Read more.
Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1) is a critical deubiquitinating enzyme that is highly expressed in the central nervous system, where it participates in protein degradation and turnover as part of the ubiquitin–proteasome system (UPS). Convincing evidence supports the role of UCH-L1 dysfunction in several neurodegenerative disorders, given its unique position at the crossroad of several aetiopathogenic pathways, including those implicated in Alzheimer’s disease (AD) onset. Indeed, UCH-L1 depletion correlates with decreased levels of triggering receptor expressed on myeloid cells 2 (TREM2), with consequent effects on neuroinflammation. Notably, UCH-L1 can affect the level of phosphorylated tau protein, thus contributing to the formation of neurofibrillary tangles (NFTs). In addition, UCH-L1 influences β-Secretase 1 (BACE1) expression, resulting in the abnormal accumulation of amyloid-β plaques in brain parenchyma. These findings underline UCH-L1’s centrality in maintaining the homeostasis of protein folding and aggregation, which are significantly impaired in AD and AD-related dementias. Given these assumptions, UCH-L1 is recognized as a potential biomarker for AD, highlighting its relevance in governing the fate of crucial pathological mediators of cognitive impairment and neurodegeneration. Herein, we contextualize the involvement of UCH-L1 in different dementia-associated pathways and summarize the state of the art of UCH-L1 as a biomarker for AD diagnosis. Full article
(This article belongs to the Special Issue Research in Alzheimer’s Disease: Advances and Perspectives)
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