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New Insights of Biomarkers in Neurodegenerative Diseases
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New Insights of Biomarkers in Neurodegenerative Diseases

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: 20 June 2025 | Viewed by 8716

Special Issue Editor

Dr. Ioannis Liampas

E-Mail Website
Guest Editor
Department of Neurology, Faculty of Medicine, University of Thessaly, Volos, Greece
Interests: dementia; Alzheimer’s disease; cognitive impairment; cognitive decline; neuropsychiatric manifestations
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Biomarkers are objectively measured biological indices of normal or pathogenic biological processes. They are associated with specific clinical endpoints: e.g., diagnostic biomarkers reflect the clinical state of an individual (whether a person has a particular disease or not), susceptibility biomarkers measure the risk of developing a disorder, prognostic biomarkers are used to determine disease progression, predictive biomarkers are utilized to identify potential responders to specific interventions, and so on. Occasionally, given their well-established clinical relevance, biomarkers are used as substitute endpoints, instead of clinical outcomes. Biological markers are considered to play an important role in clinical research and practice. In the context of neurogenerative disorders, they are necessary to improve the identification of individuals at high-risk of developing a condition and the diagnostic accuracy and categorization of patients. Currently, among neurodegenerative disorders, biomarkers specific for Alzheimer’s disease have been studied more rigorously. This collection aims to cover the most recent advances in the field of biomarkers for neurodegenerative disorders. Any types of manuscripts supported by the Journal—original research articles, brief reports, communications, narrative reviews, systematic reviews, and meta-analyses - pertaining to this topic are welcome. Potential topics include, but are not limited to: Imaging, CSF, blood and urine-based biomarkers; Clinical relevance of biomarkers; Potential use and limitations of current biomarkers; Biomarkers as surrogate endpoints; Biomarkers in drug development; Biological and clinical markers.

Dr. Ioannis Liampas
Guest Editor

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Keywords

  •  amyloid-β
  •  tau phosphorylated
  •  tau
  •  GFAP
  •  neurofilaments
  •  TDP-43
  •  progranulin
  •  a-synuclein
  •  magnetic resonance imaging
  •  positron emission tomography
  •  dopamine transporter scan

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Published Papers (5 papers)

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19 pages, 5458 KiB  
Article
Differentially Expressed Genes in Rat Brain Regions with Different Degrees of Ischemic Damage
by Ivan B. Filippenkov, Yana Yu. Shpetko, Vasily V. Stavchansky, Alina E. Denisova, Vadim V. Yuzhakov, Natalia K. Fomina, Leonid V. Gubsky, Svetlana A. Limborska and Lyudmila V. Dergunova
Int. J. Mol. Sci. 2025, 26(5), 2347; https://doi.org/10.3390/ijms26052347 - 6 Mar 2025
Viewed by 651
Abstract
Ischemic stroke is a multifactorial disease that leads to brain tissue damage and severe neurological deficit. Transient middle cerebral artery occlusion (tMCAO) models are actively used for the molecular, genetic study of stroke. Previously, using high-throughput RNA sequencing (RNA-Seq), we revealed 3774 differentially [...] Read more.
Ischemic stroke is a multifactorial disease that leads to brain tissue damage and severe neurological deficit. Transient middle cerebral artery occlusion (tMCAO) models are actively used for the molecular, genetic study of stroke. Previously, using high-throughput RNA sequencing (RNA-Seq), we revealed 3774 differentially expressed genes (DEGs) in the penumbra-associated region of the frontal cortex (FC) of rats 24 h after applying the tMCAO model. Here, we studied the gene expression pattern in the striatum that contained an ischemic focus. Striatum samples were obtained from the same rats from which we previously obtained FC samples. Therefore, we compared DEG profiles between two rat brain tissues 24 h after tMCAO. Tissues were selected based on magnetic resonance imaging (MRI) and histological examination (HE) data. As a result, 4409 DEGs were identified 24 h after tMCAO in striatum. Among them, 2609 DEGs were overlapped in the striatum and FC, whereas more than one thousand DEGs were specific for each studied tissue. Furthermore, 54 DEGs exhibited opposite changes at the mRNA level in the two brain tissues after tMCAO. Thus, the spatial regulation of the ischemic process in the ipsilateral hemisphere of rat brain at the transcriptome level was revealed. We believe that the targeted adjustment of the genome responses identified can be the key for the induction of regeneration processes in brain cells after stroke. Full article
(This article belongs to the Special Issue New Insights of Biomarkers in Neurodegenerative Diseases)
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17 pages, 1947 KiB  
Article
Influence of Physiological Variables and Comorbidities on Plasma Aβ40, Aβ42, and p-tau181 Levels in Cognitively Unimpaired Individuals
by Francisco Martínez-Dubarbie, Armando Guerra-Ruiz, Sara López-García, Juan Irure-Ventura, Carmen Lage, Marta Fernández-Matarrubia, Ana Pozueta-Cantudo, María García-Martínez, Andrea Corrales-Pardo, María Bravo, Juan Martín-Arroyo, Jon Infante, Marcos López-Hoyos, María Teresa García-Unzueta, Pascual Sánchez-Juan and Eloy Rodríguez-Rodríguez
Int. J. Mol. Sci. 2024, 25(3), 1481; https://doi.org/10.3390/ijms25031481 - 25 Jan 2024
Cited by 7 | Viewed by 1882
Abstract
Plasma biomarkers for Alzheimer’s disease (AD) are a promising tool that may help in early diagnosis. However, their levels may be influenced by physiological parameters and comorbidities that should be considered before they can be used at the population level. For this purpose, [...] Read more.
Plasma biomarkers for Alzheimer’s disease (AD) are a promising tool that may help in early diagnosis. However, their levels may be influenced by physiological parameters and comorbidities that should be considered before they can be used at the population level. For this purpose, we assessed the influences of different comorbidities on AD plasma markers in 208 cognitively unimpaired subjects. We analyzed both plasma and cerebrospinal fluid levels of Aβ40, Aβ42, and p-tau181 using the fully automated Lumipulse platform. The relationships between the different plasma markers and physiological variables were studied using linear regression models. The mean differences in plasma markers according to comorbidity groups were also studied. The glomerular filtration rate showed an influence on plasma Aβ40 and Aβ42 levels but not on the Aβ42/Aβ40 ratio. The amyloid ratio was significantly lower in diabetic and hypertensive subjects, and the mean p-tau181 levels were higher in hypertensive subjects. The glomerular filtration rate may have an inverse relationship on plasma Aβ40 and Aβ42 levels but not on the amyloid ratio, suggesting that the latter is a more stable marker to use in the general population. Cardiovascular risk factors might have a long-term effect on the amyloid ratio and plasma levels of p-tau181. Full article
(This article belongs to the Special Issue New Insights of Biomarkers in Neurodegenerative Diseases)
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12 pages, 1292 KiB  
Article
Objective Physical Function in the Alzheimer’s Disease Continuum: Association with Cerebrospinal Fluid Biomarkers in the ALBION Study
by Stefanos N. Sampatakakis, Eirini Mamalaki, Eva Ntanasi, Faidra Kalligerou, Ioannis Liampas, Mary Yannakoulia, Antonios N. Gargalionis and Nikolaos Scarmeas
Int. J. Mol. Sci. 2023, 24(18), 14079; https://doi.org/10.3390/ijms241814079 - 14 Sep 2023
Cited by 1 | Viewed by 2547
Abstract
Cognitive and physical decline, both indicators of aging, seem to be associated with each other. The aim of the present study was to investigate whether physical function parameters (walking time and handgrip strength) are related to cerebrospinal fluid (CSF) biomarkers (amyloid-beta Aβ42 [...] Read more.
Cognitive and physical decline, both indicators of aging, seem to be associated with each other. The aim of the present study was to investigate whether physical function parameters (walking time and handgrip strength) are related to cerebrospinal fluid (CSF) biomarkers (amyloid-beta Aβ42, Tau, PhTau) in individuals in the Alzheimer’s disease (AD) continuum. The sample was drawn from the Aiginition Longitudinal Biomarker Investigation of Neurodegeneration study, comprising 163 individuals aged 40–75 years: 112 cognitively normal (CN) and 51 with mild cognitive impairment (MCI). Physical function parameters were measured at baseline, a lumbar puncture was performed the same day and CSF biomarkers were analyzed using automated methods. The association between walking time, handgrip strength and CSF biomarkers was evaluated by linear correlation, followed by multivariate linear regression models adjusted for age, sex, education and APOEe4 genotype. Walking time was inversely related to CSF Aβ42 (lower CSF values correspond to increased brain deposition) in all participants (p < 0.05). Subgroup analysis showed that this association was stronger in individuals with MCI and participants older than 60 years old, a result which remained statistically significant after adjustment for the aforementioned confounding factors. These findings may open new perspectives regarding the role of mobility in the AD continuum. Full article
(This article belongs to the Special Issue New Insights of Biomarkers in Neurodegenerative Diseases)
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9 pages, 1953 KiB  
Case Report
Chronic Central Nervous System Graft-Versus-Host Disease to Unravel Progressive Visual Loss and Ischemic Stroke Recurrence Post-Allogeneic Hematopoietic Stem Cell Transplant: A Case Report
by Francesco Crescenzo, Alessandra Danese, Francesco Dall’Ora and Michelangelo Turazzini
Int. J. Mol. Sci. 2025, 26(5), 2289; https://doi.org/10.3390/ijms26052289 - 4 Mar 2025
Cited by 1 | Viewed by 776
Abstract
Chronic graft-versus-host disease (cGVHD) is a prognostically negative event following hematopoietic stem cell transplant (HSCT). While cGVHD mainly affects the muscles, skin, oral mucosa, eyes, lungs, gastrointestinal tract, and liver, central nervous system (CNS) involvement remains possible and, moreover, is rare when it [...] Read more.
Chronic graft-versus-host disease (cGVHD) is a prognostically negative event following hematopoietic stem cell transplant (HSCT). While cGVHD mainly affects the muscles, skin, oral mucosa, eyes, lungs, gastrointestinal tract, and liver, central nervous system (CNS) involvement remains possible and, moreover, is rare when it occurs isolated. CNS-cGVHD can manifest with a wide spectrum of CNS disorders, including cerebrovascular diseases, autoimmune demyelinating diseases, and immune-mediated encephalitis. We present a case of 65-year-old man previously treated with HSCT presenting with progressive cerebrovascular disorder and optic neuropathy without any clear alternative causal processes except for immune-mediated CNS microangiopathy in the context of possible CNS-cGVHD, along with suggestive imaging and instrumental and laboratory findings. Starting one year after HSCT for acute myeloid leukemia, when the first cerebral ischemic event occurred and was then associated with a reduction in visual acuity, an extensive diagnostic work-up had remained inconclusive over many years, leading us to the hypothesis of CNS-cGVHD and, therefore, to the start of immunosuppressive therapy. Our experience highlighted not ignoring the possibility of cGVHD as the underlying mechanism of CNS disorder, even in the absence of other systemic presentations, once more common etiologies of CNS pathological processes have been ruled out. Full article
(This article belongs to the Special Issue New Insights of Biomarkers in Neurodegenerative Diseases)
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66 pages, 14003 KiB  
Perspective
ACH2.0/E, the Consolidated Theory of Conventional and Unconventional Alzheimer’s Disease: Origins, Progression, and Therapeutic Strategies
by Vladimir Volloch and Sophia Rits-Volloch
Int. J. Mol. Sci. 2024, 25(11), 6036; https://doi.org/10.3390/ijms25116036 - 30 May 2024
Cited by 2 | Viewed by 1840
Abstract
The centrality of amyloid-beta (Aβ) is an indisputable tenet of Alzheimer’s disease (AD). It was initially indicated by the detection (1991) of a mutation within Aβ protein precursor (AβPP) segregating with the disease, which served as a basis for the long-standing Amyloid Cascade [...] Read more.
The centrality of amyloid-beta (Aβ) is an indisputable tenet of Alzheimer’s disease (AD). It was initially indicated by the detection (1991) of a mutation within Aβ protein precursor (AβPP) segregating with the disease, which served as a basis for the long-standing Amyloid Cascade Hypothesis (ACH) theory of AD. In the intervening three decades, this notion was affirmed and substantiated by the discovery of numerous AD-causing and AD-protective mutations with all, without an exception, affecting the structure, production, and intraneuronal degradation of Aβ. The ACH postulated that the disease is caused and driven by extracellular Aβ. When it became clear that this is not the case, and the ACH was largely discredited, a new theory of AD, dubbed ACH2.0 to re-emphasize the centrality of Aβ, was formulated. In the ACH2.0, AD is caused by physiologically accumulated intraneuronal Aβ (iAβ) derived from AβPP. Upon reaching the critical threshold, it triggers activation of the autonomous AβPP-independent iAβ generation pathway; its output is retained intraneuronally and drives the AD pathology. The bridge between iAβ derived from AβPP and that generated independently of AβPP is the neuronal integrated stress response (ISR) elicited by the former. The ISR severely suppresses cellular protein synthesis; concurrently, it activates the production of a small subset of proteins, which apparently includes components necessary for operation of the AβPP-independent iAβ generation pathway that are absent under regular circumstances. The above sequence of events defines “conventional” AD, which is both caused and driven by differentially derived iAβ. Since the ISR can be elicited by a multitude of stressors, the logic of the ACH2.0 mandates that another class of AD, referred to as “unconventional”, has to occur. Unconventional AD is defined as a disease where a stressor distinct from AβPP-derived iAβ elicits the neuronal ISR. Thus, the essence of both, conventional and unconventional, forms of AD is one and the same, namely autonomous, self-sustainable, AβPP-independent production of iAβ. What distinguishes them is the manner of activation of this pathway, i.e., the mode of causation of the disease. In unconventional AD, processes occurring at locations as distant from and seemingly as unrelated to the brain as, say, the knee can potentially trigger the disease. The present study asserts that these processes include traumatic brain injury (TBI), chronic traumatic encephalopathy, viral and bacterial infections, and a wide array of inflammatory conditions. It considers the pathways which are common to all these occurrences and culminate in the elicitation of the neuronal ISR, analyzes the dynamics of conventional versus unconventional AD, shows how the former can morph into the latter, explains how a single TBI can hasten the occurrence of AD and why it takes multiple TBIs to trigger the disease, and proposes the appropriate therapeutic strategies. It posits that yet another class of unconventional AD may occur where the autonomous AβPP-independent iAβ production pathway is initiated by an ISR-unrelated activator, and consolidates the above notions in a theory of AD, designated ACH2.0/E (for expanded ACH2.0), which incorporates the ACH2.0 as its special case and retains the centrality of iAβ produced independently of AβPP as the driving agent of the disease. Full article
(This article belongs to the Special Issue New Insights of Biomarkers in Neurodegenerative Diseases)
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