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Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition
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Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition

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: closed (1 December 2021) | Viewed by 38379

Special Issue Editors

Prof. Dr. Hanna Rosenmann

E-Mail Website
Guest Editor
Department of Neurology, The Agnes Ginges Center for Human Neurogenetics, Hadassah Hebrew University Medical Center, Jerusalem 9112001, Israel
Interests: Alzheimer's disease; tauopathy; neurodegeneration; animal models
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Frenkel Dan

E-Mail Website
Guest Editor
Department of Neurobiology, Faculty of Life Sciences, Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 69978, Israel
Interests: neuroinflammation; astrocyte; microglia; Alzheimer’s disease; animal model
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although Alzheimer's disease (AD) and other dementias are being intensively investigated, there is not yet a drug that efficiently interferes with disease pathogenesis. Most cases of AD are sporadic and less than 5%, among them carrying mutations that affect beta amyloid, are early‐onset familial AD that occur before the age of 65 years. Unfortunately, thus far, most of the newly developed drugs for AD treatment have failed in clinical trials. There is an urgent need for new therapies for treating dementias, particularly AD. Otherwise, this disease will continue to attack 5% of people aged over 65 and more than 40% of those aged over 85. Genetic risk factors, such as the presence of ApoE4 or mutations in inflammatory markers, such as TREM2, have been shown to affect disease development and progress. However, preventive approaches, such as maintaining good health (e.g., reducing cardiovascular and metabolic risk factors, enhancing physical and mental activities), seem to have a major impact on reducing disease incidence and delaying its onset. Many research approaches may be suitable for combating dementias, such as identifying disease-causing compounds (toxins), finding new targets, developing new drugs (mono/multi-target) by drug screening or by drug design, cell or organelle therapy, and device development, as well as other creative and innovative unconventional approaches.

This Special Issue will be dedicated to gathering novel therapeutic approaches to treat Alzheimer's disease and other dementias. We welcome submissions, including original papers and reviews, on these essential topics.

Prof. Hanna Rosenmann
Prof. Dr. Dan Frenkel
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • Prevention of dementia
  • Treatment of dementia
  • Amyloid
  • Tangles
  • Tauopathies
  • Mild cognitive impairment
  • Neurodegenerative pathways
  • Toxic elements inducing dementia
  • Drug screening
  • Drug design
  • Cell or organelle therapy
  • Device development
  • Neurodegeneration
  • Neuroinflammation

Published Papers (10 papers)

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Research

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14 pages, 2293 KiB  
Article
Imbalance in Sirt1 Alternative Splicing in Response to Chronic Stress during the Adolescence Period in Female Mice
by Shir Shlomi, Roni Toledano, Keren Nitzan, Sigal Dror Shahaf, Emanuela P. Break, Dan Frenkel and Ravid Doron
Int. J. Mol. Sci. 2022, 23(9), 4945; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094945 - 29 Apr 2022
Cited by 3 | Viewed by 1594
Abstract
Stressful unpredictable life events have been implicated in numerous diseases. It is now becoming clear that some life periods are more vulnerable than others. As adolescence is a sensitive period in brain development, the long-term effects of stress during this period could be [...] Read more.
Stressful unpredictable life events have been implicated in numerous diseases. It is now becoming clear that some life periods are more vulnerable than others. As adolescence is a sensitive period in brain development, the long-term effects of stress during this period could be significant. We investigated the long-term effects of exposure to unpredictable chronic mild stress in adolescent mice on alternative splicing of Sirtuin 1. One-month-old mice were exposed to 4 weeks of UCMS and examined for anxiety and cognition at the age of 2, 4 and 6 months. We found a rise in anxious behavior immediately after the exposure to stress. Notably, there was a long-term impairment of performance in cognitive tasks and an imbalance in Sirtuin 1 and TrkB receptor alternative splicing in the stress-exposed mice compared with controls. To conclude, our results show that exposure to unpredictable chronic mild stress during adolescence affects cognition in adulthood. Understanding pathways affiliated with stress may help minimize the long-term emotional effects of an unpredictable, stressful event. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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38 pages, 8328 KiB  
Article
The Phenoxyalkyltriazine Antagonists for 5-HT6 Receptor with Promising Procognitive and Pharmacokinetic Properties In Vivo in Search for a Novel Therapeutic Approach to Dementia Diseases
by Sylwia Sudoł, Agnieszka Cios, Magdalena Jastrzębska-Więsek, Ewelina Honkisz-Orzechowska, Barbara Mordyl, Natalia Wilczyńska-Zawal, Grzegorz Satała, Katarzyna Kucwaj-Brysz, Anna Partyka, Gniewomir Latacz, Agnieszka Olejarz-Maciej, Anna Wesołowska and Jadwiga Handzlik
Int. J. Mol. Sci. 2021, 22(19), 10773; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910773 - 05 Oct 2021
Cited by 11 | Viewed by 2386
Abstract
Among the serotonin receptors, one of the most recently discovered 5-HT6 subtype is an important protein target and its ligands may play a key role in the innovative treatment of cognitive disorders. However, none of its selective ligands have reached the pharmaceutical [...] Read more.
Among the serotonin receptors, one of the most recently discovered 5-HT6 subtype is an important protein target and its ligands may play a key role in the innovative treatment of cognitive disorders. However, none of its selective ligands have reached the pharmaceutical market yet. Recently, a new chemical class of potent 5-HT6 receptor agents, the 1,3,5-triazine-piperazine derivatives, has been synthesized. Three members, the ortho and meta dichloro- (1,2) and the unsubstituted phenyl (3) derivatives, proved to be of special interest due to their high affinities (1,2) and selectivity (3) toward 5-HT6 receptor. Thus, a broader pharmacological profile for 1–3, including comprehensive screening of the receptor selectivity and drug-like parameters in vitro as well as both, pharmacokinetic and pharmacodynamic properties in vivo, have been investigated within this study. A comprehensive analysis of the obtained results indicated significant procognitive-like activity together with beneficial drug-likeness in vitro and pharmacokinetics in vivo profiles for both, (RS)-4-[1-(2,3-dichlorophenoxy)propyl]-6-(4-methylpiperazin-1-yl)-1,3,5-triazin-2-amine (2) and (RS)-4-(4-methylpiperazin-1-yl)-6-(1-phenoxypropyl)-1,3,5-triazin-2-amine (3), but insensibly predominant for compound 2. Nevertheless, both compounds (2 and 3) seem to be good Central Nervous System drug candidates in search for novel therapeutic approach to dementia diseases, based on the 5-HT6 receptor target. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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11 pages, 2990 KiB  
Article
Therapeutic Effects of Aripiprazole in the 5xFAD Alzheimer’s Disease Mouse Model
by Ye Ji Jeong, Yeonghoon Son, Hye-Jin Park, Se Jong Oh, Jae Yong Choi, Young-Gyu Ko and Hae-June Lee
Int. J. Mol. Sci. 2021, 22(17), 9374; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179374 - 29 Aug 2021
Cited by 5 | Viewed by 2741
Abstract
Global aging has led to growing health concerns posed by Alzheimer’s disease (AD), the most common type of dementia. Aripiprazole is an atypical FDA-approved anti-psychotic drug with potential against AD. To investigate its therapeutic effects on AD pathology, we administered aripiprazole to 5xFAD [...] Read more.
Global aging has led to growing health concerns posed by Alzheimer’s disease (AD), the most common type of dementia. Aripiprazole is an atypical FDA-approved anti-psychotic drug with potential against AD. To investigate its therapeutic effects on AD pathology, we administered aripiprazole to 5xFAD AD model mice and examined beta-amyloid (βA)-induced AD-like phenotypes, including βA production, neuroinflammation, and cerebral glucose metabolism. Aripiprazole administration significantly decreased βA accumulation in the brains of 5xFAD AD mice. Aripiprazole significantly modified amyloid precursor protein processing, including carboxyl-terminal fragment β and βA, a disintegrin and metalloproteinase domain-containing protein 10, and beta-site APP cleaving enzyme 1, as determined by Western blotting. Neuroinflammation, as evidenced by ionized calcium binding adapter molecule 1 and glial fibrillary acidic protein upregulation was dramatically inhibited, and the neuron cell layer of the hippocampal CA1 region was preserved following aripiprazole administration. In 18F-fluorodeoxyglucose positron emission tomography, after receiving aripiprazole, 5xFAD mice showed a significant increase in glucose uptake in the striatum, thalamus, and hippocampus compared to vehicle-treated AD mice. Thus, aripiprazole effectively alleviated βA lesions and prevented the decline of cerebral glucose metabolism in 5xFAD AD mice, suggesting its potential for βA metabolic modification and highlighting its therapeutic effect over AD progression. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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14 pages, 3632 KiB  
Article
Nasal Rifampicin Improves Cognition in a Mouse Model of Dementia with Lewy Bodies by Reducing α-Synuclein Oligomers
by Tomohiro Umeda, Yukari Hatanaka, Ayumi Sakai and Takami Tomiyama
Int. J. Mol. Sci. 2021, 22(16), 8453; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168453 - 06 Aug 2021
Cited by 11 | Viewed by 2677
Abstract
α-Synuclein oligomers are thought to play an important role in the pathogenesis of dementia with Lewy bodies (DLB). There is no effective cure for DLB at present. Previously, we demonstrated that in APP- and tau-transgenic mice, oral or intranasal rifampicin reduced brain Aβ [...] Read more.
α-Synuclein oligomers are thought to play an important role in the pathogenesis of dementia with Lewy bodies (DLB). There is no effective cure for DLB at present. Previously, we demonstrated that in APP- and tau-transgenic mice, oral or intranasal rifampicin reduced brain Aβ and tau oligomers and improved mouse cognition. In the present study, we expanded our research to DLB. Rifampicin was intranasally administered to 6-month-old A53T-mutant α-synuclein-transgenic mice at 0.1 mg/day for 1 month. The mice displayed memory impairment but no motor deficit at this age, indicating a suitable model of DLB. α-Synuclein pathologies were examined by the immunohistochemical/biochemical analyses of brain tissues. Cognitive function was evaluated by the Morris water maze test. Intranasal rifampicin significantly reduced the levels of [pSer129] α-synuclein in the hippocampus and α-synuclein oligomers in the visual cortex and hippocampus. The level of the presynaptic marker synaptophysin in the hippocampus was recovered to the level in non-transgenic littermates. In the Morris water maze, a significant improvement in spatial reference memory was observed in rifampicin-treated mice. Taken together with our previous findings, these results suggest that intranasal rifampicin is a promising remedy for the prevention of neurodegenerative dementia, including Alzheimer’s disease, frontotemporal dementia, and DLB. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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13 pages, 6625 KiB  
Article
The Involvement of Insulin-Like Growth Factor 1 and Nerve Growth Factor in Alzheimer’s Disease-Like Pathology and Survival Role of the Mix of Embryonic Proteoglycans: Electrophysiological Fingerprint, Structural Changes and Regulatory Effects on Neurotrophins
by Michail Aghajanov, Senik Matinyan, Vergine Chavushyan, Margarita Danielyan, Gohar Karapetyan, Margarita Mirumyan, Katarine Fereshetyan, Hayk Harutyunyan and Konstantin Yenkoyan
Int. J. Mol. Sci. 2021, 22(13), 7084; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22137084 - 30 Jun 2021
Cited by 5 | Viewed by 2709
Abstract
Alzheimer’s disease (AD)-associated neurodegeneration is triggered by different fragments of amyloid beta (Aβ). Among them, Aβ (25–35) fragment plays a critical role in the development of neurodegeneration—it reduces synaptic integrity by disruption of excitatory/inhibitory ratio across networks and alters the growth factors synthesis. [...] Read more.
Alzheimer’s disease (AD)-associated neurodegeneration is triggered by different fragments of amyloid beta (Aβ). Among them, Aβ (25–35) fragment plays a critical role in the development of neurodegeneration—it reduces synaptic integrity by disruption of excitatory/inhibitory ratio across networks and alters the growth factors synthesis. Thus, in this study, we aimed to identify the involvement of neurotrophic factors—the insulin-like growth factor 1 (IGF-1) and nerve growth factor (NGF)—of AD-like neurodegeneration induced by Aβ (25–35). Taking into account our previous findings on the neuroprotective effects of the mix of proteoglycans of embryonic genesis (PEG), it was suggested to test its regulatory effect on IGF-1 and NGF levels. To evaluate the progress of neurodegeneration, in vivo electrophysiological investigation of synaptic activity disruption of the entorhinal cortex–hippocampus circuit at AD was performed and the potential recovery effects of PEG with relative structural changes were provided. To reveal the direct effects of PEG on brain functional activity, the electrophysiological pattern of the single cells from nucleus supraopticus, sensomotor cortex and hippocampus after acute injection of PEG was examined. Our results demonstrated that after i.c.v. injection of Aβ (25–35), the level of NGF decreased in cerebral cortex and hypothalamus, and, in contrast, increased in hippocampus, prompting its multidirectional role in case of brain damage. The concentration of IGF-1 significantly increased in all investigated brain structures. The administration of PEG balanced the growth factor levels accompanied by substantial restoration of neural tissue architecture and synaptic activity. Acute injection of PEG activated the hypothalamic nucleus supraopticus and hippocampal neurons. IGF-1 and NGF levels were found to be elevated in animals receiving PEG in an absence of amyloid exposure. We suggest that IGF-1 and NGF play a critical role in the development of AD. At the same time, it becomes clear that the neuroprotective effects of PEG are likely mediated via the regulation of neurotrophins. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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24 pages, 4275 KiB  
Article
Early Effects of the Soluble Amyloid β25-35 Peptide in Rat Cortical Neurons: Modulation of Signal Transduction Mediated by Adenosine and Group I Metabotropic Glutamate Receptors
by Carlos Alberto Castillo, Inmaculada Ballesteros-Yáñez, David Agustín León-Navarro, José Luis Albasanz and Mairena Martín
Int. J. Mol. Sci. 2021, 22(12), 6577; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126577 - 19 Jun 2021
Cited by 10 | Viewed by 2249
Abstract
The amyloid β peptide (Aβ) is a central player in the neuropathology of Alzheimer’s disease (AD). The alteration of Aβ homeostasis may impact the fine-tuning of cell signaling from the very beginning of the disease, when amyloid plaque is not deposited yet. For [...] Read more.
The amyloid β peptide (Aβ) is a central player in the neuropathology of Alzheimer’s disease (AD). The alteration of Aβ homeostasis may impact the fine-tuning of cell signaling from the very beginning of the disease, when amyloid plaque is not deposited yet. For this reason, primary culture of rat cortical neurons was exposed to Aβ25-35, a non-oligomerizable form of Aβ. Cell viability, metabotropic glutamate receptors (mGluR) and adenosine receptors (AR) expression and signalling were assessed. Aβ25-35 increased mGluR density and affinity, mainly due to a higher gene expression and protein presence of Group I mGluR (mGluR1 and mGluR5) in the membrane of cortical neurons. Intriguingly, the main effector of group I mGluR, the phospholipase C β1 isoform, was less responsive. Also, the inhibitory action of group II and group III mGluR on adenylate cyclase (AC) activity was unaltered or increased, respectively. Interestingly, pre-treatment of cortical neurons with an antagonist of group I mGluR reduced the Aβ25-35-induced cell death. Besides, Aβ25-35 increased the density of A1R and A2AR, along with an increase in their gene expression. However, while A1R-mediated AC inhibition was increased, the A2AR-mediated stimulation of AC remained unchanged. Therefore, one of the early events that takes place after Aβ25-35 exposure is the up-regulation of adenosine A1R, A2AR, and group I mGluR, and the different impacts on their corresponding signaling pathways. These results emphasize the importance of deciphering the early events and the possible involvement of metabotropic glutamate and adenosine receptors in AD physiopathology. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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Review

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37 pages, 9151 KiB  
Review
Physical Exercise, a Potential Non-Pharmacological Intervention for Attenuating Neuroinflammation and Cognitive Decline in Alzheimer’s Disease Patients
by Samo Ribarič
Int. J. Mol. Sci. 2022, 23(6), 3245; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063245 - 17 Mar 2022
Cited by 14 | Viewed by 6130
Abstract
This narrative review summarises the evidence for considering physical exercise (PE) as a non-pharmacological intervention for delaying cognitive decline in patients with Alzheimer’s disease (AD) not only by improving cardiovascular fitness but also by attenuating neuroinflammation. Ageing is the most important risk factor [...] Read more.
This narrative review summarises the evidence for considering physical exercise (PE) as a non-pharmacological intervention for delaying cognitive decline in patients with Alzheimer’s disease (AD) not only by improving cardiovascular fitness but also by attenuating neuroinflammation. Ageing is the most important risk factor for AD. A hallmark of the ageing process is a systemic low-grade chronic inflammation that also contributes to neuroinflammation. Neuroinflammation is associated with AD, Parkinson’s disease, late-onset epilepsy, amyotrophic lateral sclerosis and anxiety disorders. Pharmacological treatment of AD is currently limited to mitigating the symptoms and attenuating progression of the disease. AD animal model studies and human studies on patients with a clinical diagnosis of different stages of AD have concluded that PE attenuates cognitive decline not only by improving cardiovascular fitness but possibly also by attenuating neuroinflammation. Therefore, low-grade chronic inflammation and neuroinflammation should be considered potential modifiable risk factors for AD that can be attenuated by PE. This opens the possibility for personalised attenuation of neuroinflammation that could also have important health benefits for patients with other inflammation associated brain disorders (i.e., Parkinson’s disease, late-onset epilepsy, amyotrophic lateral sclerosis and anxiety disorders). In summary, life-long, regular, structured PE should be considered as a supplemental intervention for attenuating the progression of AD in human. Further studies in human are necessary to develop optimal, personalised protocols, adapted to the progression of AD and the individual’s mental and physical limitations, to take full advantage of the beneficial effects of PE that include improved cardiovascular fitness, attenuated systemic inflammation and neuroinflammation, stimulated brain Aβ peptides brain catabolism and brain clearance. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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27 pages, 996 KiB  
Review
Selected Natural Products in Neuroprotective Strategies for Alzheimer’s Disease—A Non-Systematic Review
by Karolina Wojtunik-Kulesza, Tomasz Oniszczuk, Jarosław Mołdoch, Iwona Kowalska, Jarosław Szponar and Anna Oniszczuk
Int. J. Mol. Sci. 2022, 23(3), 1212; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031212 - 21 Jan 2022
Cited by 6 | Viewed by 2781
Abstract
Neurodegenerative disorders such as Alzheimer’s disease (AD) are distinguished by the irreversible degeneration of central nervous system function and structure. AD is characterized by several different neuropathologies—among others, it interferes with neuropsychiatrical controls and cognitive functions. This disease is the number one neurodegenerative [...] Read more.
Neurodegenerative disorders such as Alzheimer’s disease (AD) are distinguished by the irreversible degeneration of central nervous system function and structure. AD is characterized by several different neuropathologies—among others, it interferes with neuropsychiatrical controls and cognitive functions. This disease is the number one neurodegenerative disorder; however, its treatment options are few and, unfortunately, ineffective. In the new strategies devised for AD prevention and treatment, the application of plant-based natural products is especially popular due to lesser side effects associated with their taking. Moreover, their neuroprotective activities target different pathological mechanisms. The current review presents the anti-AD properties of several natural plant substances. The paper throws light on products under in vitro and in vivo trials and compiles information on their mechanism of actions. Knowledge of the properties of such plant compounds and their combinations will surely lead to discovering new potent medicines for the treatment of AD with lesser side effects than the currently available pharmacological proceedings. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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29 pages, 1860 KiB  
Review
Novel Therapeutic Approaches for Alzheimer’s Disease: An Updated Review
by Tien-Wei Yu, Hsien-Yuan Lane and Chieh-Hsin Lin
Int. J. Mol. Sci. 2021, 22(15), 8208; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158208 - 30 Jul 2021
Cited by 66 | Viewed by 9712
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and accounts for most cases of dementia. The prevalence of AD has increased in the current rapidly aging society and contributes to a heavy burden on families and society. Despite the profound impact of AD, [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and accounts for most cases of dementia. The prevalence of AD has increased in the current rapidly aging society and contributes to a heavy burden on families and society. Despite the profound impact of AD, current treatments are unable to achieve satisfactory therapeutic effects or stop the progression of the disease. Finding novel treatments for AD has become urgent. In this paper, we reviewed novel therapeutic approaches in five categories: anti-amyloid therapy, anti-tau therapy, anti-neuroinflammatory therapy, neuroprotective agents including N-methyl-D-aspartate (NMDA) receptor modulators, and brain stimulation. The trend of therapeutic development is shifting from a single pathological target to a more complex mechanism, such as the neuroinflammatory and neurodegenerative processes. While drug repositioning may accelerate pharmacological development, non-pharmacological interventions, especially repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS), also have the potential for clinical application. In the future, it is possible for physicians to choose appropriate interventions individually on the basis of precision medicine. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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19 pages, 359 KiB  
Review
Brain Glucose Transporters: Role in Pathogenesis and Potential Targets for the Treatment of Alzheimer’s Disease
by Leszek Szablewski
Int. J. Mol. Sci. 2021, 22(15), 8142; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158142 - 29 Jul 2021
Cited by 29 | Viewed by 4232
Abstract
The most common cause of dementia, especially in elderly people, is Alzheimer’s disease (AD), with aging as its main risk factor. AD is a multifactorial neurodegenerative disease. There are several factors increasing the risk of AD development. One of the main features of [...] Read more.
The most common cause of dementia, especially in elderly people, is Alzheimer’s disease (AD), with aging as its main risk factor. AD is a multifactorial neurodegenerative disease. There are several factors increasing the risk of AD development. One of the main features of Alzheimer’s disease is impairment of brain energy. Hypometabolism caused by decreased glucose uptake is observed in specific areas of the AD-affected brain. Therefore, glucose hypometabolism and energy deficit are hallmarks of AD. There are several hypotheses that explain the role of glucose hypometabolism in AD, but data available on this subject are poor. Reduced transport of glucose into neurons may be related to decreased expression of glucose transporters in neurons and glia. On the other hand, glucose transporters may play a role as potential targets for the treatment of AD. Compounds such as antidiabetic drugs, agonists of SGLT1, insulin, siRNA and liposomes are suggested as therapeutics. Nevertheless, the suggested targets of therapy need further investigations. Full article
(This article belongs to the Special Issue Alzheimer’s Disease and Other Dementias-Novel Therapeutic Approaches-2nd Edition)
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