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Immune-dysregulation harnessing in myeloid neoplasms
(2024) Sharifi, Mohammad Jafar; Xu, Ling; Nasiri, Nahid; Ashja Arvan, Mehnoosh; Soleimanzadeh, Hadis; Ganjalikhani Hakemi, Mazdak
Myeloid malignancies arise in bone marrow microenvironments and shape these microenvironments in favor of malignant development. Immune suppression is one of the most important stages in myeloid leukemia progression. Leukemic clone expansion and immune dysregulation occur simultaneously in bone marrow microenvironments. Complex interactions emerge between normal immune system elements and leukemic clones in the bone marrow. In recent years, researchers have identified several of these pathological interactions. For instance, recent works shows that the secretion of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), from bone marrow stromal cells contributes to immune dysregulation and the selective proliferation of JAK2V617F+ clones in myeloproliferative neoplasms. Moreover, inflammasome activation and sterile inflammation result in inflamed microenvironments and the development of myelodysplastic syndromes. Additional immune dysregulations, such as exhaustion of T and NK cells, an increase in regulatory T cells, and impairments in antigen presentation are common findings in myeloid malignancies. In this review, we discuss the role of altered bone marrow microenvironments in the induction of immune dysregulations that accompany myeloid malignancies. We also consider both current and novel therapeutic strategies to restore normal immune system function in the context of myeloid malignancies.
Bioactive peptides: An alternative therapeutic approach for cancer management
(Frontiers Media SA, 2024) Ghadiri, Nooshin; Javidan, Moslem; Sheikhi, Shima; Taştan, Özge; Parodi, Alessandro; Liao, Ziwei; Tayybi Azar, Mehdi; Ganjalıkhani-Hakemi, Mazdak
Cancer is still considered a lethal disease worldwide and the patients’ quality of life is affected by major side effects of the treatments including post-surgery complications, chemo-, and radiation therapy. Recently, new therapeutic approaches were considered globally for increasing conventional cancer therapy efficacy and decreasing the adverse effects. Bioactive peptides obtained from plant and animal sources have drawn increased attention because of their potential as complementary therapy. This review presents a contemporary examination of bioactive peptides derived from natural origins with demonstrated anticancer, ant invasion, and immunomodulation properties. For example, peptides derived from common beans, chickpeas, wheat germ, and mung beans exhibited antiproliferative and toxic effects on cancer cells, favoring cell cycle arrest and apoptosis. On the other hand, peptides from marine sources showed the potential for inhibiting tumor growth and metastasis. In this review we will discuss these data highlighting the potential befits of these approaches and the need of further investigations to fully characterize their potential in clinics.
Integrated multi-omics analyses of microbial communities: A review of the current state and future directions
(Royal Society of Chemistry, 2023) Arıkan, Muzaffer; Muth, Thilo
Integrated multi-omics analyses of microbiomes have become increasingly common in recent years as the emerging omics technologies provide an unprecedented opportunity to better understand the structural and functional properties of microbial communities. Consequently, there is a growing need for and interest in the concepts, approaches, considerations, and available tools for investigating diverse environmental and host-associated microbial communities in an integrative manner. In this review, we first provide a general overview of each omics analysis type, including a brief history, typical workflow, primary applications, strengths, and limitations. Then, we inform on both experimental design and bioinformatics analysis considerations in integrated multi-omics analyses, elaborate on the current approaches and commonly used tools, and highlight the current challenges. Finally, we discuss the expected key advances, emerging trends, potential implications on various fields from human health to biotechnology, and future directions.
Helper innate lymphoid cells as cell therapy for cancer
(Wiley, 2023) Magnusson, Fay Celeste; Bahhar, Ilham
Although the first cancer immunotherapy was given in the clinic more than a century ago, this line of treatment has remained more of a distant goal than a practical therapy due to limited understanding of the tumour microenvironment and the mechanisms at play within it, which led to failures of numerous clinical trials. However, in the last two decades, the immune checkpoint inhibitors (ICIs) and chimeric antigen receptor-T cell therapies have revolutionized the treatment of cancer and provided proof-of-concept that immunotherapies are a viable option. So far, immunotherapies have majoritarily focused on utilizing T cells; however, T cells are not autonomous but rather function as part of, and therefore are influenced by, a vast cast of other immune cells, including innate lymphoid cells (ILCs). Here, we summarize the role of ILCs, especially helper ILCs, in tumour development, progression and metastasis, as well as their potential to be used as immunotherapy for cancer. By reviewing the studies that used helper ILCs as adoptive cell therapy (ACT), we highlight the rationale behind considering these cells as novel ACT for cancer as well as identify open questions and areas for future research.
Network-medicine approach for the identification of genetic association of parathyroid adenoma with cardiovascular disease and type-2 diabetes
(Oxford University Press, 2023) İmam, Nikhat; Alam, Aftab; Siddiqui, Mohd Faizan; Veg, Akhtar; Bay, Sadık; Khan, Md Jawed Ikbal; Ishrat, Romana
Primary hyperparathyroidism is caused by solitary parathyroid adenomas (PTAs) in most cases (?85%), and it has been previously reported that PTAs are associated with cardiovascular disease (CVD) and type-2 diabetes (T2D). To understand the molecular basis of PTAs, we have investigated the genetic association amongst PTAs, CVD and T2D through an integrative network-based approach and observed a remarkable resemblance. The current study proposed to compare the PTAs-associated proteins with the overlapping proteins of CVD and T2D to determine the disease relationship. We constructed the protein-protein interaction network by integrating curated and experimentally validated interactions in humans. We found the $11$ highly clustered modules in the network, which contain a total of $13$ hub proteins (TP53, ESR1, EGFR, POTEF, MEN1, FLNA, CDKN2B, ACTB, CTNNB1, CAV1, MAPK1, G6PD and CCND1) that commonly co-exist in PTAs, CDV and T2D and reached to network's hierarchically modular organization. Additionally, we implemented a gene-set over-representation analysis over biological processes and pathways that helped to identify disease-associated pathways and prioritize target disease proteins. Moreover, we identified the respective drugs of these hub proteins. We built a bipartite network that helps decipher the drug-target interaction, highlighting the influential roles of these drugs on apparently unrelated targets and pathways. Targeting these hub proteins by using drug combinations or drug-repurposing approaches will improve the clinical conditions in comorbidity, enhance the potency of a few drugs and give a synergistic effect with better outcomes. This network-based analysis opens a new horizon for more personalized treatment and drug-repurposing opportunities to investigate new targets and multi-drug treatment and may be helpful in further analysis of the mechanisms underlying PTA and associated diseases.
The savant syndrome: a gift or a disability? A deeper look into metabolic correlates of hidden cognitive capacity
(Bentham Science Publishers, 2023) Onin, İrem; Hanoğlu, Lütfü; Yuluğ, Burak
Savant syndrome is a rare and unusual condition that occurs in the presence of severe developmental disabilities, disorders, and injuries. The syndrome can be congenital from birth to childhood or acquired as a result of a brain injury or damage to the central nervous system. There are several findings that indicate that savant syndrome usually occurs with significant brain metabolism alterations resulting in critical brain network changes. These types of changes in the brain are usually explained by the “tyranny of the left hemisphere” theory, which indicates the inhibition of the left hemisphere to allow the right hemisphere to develop savant abilities. Another way to temporarily simulate these types of changes in the brain can be through different neuro-modulation techniques such as transcranial magnetic stimulation and transcranial direct current stimulation. Such neuromodulation techniques might help us discover the “hidden talent” potential through modulating the brain network metabolism. We herein discussed the types of savant syndrome along with its relation to specific neurometabolic network alterations. Furthermore, we provide a perspective on how newly developed neuromodulation and cognitive rehabilitation techniques can help simulate savant syndrome in healthy individuals through modulating the brain network activity.
Extracellular vesicles derived from neural progenitor cells--a preclinical evaluation for stroke treatment in mice (vol 12, pg 185, 2021)
(Springer, 2022) Zheng, Xuan; Zhang, Lin; Kuang, Yaoyun; Venkataramani, Vivek; Jin, Fengyan; Hein, Katharina; Zafeiriou, Maria Patapia; Lenz, Christof; Moebius, Wiebke; Kılıç, Ertuğrul; Hermann, Dirk Matthias; Weber, Martin S.; Urlaub, Henning; Zimmermann, Wolfram Hubertus; BäHR, Mathias; Doeppner, Thorsten Roland
In the version of this article initially published, there were errors on pages 5 and 6.
Protein and gene delivery systems for neurodegenerative disorders: Where do we stand today?
(MDPI, 2022) Siafaka, Panoraia I.; Okur, Mehmet Evren; Dilsiz Erim, Pelin; Çağlar, Emre Şefik; Özgenç, Emre; Gündoğdu, Evren; Parlar Köprülü, Rabia Edibe; Karantaş, Ioannis D.; Üstündağ Okur, Neslihan
It has been estimated that every year, millions of people are affected by neurodegenerative disorders, which complicate their lives and their caregivers’ lives. To date, there has not been an approved pharmacological approach to provide the complete treatment of neurodegenerative disorders. The only available drugs may only relieve the symptoms or slow down the progression of the disease. The absence of any treatment is quite rational given that neurodegeneration occurs by the progressive loss of the function or structure of the nerve cells of the brain or the peripheral nervous system, which eventually leads to their death either by apoptosis or necrotic cell death. According to a recent study, even though adult brain cells are injured, they can revert to an embryonic state, which may help to restore their function. These interesting findings might open a new path for the development of more efficient therapeutic strategies to combat devastating neurodegenerative disorders. Gene and protein therapies have emerged as a rapidly growing field for various disorders, especially neurodegenerative diseases. Despite these promising therapies, the complete treatment of neurodegenerative disorders has not yet been achieved. Therefore, the aim of this review is to address the most up-to-date data for neurodegenerative diseases, but most importantly, to summarize the available delivery systems incorporating proteins, peptides, and genes that can potentially target such diseases and pass into the blood–brain barrier. The authors highlight the advancements, at present, on delivery based on the carrier, i.e., lipid, polymeric, and inorganic, as well as the recent studies on radiopharmaceutical theranostics.
Detecting and targeting neurodegenerative disorders using electrospun nanofibrous matrices: Current status and applications
(Taylor & Francis Ltd, 2021) Siafaka, Panoraia I.; Özcan Bülbül, Ece; Dilsiz, Pelin; Karantas, Ioannis D.; Okur, Mehmet Evren; Üstündağ Okur, Neslihan
Neurodegeneration is defined as the progressive atrophy and loss of function of neurons; it is present in neurodegenerative disorders such as Multiple Sclerosis, Alzheimer's, Huntington's, and Parkinson's diseases. The detection of such disorders is performed by various imaging modalities while their therapeutic management is quite challenging. Besides, the pathogenesis of neurodegenerative disorders is still under ongoing research due to complex and multi-factorial mechanisms. Currently, targeting the specific proteins responsible for neurodegeneration is of great interest to many researchers. Furthermore, nanotechnology-based approaches for targeting the affected neurons became an emerging field of interest. Nanostructures of various forms have been developed aiming to act as therapeutics for neurodegeneration, in which electrospun nanofibers seem to play an important role as biomedical products for both detection and management of the diseases. Electrospinning is an intriguing method able to produce nanofibers with a wide range of sizes and morphological characteristics. Such nanofibrous matrices can be delivered through different administration routes to target various diseases. In this review, the most recent advancements in electrospun nanofibrous systems that target or detect multiple neurodegenerative diseases have been enlightened and an introduction to the general aspects of neurodegenerative diseases and the electrospinning process has been made. Finally, future perspectives of neurodegeneration targeting were also discussed.
Mesenchymal stem cell applications in polycystic ovary syndrome treatment
(Ondokuz Mayıs Üniversitesi, 2021) Bülbül, Muhammet Volkan; Yıldırım, Berna; Kolbaşı, Bircan; Keskin, İlknur
Mesenchymal stem cells (MSCs) are highly capable of self-renewal and differentiation. They can be isolated from a variety of sources such as adipose tissue, bone marrow, umbilical cord, tooth pulp and can be cultured under in vitro conditions. MSCs have anti-inflammatory, anti-apoptotic, angiogenic, immunomodulatory and many more therapeutic effects because of paracrine factors they secrete. Today, mesenchymal stem cells are used for treatment in more than twenty diseases, from spinal cord injuries to diabetes. However, there is little mention in the literature of the use of these cells in female reproductive system diseases. In this review, a limited number of clinical and experimental studies on the use of mesenchymal stem cells in the treatment of polycystic ovary syndrome, which is quite common in women, were examined and analyzed.
EEG measures for clinical research in major vascular cognitive impairment: recommendations by an expert panel
(Elsevier Inc., 2021) Babiloni, Claudio C.; Arakaki, Xianghong; Bonanni, Laura; Buján, Ana; Carrillo, María C.; del Percio, Claudio; Edelmayer, Rebecca M.; Egan, Gary; Elahh, Fanny M.; Evans, Alan Charles; Ferri, Raffaele; Frisoni, Glovannl B.; Güntekin, Bahar; Hainsworth, Atticus Henry; Hampel, Harald; Jeli?, Vesna; Jeong, Jaeseung; Kim, Doh-kwan; Kramberger, Milica Gregori?; Kumar, Sanjeev; Lizio, Roberta; Nobili, Flavio Mariano; Noce, Giuseppe; Puce, Aina; Ritter, Petra; Smit, Dirk J.A.; Soricelli, Andrea; Teipel, S.; Tucci, Federico
Vascular contribution to cognitive impairment (VCI) and dementia is related to etiologies that may affect the neurophysiological mechanisms regulating brain arousal and generating electroencephalographic (EEG) activity. A multidisciplinary expert panel reviewed the clinical literature and reached consensus about the EEG measures consistently found as abnormal in VCI patients with dementia. As compared to cognitively unimpaired individuals, those VCI patients showed (1) smaller amplitude of resting state alpha (8–12 Hz) rhythms dominant in posterior regions; (2) widespread increases in amplitude of delta (< 4 Hz) and theta (4–8 Hz) rhythms; and (3) delayed N200/P300 peak latencies in averaged event-related potentials, especially during the detection of auditory rare target stimuli requiring participants’ responses in “oddball” paradigms. The expert panel formulated the following recommendations: (1) the above EEG measures are not specific for VCI and should not be used for its diagnosis; (2) they may be considered as “neural synchronization” biomarkers to enlighten the relationships between features of the VCI-related cerebrovascular lesions and abnormalities in neurophysiological brain mechanisms; and (3) they may be tested in future clinical trials as prognostic biomarkers and endpoints of interventions aimed at normalizing background brain excitability and vigilance in wakefulness.
Experimental data of labeling the heart and cardiac cultures with a retrograde tracer in vitro and in vivo
(Elsevier Inc., 2021) Akgül Çağlar, Tuba; Günal, Mehmet Yalçın; Turhan, Mehmet Uğurcan; Öztürk, Gürkan; Çağavi, Esra
Retrograde dyes are often used in basic research to investigate neuronal innervations of an organ. This article describes the experimental data on the application of retrograde dyes on the mouse heart in vivo and on the cardiac or neuronal cultures in vitro. By providing this information, cardiac or inneinnervations can be evaluated in vivo. Therefore, unknown cellular and molecular mechanisms and systemic interactions in the body can be investigated. In particular, we provided practical tips to lower mortality risks following the cardiac surgery and evaluated the staining capacity and fluorescent characteristics of the Di-8-ANEPPQ dye in the cardiac tissue and cell cultures. First, primary cultures of mouse nodose ganglia (NG) neurons and mouse neonatal cardiomyocytes were stained with Di-8-ANEPPQ. The Di-8-ANEPPQ signal from live cultures were visualized using spinning disk confocal microscopy to verify the lipophilic and fluorescent labeling capacity of Di-8-ANEPPQ. Next, the excitation and emission data of Di-8-ANEPPQ were collected between 415 nm and 690 nm using power spectrum module of confocal microscopy. This spectrum analysis could be useful for the researchers who plan to use Di-8-ANEPPQ in combination with other fluorescent dyes to eliminate any florescent overlap. In order to label the heart tissue with tracer dyes Di-8-ANEPPQ or DiI in vivo, the heart was exposed without damaging lungs or other tissues following anesthetization, then the retrograde dye was applied as a paste for DiI or injected to the apex of the heart for Di-8-ANEPPQ and the operation area was sutured. The surgical procedure required intubation to control the respiratory reflex without the need to perform a tracheotomy and yielded high viability. Following labeling the heart in vivo, the heart was dissected, and images of injection area were captured using confocal microscopy. All fluorescent images of Di-8-ANEPPQ labeled cells were analyzed by using the Fiji software. Overall, these data provide applicable data to other investigators to trace the sensory neurons innervating not only the heart but also other organs using Di-8-ANEPPQ. These data support the original research article titled “Evaluation of bilateral cardiac afferent distribution at the spinal and vagal ganglia by retrograde labeling” that was accepted for publication in Brain Research Journal [1].
NextGen Voices: Quality mentoring
(New York, N.Y., 2018) Segal, Lauren; Agarwal, Divyansh; Isaacson, Kyle J; Oehmke, Theresa B; Kumar, Brijesh; Chen, Jennifer Shuen; Cusimano, Joseph Michael; Negi, Swati; Tiper, Irina; Bakermans, Adrianus J; Jensen, Mark Martin; Sanganyado, Edmond; Zaidi, Syed Shan-E-Ali; Romero-Molina, Carmen; Martinez, Santiago Esteban; Anderson, Sarah Marie; Santos, Guilherme Martins; de Lella Ezcurra, Ana Laura; Farragher, Janine; Sharma, Vandana; Duncan, Gregg; Dutton-Regester, Ken; Kim, Sun Ae; Yu, Sha; Schwendimann, Beat a; K V Reichardt, Juergen; Halder, Antarip; Dennis, Allison F; Ellwanger, Joel Henrique; Chiu, Yu-Han; Kerman, Bilal Ersen
In her Working Life, “Paying it forward as a mentor” (3 August, p. 522),B. Abderrahman describes how a mentor’s encouragement can help shapea career. She then explains how her positive mentorship experienceinspired her to mentor others. We asked young scientists to describe onequality of a mentor you’ve had that you will try to emulate when youbecome a mentor yourself. Respondents from around the world wrotein appreciation of their patient, honest, humble, and supportive.
Physiological and pharmacological roles of melatonin in the pathophysiological components of cellular injury after ischemic stroke
(NLM (Medline), 2020) Kılıç, Ertuğrul; Ça?layan, Berrak; Beker, Mustafa Çağlar
Apart from its metabolic or physiological functions, melatonin has a potent cytoprotective activity in the physiological and pathological conditions. It is synthetized by the pineal gland and released into the blood circulation but particularly cerebrospinal fluid in a circadian manner. It can also easily diffuse through cellular membranes due its small size and lipophilic structure. Its cytoprotective activity has been linked to its potent free radical scavenger activity with the desirable characteristics of a clinically- reliable antioxidant. Melatonin detoxifies oxygen and nitrogen-based free radicals and oxidizing agents, including the highly toxic hydroxyl-and peroxynitrite radicals, initiating cellular damage. However, the cytoprotective activity of melatonin is complex and cannot be solely limited to its free radical scavenger activity. It regulates cellular signaling pathways through receptor– dependent and independent mechanisms. Most of these downstream molecules, such as PI3K/AKT pathway components, also contribute to the cytoprotective effects of melatonin. In this term, melatonin is a promising molecule for the treatment of neurodegenerative disorders, such as ischemic stroke, which melatonin reduces ischemic brain injury in animal models of ischemic stroke. It regulates also circadian rhythm proteins after ischemic stroke, playing roles in cellular survival. In this context, present article summarizes the possible role of melatonin in the pathophysiological events after ischemic stroke.
The pleiotropic effects of TNF alpha in breast cancer subtypes is regulated by TNFAIP3/A20 (vol 38, pg 469, 2018)
(Nature Publishing Group, 2019) Lee, Eunmi; Ouzounova, Maria; Piranlıoğlu, Raziye; Ma, Minh Thu; Güzel, Mustafa; Marasco, Daniela; Chadli, Ahmed; Gestwicki, Jason E.; Cowell, John Kenneth; Wicha, Max S.; Hassan, Khaled A.; Korkaya, Hasan
Following publication of this article the authors noted that the Acknowledgments section had been omitted. This section should read as follows.
Early diagnosis of Alzheimer's disease: the role of biomarkers including advanced EEG signal analysis. Report from the IFCN-sponsored panel of experts
(Elsevier Ireland Ltd., 2020) Rossini, Paolo Maria; Di Iorio, Riccardo; Vecchio, F.; Anfossi, Maria; Babiloni, C.; Bozzali, M.; Bruni, Amalia Cecilia; Cappa, Stefano F.; Escudero, Julien; Fraga, Francisco Jose; Giannakopoulos, Panteleimon; Güntekin, Bahar; Logroscino, Giancarlo; Marra, Camillo; Miraglia, F.; Panza, Francesco; Tecchio, F.; Pascual-Leone, Alvaro; Dubois, Bruno
Alzheimer's disease (AD) is the most common neurodegenerative disease among the elderly with a progressive decline in cognitive function significantly affecting quality of life. Both the prevalence and emotional and financial burdens of AD on patients, their families, and society are predicted to grow significantly in the near future, due to a prolongation of the lifespan. Several lines of evidence suggest that modifications of risk-enhancing life styles and initiation of pharmacological and nonpharmacological treatments in the early stage of disease, although not able to modify its course, helps to maintain personal autonomy in daily activities and significantly reduces the total costs of disease management. Moreover, many clinical trials with potentially disease-modifying drugs are devoted to prodromal stages of AD. Thus, the identification of markers of conversion from prodromal form to clinically AD may be crucial for developing strategies of early interventions. The current available markers, including volumetric magnetic resonance imaging (MRI), positron emission tomography (PET), and cerebral spinal fluid (CSF) analysis are expensive, poorly available in community health facilities, and relatively invasive. Taking into account its low cost, widespread availability and non-invasiveness, electroencephalography (EEG) would represent a candidate for tracking the prodromal phases of cognitive decline in routine clinical settings eventually in combination with other markers. In this scenario, the present paper provides an overview of epidemiology, genetic risk factors, neuropsychological, fluid and neuroimaging biomarkers in AD and describes the potential role of EEG in AD investigation, trying in particular to point out whether advanced analysis of EEG rhythms exploring brain function has sufficient specificity/sensitiv ity/accuracy for the early diagnosis of AD.
Toward a personalized medicine in wake-up stroke?
(Bentham Science Publishers Ltd., 2017) Yuluğ, Burak; Hano?lu, Lütfü; Kılıç, Ertuğrul
Ischemic stroke (IS), especially wake-up stroke, is reported to occur with a maximal peak in the morning hoursand usually associated with worse clinical outcome [1-3].Many proposed mechanisms are reported to be responsiblefor the impaired clinical outcomes in IS patients, includinghemostatic and hemodynamic factors. Despite this fact, recent reports have pointed out that circadian pattern independently affects the outcome of IS that persists even whencontrolling for vascular risk factors and different treatmentmodalities (such as anti-platelet or anticoagulant treatment)
The neuroprotective effect of focused ultrasound: New perspectives on an old tool
(Pergamon-Elsevier Science Ltd., 2017) Yuluğ, Burak; Hanoğlu, Lütfü; Kılıç, Ertuğrul
Introduction Transcranial focused ultrasound (tFUS) is a novel technique that can noninvasively modulate the cortical function. Moreover, there are rapidly replicating evidence suggesting the role of tFUS for targeted neuroprotective drug delivery by increasing the permeability of the central nervous system barrier that results with increased neuroprotective activity. In contrast to the indirect neuroprotective effect, there is rare evidence suggesting the direct parenchymal neuroprotective effect of transcranial focused ultrasound (tFUS). In the light of these findings, we aimed to review the direct and indirect neuroprotective effect of FUS in various animal models of Stroke, Parkinson's Disease, Alzheimer's Disease and Major Depressive Disorder.Methods: A literary search was conducted, utilizing search terms "animal", "focused ultrasound", "neuroprotection", "Alzheimer's Disease", "Parkinson's Disease ", "Stroke", "Neurodegenerative disease" and "Major Depressive Disorder". Items were excluded if they failed to: (1) include patients, (2) editorials, and letters.Results: This mini-review article presents an up-to-date review of the neuroprotective effects of tFUS in animal studies and suggests the dual neurotherapeutic role of tFUS in various neurodegenerative diseases.Conclusion: Future well-conducted human studies are emergently needed to assess the neuroprotective effects of FUS.
Elevated ?-hydroxybutyric acid with no ketoacidosis in type 2 diabetic patients using sodium-glucose cotransporter-2 inhibitors
(Elsevier, 2019) Thapa, Simant Singh; Lal, Amos; Ömer, Abdulkadir; Trivedi, Nitin
SGLT2 inhibitor (SGLT2i) class of medications are known to cause to euglycemic diabetic ketoacidosis (euDKA) as reported in the article by Lin et al. in your esteemed publication about this entity being reported for the first time in Taiwanese population.1 We wish to share the findings from our center to further expand the spectrum of findings associated with SGLT2i therapy. SGLT2i treatment in patients with preexisting atherosclerotic heart disease and those with high risk of cardiovascular events is associated with a reduction in cardiovascular (CV) mortality, heart failure hospitalizations, and death from any cause.
A different view on the pathophysiology of Parkinson’s disease: A descendent neurochemical hypothesis?
(Wolters Kluwer, 2019) Yuluğ, Burak; Ozansoy, Mehmet; Çankaya, Şeyda
It has been already shown that Parkinson’s disease (PD) is characterized by a prominent degeneration in substantia nigra (SN)neurons. Growing evidence suggests that there is a latent period of PD associated with slight non-motor findings such as olfactorydys function (Dickson et al., 2018). However, the potential biomarker role of olfactory dysfunction in PD has been a topic of great interest in the last years (Raskin et al., 1990; Dicksonet al., 2018). The classical hypothesis of Braak suggests that PD begins as a synucleinopathy in the lower brainstem or in the olfactorybulb (OB) that progresses rostrally to the SN and amygdalato cause parkinsonism at a later stage of the disease (Burkeet al., 2008). However, Braak’s hypothesis should be cautiously interpreted since this scheme is not based on the distribution of neuronal cell loss, but on the distribution of the accumulation of abnormal ?-synuclein aggregates which leaves unanswered how it relates to the progression of neurochemical changes.

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