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Targeted Diagnosis and Treatment of Dementia: Current Concepts and New Horizons

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Mental Health".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3063

Special Issue Editor

Dr. Eli Wertman

E-Mail Website
Guest Editor
1. Department of Neurology, Section of Neuropsychology, Hadassah University Hospital, Jerusalem, Israel
2. Department of Psychology, The Hebrew University, Jerusalem, Israel
Interests: dementia; predementia; pre-dementia

Special Issue Information

Dear Colleagues,

This Special Issue, titled “Targeted Diagnosis and Treatment of Dementia: Current Concepts and New Horizons”, presents a comprehensive review that focuses on targeted aspects of diagnosing and treating dementia and their relevant issues. Dementia is a complex disorder that is characterized by cognitive decline, behavioral changes, and functional impairments, which heavily impacts patients, their caregivers, and socioeconomic domains. Recent clinical and biological research have opened up new horizons for alleviating the pain felt by patients and reducing the costs of dementia. This review will discuss state-of-the-art findings, emerging domains, and future directions, e.g., the diagnostic tools and criteria relevant to clinical practice, including cognitive, behavioral, and functional assessments, neuroimaging techniques, and the contribution from biomarkers towards a diagnosis. It will also explore the current treatment options that are available, such as pharmacological and non-pharmacological interventions, supportive care strategies, and dynamic pre-symptomatic and para-symptomatic prevention . Developing concepts in highly prevalent  late-onset dementia will include its high multimorbidity, multisyndromal presentation, heterogeneity, the interaction between its behavioral, neurological, neuropsychological, psychiatric, geriatric, systemic, and social components, and its complex effect on diagnostic approaches, treatment, case management, and potential remediability. Relevant pathophysiological models, emerging disease-modifying treatments, and future directions of research are welcome. This review aims to help in consolidating the essential and appropriate steps for diagnostic work-up, treatment decisions, and follow-up.

Dr. Eli Wertman
Guest Editor

Manuscript Submission Information

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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. Journal of Clinical Medicine 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 2600 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

  • dementia
  • pre-dementia
  • diagnosis
  • targeted therapies
  • cognitive assessment
  • behavioral syndromes neuroimaging
  • multimorbidity
  • pharmacological interventions
  • non-pharmacological approaches
  • case management
  • supportive care
  • remediability

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Published Papers (3 papers)

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16 pages, 2372 KiB  
Article
Cognitive Functioning in Toxic Oil Syndrome Survivors: A Case-Control Study Four Decades After the Epidemic
by José Lapeña-Motilva, Mariano Ruiz-Ortiz, Glen M. Doniger, María Antonia Nogales, Verónica Giménez de Bejar, Sonia Álvarez-Sesmero, Montserrat Morales, Fernando Bartolomé, Carolina Alquézar, Durjoy Lahiri, Cecilia García-Cena and Julián Benito-León
J. Clin. Med. 2025, 14(11), 3746; https://doi.org/10.3390/jcm14113746 - 27 May 2025
Abstract
Background: Toxic oil syndrome (TOS) was a major food-borne epidemic that occurred in Spain in May 1981, caused by the ingestion of rapeseed oil adulterated with aniline. While the somatic sequelae of TOS have been well documented, its long-term cognitive consequences remain poorly [...] Read more.
Background: Toxic oil syndrome (TOS) was a major food-borne epidemic that occurred in Spain in May 1981, caused by the ingestion of rapeseed oil adulterated with aniline. While the somatic sequelae of TOS have been well documented, its long-term cognitive consequences remain poorly understood more than four decades after exposure. Methods: In this case-control study, 50 individuals with clinically confirmed TOS were compared to 50 healthy controls matched for age, sex, and education. All participants completed a comprehensive neuropsychological assessment, along with questionnaires evaluating fatigue, anxiety, depression, and health-related quality of life. Multivariate regression models were adjusted for demographic and vascular risk factors, as well as for mood symptoms, fatigue, and use of central nervous system-acting medications. Structural equation modeling was used to explore the potential mediating effects of affective and fatigue symptoms on cognitive performance. Results: TOS survivors showed significantly poorer performance than controls in attention, executive function, processing speed, and global cognition after adjusting for demographic and vascular risk factors. However, these differences were no longer statistically significant after additional adjustment for fatigue, depression, anxiety, and central nervous system-acting medications. Structural equation modeling analyses revealed that affective symptoms—particularly fatigue—substantially mediated the relationship between TOS and cognitive performance. Conclusions: The cognitive profile observed mirrors that of disorders characterized by subcortical dysfunction and impaired neural connectivity, such as multiple sclerosis and vascular cognitive impairment. Although early postmortem studies in TOS did not demonstrate overt white matter lesions, our findings raise the possibility of long-lasting alterations involving both white and gray matter networks. These results emphasize the need to consider mood and fatigue symptoms when evaluating cognition in TOS survivors and point to the potential for widespread, enduring neurobiological effects stemming from the original toxic exposure. Full article
(This article belongs to the Special Issue Targeted Diagnosis and Treatment of Dementia: Current Concepts and New Horizons)
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30 pages, 1179 KiB  
Article
Relationship Between Depression and Decreased Activity Level and Cognitive Impairment in Patients with Diabetes Mellitus Type 2 and/or Atrial Fibrillation
by Marius Militaru, Daniel Florin Lighezan, Cristina Tudoran, Flavia Zara, Adina Bucur and Anda Gabriela Militaru
J. Clin. Med. 2025, 14(2), 563; https://doi.org/10.3390/jcm14020563 - 16 Jan 2025
Viewed by 1003
Abstract
Background: The interdependence between type 2 diabetes mellitus (DM-2), atrial fibrillation (AF), and cognitive decline (CD)/dementia is a debated topic. In this study, we highlighted the influence of DM-2 and FA individually and in association on the severity of CD/dementia. Methods: This study [...] Read more.
Background: The interdependence between type 2 diabetes mellitus (DM-2), atrial fibrillation (AF), and cognitive decline (CD)/dementia is a debated topic. In this study, we highlighted the influence of DM-2 and FA individually and in association on the severity of CD/dementia. Methods: This study comprises 248 patients with very high cardiovascular risk (VHCVR) according to Systematic Coronary Risk Evaluation (SCORE2), of whom 184 had DM-2 and/or AF, and 64 were age-matched controls (without DM-2/AF), admitted to the Municipal Hospital Timisoara. Results: Mini-Mental-State-Examination (MMSE), Montreal Cognitive Assessment (MoCA), Activities of Daily Living Score (ADL), and Instrumental Activities of Daily Living Score (IADL) were significantly decreased, and Geriatric Depression Scale (GDS-15) increased in patients with DM-2 and AF in comparison to controls (p < 0.05), with the subjects with DM-2 and AF having more severe CD compared to those with only one of these two pathologies. The logistic regression model showed that the risk of CD (MMSE < 27) or dementia (MMSE < 24) increased significantly in patients with DM-2 and/or AF depending on the SCORE2 values, ADL, and GDS-15. In DM-2 and/or AF patients, an increase of 1% in SCORE2 was associated with an elevation of 2.40% in the odds of CD and of 4.30% of dementia. In these patients, depression (GDS score) increased the risk of CD by 36.3%, and if ADL improved, the risk of CD decreased by 44.0%. Conclusions: Our findings suggest a direct association between CD, DM-2, and AF with SCORE2, cognitive parameters, ADL, and depression. In patients with DM-2 and/or AF, it is important to identify subclinical CD to prevent the evolution to dementia. Full article
(This article belongs to the Special Issue Targeted Diagnosis and Treatment of Dementia: Current Concepts and New Horizons)
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10 pages, 224 KiB  
Commentary
Neuroinflammation: A Driving Force in the Onset and Progression of Alzheimer’s Disease
by Campbell Long, Arianne Fritts, Jessica Broadway, Olga Brawman-Mintzer and Jacobo Mintzer
J. Clin. Med. 2025, 14(2), 331; https://doi.org/10.3390/jcm14020331 - 8 Jan 2025
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Abstract
Background/Objectives: The goal of this commentary is to highlight several key components of the inflammatory process as it relates to amyloid toxicity in Alzheimer’s disease (AD), including the role of neuroinflammatory factors and peripheral inflammatory events. Methods: Google Scholar and PubMed [...] Read more.
Background/Objectives: The goal of this commentary is to highlight several key components of the inflammatory process as it relates to amyloid toxicity in Alzheimer’s disease (AD), including the role of neuroinflammatory factors and peripheral inflammatory events. Methods: Google Scholar and PubMed were used to find articles with the following keywords: Alzheimer’s disease, amyloids, neuroinflammation, peripheral inflammation, microglia, cytokines, and treatments. Sources that were case reports, not peer-reviewed, or older than 30 years were excluded. Abstracts were reviewed first for their relevance before the full text was considered. Methods sections were reviewed to ensure the interventional papers included were randomized controlled trials, meta-analyses, or systematic reviews; however, several literature reviews were also included due to the relevance of their background information. Results: Based on the literature review, we chose to concentrate on microglia, cytokine signaling, and peripheral inflammation markers. We found that microglia activation and subsequent microglia-driven inflammation play a pivotal role in the pathomechanism of AD. Additionally, cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a) appear to contribute to amyloid accumulation and cell damage. Finally, the increased permeability of the blood–brain barrier (BBB) allows for the peripheral inflammatory process to contribute to the inflammation of the central nervous system (CNS) and amyloid-beta (Aβ) accumulation. Conclusions: Current evidence suggests that the immune system plays a pivotal role in the pathogenesis of AD, both in the CNS and the periphery. Full article
(This article belongs to the Special Issue Targeted Diagnosis and Treatment of Dementia: Current Concepts and New Horizons)
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