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Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies

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

Deadline for manuscript submissions: closed (1 August 2024) | Viewed by 23164

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Dr. Ines Moreno-Gonzalez

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1. Department of Cell Biology, Faculty of Sciences, University of Malaga, IBIMA, 29010 Malaga, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 29010 Malaga, Spain
3. Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77030, USA
Interests: Alzheimer's disease; neurodegeneratrive diseases; amyloid beta; tau; neuroinflammation; risk factors; transgenic animals; preclinical trials

Dr. Claudia Duran-Aniotz

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Guest Editor

Latin American Brain Health Institute (BrainLat), Center for Social and Cognitive Neuroscience (CSCN), Universidad Adolfo Ibanez, Santiago 7941169, Chile
Interests: biomarkers; dementia; neurodegeneration; Tau; amyloid

Dr. Joana A. Loureiro

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Guest Editor

1. LEPABE—Laboratory for Process Engineering, Environment, Biotechnology and Energy, R. Dr. Roberto Frias, 4200-465 Porto, Portugal
2. ALiCE—Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal
Interests: nanotechnology and interfacial phenomena; effects of fluorinated systems and peptides on the aggregation of amyloid beta peptides; conformational studies of protein and peptide self-organized systems and polymer surfaces; design and production of inorganic and polymeric nanosystems for pharmaceutical and food applications
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Dear Colleagues,

Alzheimer's disease (AD) is the most common form of dementia that accounts for around 50 million cases worldwide. Increasing life expectancy will triple this number by 2050. As long as we remain unable to reverse or prevent AD, its clinical, social, and economic burden will steadily increase hopelessly. The majority of AD cases are sporadic, indicating that the molecular mechanisms that trigger the late onset of the disease are still unknown. Currently, there is no definitive cure for AD, and current clinical interventions help to palliate some clinical symptoms. Prevention and modification of potential risk factors may reduce the probability of developing this type of dementia, but new and more effective therapeutic strategies are needed to prevent, slow down, or even halt the progression of the disease. This Special Issue aims to shed light on the recently described molecular mechanisms that are involved in Alzheimer's pathology, as well as collecting the latest advances in therapeutic interventions to combat this devastating condition.

Dr. Ines Moreno-Gonzalez
Dr. Claudia Duran-Aniotz
Prof. Dr. Joana A. Loureiro
Guest Editors

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Keywords

Alzheimer's disease
neurodegeneration
risk factors
therapy

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Published Papers (9 papers)

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17 pages, 1664 KiB

Open AccessArticle

Predicting Longitudinal Cognitive Decline and Alzheimer’s Conversion in Mild Cognitive Impairment Patients Based on Plasma Biomarkers

by Min-Koo Park, Jinhyun Ahn, Young-Ju Kim, Ji-Won Lee, Jeong-Chan Lee, Sung-Joo Hwang and Keun-Cheol Kim

Cells 2024, 13(13), 1085; https://doi.org/10.3390/cells13131085 - 22 Jun 2024

Viewed by 1661

Abstract

The increasing burden of Alzheimer’s disease (AD) emphasizes the need for effective diagnostic and therapeutic strategies. Despite available treatments targeting amyloid beta (Aβ) plaques, disease-modifying therapies remain elusive. Early detection of mild cognitive impairment (MCI) patients at risk for AD conversion is crucial, especially with anti-Aβ therapy. While plasma biomarkers hold promise in differentiating AD from MCI, evidence on predicting cognitive decline is lacking. This study’s objectives were to evaluate whether plasma protein biomarkers could predict both cognitive decline in non-demented individuals and the conversion to AD in patients with MCI. This study was conducted as part of the Korean Longitudinal Study on Cognitive Aging and Dementia (KLOSCAD), a prospective, community-based cohort. Participants were based on plasma biomarker availability and clinical diagnosis at baseline. The study included MCI (n = 50), MCI-to-AD (n = 21), and cognitively unimpaired (CU, n = 40) participants. Baseline plasma concentrations of six proteins—total tau (tTau), phosphorylated tau at residue 181 (pTau181), amyloid beta 42 (Aβ42), amyloid beta 40 (Aβ40), neurofilament light chain (NFL), and glial fibrillary acidic protein (GFAP)—along with three derivative ratios (pTau181/tTau, Aβ42/Aβ40, pTau181/Aβ42) were analyzed to predict cognitive decline over a six-year follow-up period. Baseline protein biomarkers were stratified into tertiles (low, intermediate, and high) and analyzed using a linear mixed model (LMM) to predict longitudinal cognitive changes. In addition, Kaplan–Meier analysis was performed to discern whether protein biomarkers could predict AD conversion in the MCI subgroup. This prospective cohort study revealed that plasma NFL may predict longitudinal declines in Mini-Mental State Examination (MMSE) scores. In participants categorized as amyloid positive, the NFL biomarker demonstrated predictive performance for both MMSE and total scores of the Korean version of the Consortium to Establish a Registry for Alzheimer’s Disease Assessment Packet (CERAD-TS) longitudinally. Additionally, as a baseline predictor, GFAP exhibited a significant association with cross-sectional cognitive impairment in the CERAD-TS measure, particularly in amyloid positive participants. Kaplan–Meier curve analysis indicated predictive performance of NFL, GFAP, tTau, and Aβ42/Aβ40 on MCI-to-AD conversion. This study suggests that plasma GFAP in non-demented participants may reflect baseline cross-sectional CERAD-TS scores, a measure of global cognitive function. Conversely, plasma NFL may predict longitudinal decline in MMSE and CERAD-TS scores in participants categorized as amyloid positive. Kaplan–Meier curve analysis suggests that NFL, GFAP, tTau, and Aβ42/Aβ40 are potentially robust predictors of future AD conversion. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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18 pages, 1994 KiB

Open AccessArticle

Cannabinerol Prevents Endoplasmic Reticulum and Mitochondria Dysfunctions in an In Vitro Model of Alzheimer’s Disease: A Network-Based Transcriptomic Analysis

by Luigi Chiricosta, Aurelio Minuti, Agnese Gugliandolo, Stefano Salamone, Federica Pollastro, Emanuela Mazzon and Osvaldo Artimagnella

Cells 2024, 13(12), 1012; https://doi.org/10.3390/cells13121012 - 10 Jun 2024

Cited by 1 | Viewed by 1154

Abstract

Neurodegenerative disorders are affecting millions of people worldwide, impacting the healthcare system of our society. Among them, Alzheimer’s disease (AD) is the most common form of dementia, characterized by severe cognitive impairments. Neuropathological hallmarks of AD are β-amyloid (Aβ) plaques and neurofibrillary tangles, as well as endoplasmic reticulum and mitochondria dysfunctions, which finally lead to apoptosis and neuronal loss. Since, to date, there is no definitive cure, new therapeutic and prevention strategies are of crucial importance. In this scenario, cannabinoids are deeply investigated as promising neuroprotective compounds for AD. In this study, we evaluated the potential neuroprotective role of cannabinerol (CBNR) in an in vitro cellular model of AD via next-generation sequencing. We observed that CBNR pretreatment counteracts the Aβ-induced loss of cell viability of differentiated SH-SY5Y cells. Moreover, a network-based transcriptomic analysis revealed that CBNR restores normal mitochondrial and endoplasmic reticulum functions in the AD model. Specifically, the most important genes regulated by CBNR are related mainly to oxidative phosphorylation (COX6B1, OXA1L, MT-CO2, MT-CO3), protein folding (HSPA5) and degradation (CUL3, FBXW7, UBE2D1), and glucose (G6PC3) and lipid (HSD17B7, ERG28, SCD) metabolism. Therefore, these results suggest that CBNR could be a new neuroprotective agent helpful in the prevention of AD dysfunctions. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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27 pages, 5066 KiB

Open AccessArticle

Neuroprotection of Cholinergic Neurons with a Tau Aggregation Inhibitor and Rivastigmine in an Alzheimer’s-like Tauopathy Mouse Model

by Maciej Zadrozny, Patrycja Drapich, Anna Gasiorowska-Bien, Wiktor Niewiadomski, Charles R. Harrington, Claude M. Wischik, Gernot Riedel and Grazyna Niewiadomska

Cells 2024, 13(7), 642; https://doi.org/10.3390/cells13070642 - 6 Apr 2024

Cited by 1 | Viewed by 1861

Abstract

Basal forebrain cholinergic dysfunction, most likely linked with tau protein aggregation, is a characteristic feature of Alzheimer’s disease (AD). Recent evidence suggests that tau protein is a putative target for the treatment of dementia, and the tau aggregation inhibitor, hydromethylthionine mesylate (HMTM), has emerged as a potential disease-modifying treatment. However, its efficacy was diminished in patients already receiving approved acetylcholinesterase inhibitors. In this study, we ask whether this negative interaction can also be mimicked in experimental tau models of AD and whether the underlying mechanism can be understood. From a previous age profiling study, 6-month-old line 1 (L1) tau transgenic mice were characterized by a severe reduction in several cholinergic markers. We therefore assessed whether long-term pre-exposure with the acetylcholinesterase inhibitor rivastigmine alone and in conjunction with the tau aggregation inhibitor HMTM can reverse cholinergic deficits in L1. Rivastigmine and HMTM, and combinations of the two compounds were administered orally for 11 weeks to both L1 and wild-type mice. The brains were sectioned with a focus on the basal forebrain, motor cortex and hippocampus. Immunohistochemical staining and quantification of choline acetyltransferase (ChAT), tyrosine kinase A (TrkA)-positive neurons and relative optical intensity (ROI) for vesicular acetylcholine transporter (VAChT), and acetylcholinesterase (AChE) reactivity confirmed reversal of the diminished cholinergic phenotype of interneurons (nucleus accumbens, striatum) and projection neurons (medial septum, nucleus basalis magnocellularis) by HMTM, to a greater extent than by rivastigmine alone in L1 mice. Combined administration did not yield additivity but, in most proxies, led to antagonistic effects in which rivastigmine decreased the benefits shown with HMTM alone. Local markers (VAChT and AChE) in target structures of the basal forebrain, motor cortex and hippocampal CA3 seemed to be normalized by HMTM, but not by rivastigmine or the combination of both drugs. HMTM, which was developed as a tau aggregation inhibitor, strongly decreased the tau load in L1 mice, however, not in combination with rivastigmine. Taken together, these data confirm a cholinergic phenotype in L1 tau transgenic mice that resembles the deficits observed in AD patients. This phenotype is reversible by HMTM, but at the same time appears to be subject to a homeostatic regulation induced by chronic pre-treatment with an acetylcholinesterase inhibitor, which interferes with the efficacy of HMTM. The strongest phenotypic reversal coincided with a normalization of the tau load in the cortex and hippocampus of L1, suggesting that tau accumulation underpins the loss of cholinergic markers in the basal forebrain and its projection targets. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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17 pages, 4865 KiB

Open AccessArticle

Age-Dependent and Aβ-Induced Dynamic Changes in the Subcellular Localization of HMGB1 in Neurons and Microglia in the Brains of an Animal Model of Alzheimer’s Disease

by Song-I Seol, Dashdulam Davaanyam, Sang-A Oh, Eun-Hwa Lee, Pyung-Lim Han, Seung-Woo Kim and Ja-Kyeong Lee

Cells 2024, 13(2), 189; https://doi.org/10.3390/cells13020189 - 18 Jan 2024

Viewed by 2027

Abstract

HMGB1 is a prototypical danger-associated molecular pattern (DAMP) molecule that co-localizes with amyloid beta (Aβ) in the brains of patients with Alzheimer’s disease. HMGB1 levels are significantly higher in the cerebrospinal fluid of patients. However, the cellular and subcellular distribution of HMGB1 in relation to the pathology of Alzheimer’s disease has not yet been studied in detail. Here, we investigated whether HMGB1 protein levels in brain tissue homogenates (frontal cortex and striatum) and sera from Tg-APP/PS1 mice, along with its cellular and subcellular localization in those regions, differed. Total HMGB1 levels were increased in the frontal cortices of aged wildtype (7.5 M) mice compared to young (3.5 M) mice, whereas total HMGB1 levels in the frontal cortices of Tg-APP/PS1 mice (7.5 M) were significantly lower than those in age-matched wildtype mice. In contrast, total serum HMGB1 levels were enhanced in aged wildtype (7.5 M) mice and Tg-APP/PS1 mice (7.5 M). Further analysis indicated that nuclear HMGB1 levels in the frontal cortices of Tg-APP/PS1 mice were significantly reduced compared to those in age-matched wildtype controls, and cytosolic HMGB1 levels were also significantly decreased. Triple-fluorescence immunohistochemical analysis indicated that HMGB1 appeared as a ring shape in the cytoplasm of most neurons and microglia in the frontal cortices of 9.5 M Tg-APP/PS1 mice, indicating that nuclear HMGB1 is reduced by aging and in Tg-APP/PS1 mice. Consistent with these observations, Aβ treatment of both primary cortical neuron and primary microglial cultures increased HMGB1 secretion in the media, in an Aβ-dose-dependent manner. Our results indicate that nuclear HMGB1 might be translocated from the nucleus to the cytoplasm in both neurons and microglia in the brains of Tg-APP/PS1 mice, and that it may subsequently be secreted extracellularly. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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14 pages, 1830 KiB

Open AccessArticle

Altering Brain Amyloidosis by Intra-Lingual and Extra-Nasal Exposure of Aβ Aggregates

by Nazaret Gamez, Javiera Bravo-Alegria, Yumeng Huang, Nelson Perez-Urrutia, Deepa Dongarwar, Claudio Soto and Rodrigo Morales

Cells 2022, 11(21), 3442; https://doi.org/10.3390/cells11213442 - 31 Oct 2022

Cited by 2 | Viewed by 2017

Abstract

Extensive experimental and human-derived evidence suggest that misfolded Aβ particles spread similarly to infectious prions. Moreover, peripheral administration of Aβ seeds accelerates brain amyloidosis in both susceptible experimental animals and humans. The mechanisms and elements governing the transport of misfolded Aβ from the periphery to the brain are not fully understood, although circulation and retrograde axonal transport have been proposed. Here, we demonstrate that injection of Aβ seeds in the tongue, a highly innervated organ, substantially accelerates the appearance of plaques in Tg2576 mice. In addition, the extra-nasal exposure of Aβ aggregates increased amyloid pathology in the olfactory bulb. Our results show that exposing highly innervated tissues to Aβ seeds accelerates AD-like pathological features, and suggest that Aβ seeds can be transported from peripheral compartments to the brain by retrograde axonal transport. Research in this direction may be relevant on different fronts, including disease mechanisms, diagnosis, and risk-evaluation of potential iatrogenic transmission of Aβ misfolding. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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13 pages, 1429 KiB

Open AccessArticle

A Method for Bridging Population-Specific Genotypes to Detect Gene Modules Associated with Alzheimer’s Disease

by Yulin Dai, Peilin Jia, Zhongming Zhao and Assaf Gottlieb

Cells 2022, 11(14), 2219; https://doi.org/10.3390/cells11142219 - 16 Jul 2022

Cited by 3 | Viewed by 2327

Abstract

Background: Genome-wide association studies have successfully identified variants associated with multiple conditions. However, generalizing discoveries across diverse populations remains challenging due to large variations in genetic composition. Methods that perform gene expression imputation have attempted to address the transferability of gene discoveries across populations, but with limited success. Methods: Here, we introduce a pipeline that combines gene expression imputation with gene module discovery, including a dense gene module search and a gene set variation analysis, to address the transferability issue. Our method feeds association probabilities of imputed gene expression with a selected phenotype into tissue-specific gene-module discovery over protein interaction networks to create higher-level gene modules. Results: We demonstrate our method’s utility in three case-control studies of Alzheimer’s disease (AD) for three different race/ethnic populations (Whites, African descent and Hispanics). We discovered 182 AD-associated genes from gene modules shared between these populations, highlighting new gene modules associated with AD. Conclusions: Our innovative framework has the potential to identify robust discoveries across populations based on gene modules, as demonstrated in AD. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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14 pages, 989 KiB

Open AccessEditor’s ChoiceArticle

Cerebrospinal Fluid Proteome Alterations Associated with Neuropsychiatric Symptoms in Cognitive Decline and Alzheimer’s Disease

by Magdalena Mroczek, Christopher Clark, Loïc Dayon, Gene L. Bowman and Julius Popp

Cells 2022, 11(6), 1030; https://doi.org/10.3390/cells11061030 - 18 Mar 2022

Cited by 10 | Viewed by 2906

Abstract

Although neuropsychiatric symptoms (NPS) are common and severely affect older people with cognitive decline, little is known about their underlying molecular mechanisms and relationships with Alzheimer’s disease (AD). The aim of this study was to identify and characterize cerebrospinal fluid (CSF) proteome alterations related to NPS. In a longitudinally followed-up cohort of subjects with normal cognition and patients with cognitive impairment (MCI and mild dementia) from a memory clinic setting, we quantified a panel of 790 proteins in CSF using an untargeted shotgun proteomic workflow. Regression models and pathway enrichment analysis were used to investigate protein alterations related to NPS, and to explore relationships with AD pathology and cognitive decline at follow-up visits. Regression analysis selected 27 CSF proteins associated with NPS. These associations were independent of the presence of cerebral AD pathology (defined as CSF p-tau181/Aβ1–42 > 0.0779, center cutoff). Gene ontology enrichment showed abundance alterations of proteins related to cell adhesion, immune response, and lipid metabolism, among others, in relation to NPS. Out of the selected proteins, three were associated with accelerated cognitive decline at follow-up visits after controlling for possible confounders. Specific CSF proteome alterations underlying NPS may both represent pathophysiological processes independent from AD and accelerate clinical disease progression. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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Review

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17 pages, 1975 KiB

Open AccessReview

Sequence of Molecular Events in the Development of Alzheimer’s Disease: Cascade Interactions from Beta-Amyloid to Other Involved Proteins

by Soghra Bagheri, Ali Akbar Saboury and Luciano Saso

Cells 2024, 13(15), 1293; https://doi.org/10.3390/cells13151293 - 31 Jul 2024

Viewed by 1442

Abstract

Alzheimer’s disease is the primary neurodegenerative disease affecting the elderly population. Despite the first description of its pathology over a century ago, its precise cause and molecular mechanism remain unknown. Numerous factors, including beta-amyloid, tau protein, the APOEε4 gene, and different metals, have been extensively investigated in relation to this disease. However, none of them have been proven to have a decisive causal relationship. Furthermore, no single theory has successfully integrated these puzzle pieces thus far. In this review article, we propose the most probable molecular mechanism for AD, which clearly shows the relationship between the main aspects of the disease, and addresses fundamental questions such as: Why is aging the major risk factor for the disease? Are amyloid plaques and tau tangles the causes or consequences of AD? Why are the distributions of senile plaques and tau tangles in the brain different and independent of each other? Why is the APOEε4 gene a risk factor for AD? Finally, why is the disease more prevalent in women? Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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22 pages, 799 KiB

Open AccessReview

New Insights into Neuroinflammation Involved in Pathogenic Mechanism of Alzheimer’s Disease and Its Potential for Therapeutic Intervention

by Tiantian Li, Li Lu, Eloise Pember, Xinuo Li, Bocheng Zhang and Zheying Zhu

Cells 2022, 11(12), 1925; https://doi.org/10.3390/cells11121925 - 14 Jun 2022

Cited by 45 | Viewed by 5792

Abstract

Alzheimer’s disease (AD) is the most common form of dementia, affecting more than 50 million people worldwide with an estimated increase to 139 million people by 2050. The exact pathogenic mechanisms of AD remain elusive, resulting in the fact that the current therapeutics solely focus on symptomatic management instead of preventative or curative strategies. The two most widely accepted pathogenic mechanisms of AD include the amyloid and tau hypotheses. However, it is evident that these hypotheses cannot fully explain neuronal degeneration shown in AD. Substantial evidence is growing for the vital role of neuroinflammation in AD pathology. The neuroinflammatory hypothesis provides a new, exciting lead in uncovering the underlying mechanisms contributing to AD. This review aims to highlight new insights into the role of neuroinflammation in the pathogenesis of AD, mainly including the involvement of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), nucleotide-binding oligomerization domain, leucine-rich repeat-containing protein 3 (NLRP3)/caspase-1 axis, triggering receptor expressed on myeloid cells 2 (TREM2) and cGAS-STING as key influencers in augmenting AD development. The inflammasomes related to the pathways of NF-κB, NLRP3, TREM2, and cGAS-STING as biomarkers of the neuroinflammation associated with AD, as well as an overview of novel AD treatments based on these biomarkers as potential drug targets reported in the literature or under clinical trials, are explored. Full article

(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)

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