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juniperpublishers-crdoj · 5 years ago

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Impaired Cerebral Autoregulation-A Common Neurovascular Pathway in Diabetes may Play a Critical Role in Diabetes-Related Alzheimer’s Disease

Authored by Fan Fan

Abstract

Alzheimer’s disease (AD) is the leading cause of progressive degenerative dementia. The hallmark pathological features include beta amyloid deposition and neurofibrillary tangles. There has been astrong association of AD with Diabetes (DM) based on human studies and animal experiments. The hallmark features of AD seem to have an exaggerated presence in AD with DM, especially type 2 diabetes (T2D). In addition, insulin resistance is a common feature in both diseases and as such AD has been called type 3 diabetes. Furthermore, impairment of cerebral autoregulation has been reported in both animal and human diabetic subjects. Cerebral vascular impairment has also been implicated in the pathophysiology of AD. There is an urgent need to develop animal models of AD and DM to explore the neuropathological mechanisms of these disease and utilize such models to develop treatment strategies.

Keywords:Autoregulation; Myogenic response; Diabetes; Alzheimer’s; Dementia; Rat model; T2DN

AbbreviationsAD: Alzheimer’s Disease; DM: Diabetes; T2D: Type 2 diabetes; Aβ: Amyloid Beta; VSMC: Vascular Smooth Muscle Cells; CO2: Carbon Dioxide; ARIC-NCS: Atherosclerosis Risk in Communities-Neurocognitive Study; BBB: Blood Brain Barrier; APP: Amyloid Precursor Protein; MCA: Middle Cerebral Artery

Introduction

Alzheimer’s disease (AD) and diabetes (DM) are two of the leading ageing related disorders. AD prevalence accounts for an estimated 5.4 million Americans in 2016 [1], where as DM affects more than 29 million Americans in 2013 [2]. AD is the only leading cause of death (6th overall) [3] that lacks any therapy to slow or reverse its progression [4] followed by DM as the 7th leading cause of death in United States (US). The Medicare cost for the treatment of dementia and AD is $159 billion annually and is projected to rise to $511 billion by 2040 [5,6]. Similarly, DM prevalence is projected to triple by 2050 which costed the nation $245 billion per year in 2012 [2]. These untreatable chronic disorders will become a major economic burden long term.Thus, there is an urgent need to understand the mechanisms of these diseases in order to develop new therapeutic strategies that delay their progression.

Overall, we confirm the results presented on acute pancreatitis risk with DPP-4 inhibitors [10] and extend these findings to GLP-1 receptor agonists (lixisenatide, liraglutide, and semaglutide). Major alterations of the risk for acute pancteatitis or pancreatic cancer are not obvious from our analysis, with the exception of a slightly elevated risk for acute pancreatitis with DPP-4 inhibiutors as previously reported by Tkaz et al. [11]. Interestingly, the present analysis is slightly at variance with a previous analysis based on phase 3 trials with the same drugs, coming to the conclusion that, most likely, there is some elevation in risk for GLP-1 receptor agonists, but not for DPP-4 inhibitors [12]. We do not suggest the results regarding pancreatic cancer to indicate that this is proof for a protective effect (although formally, the estimates would support such conclusion). Rather, we suggest to take this as evidence against previous estimates of that risk [2,3]. The methods underlying these conclusions have been heavily criticised [13], but until now, no competing data have been available that would allow to derive independent analyses and conclusions based on state-of-the art methodology. The recent report of trials aiming at long-term exposure to incretin-based medications, as a by-product of cardio-vascular data, the primary motivation and endpoint, has yielded valuable information that is highly reassuring with respect to a potentially elevated cancer risk as a consequence of stimulating GLP-1 receptors.This, together with the proven benefits regarding cardiovascular outcomes reported for liraglutide [9] and semaglutide [14], will be important determinants of the present benefit-risk estimation for incretin-based medications.

Introduction

High comorbidity of DM and AD

AD is one of the most common forms of progressive degenerative brain disorders resulting in dementia [7,8]. AD is characterized by a decline in short term memory, problem-solving, complex cognitive skills and later language dysfunction. Loss in ability to perform everyday activities requires constant nursing and long -term dependence. This decline occurs because of wide spread cortical neuronal loss in areas of brain responsible for cognitive function. Whereas, DM is a variable disorder of carbohydrate metabolism resulting in hyperglycemia, which, if persists chronically, can lead to systemic complications including cognitive impairment T2D, which begins as insulin resistance and is the most common form of DM. Numerous studies demonstrate that diabetics are at an increased risk of developing AD especially in the elderly. As a result, AD has been proposed as Type 3 DM in appropriate context [9]. Recent animal studies are proposing an increased association of T2D with AD [10,11]. This association has also been corroborated in human epidemiological studies [12,13].

A clear mechanism underlying AD has yet to be fully understood. Earlier hypotheses of neuro degeneration in AD relied heavily on cholinergic deficiency, extracellular amyloid beta (Aβ) plaque formation, and hyperphosphorylated Tau protein induced neurofibrillary tangles [14]. However, current treatments and clinical trials targeting these pathways, such as using inhibitors of acetylcholinesterase [15], and γ secretase [16-19] or immunotherapy targeting to Aβ and Tau [18], have not been proved to be able to stop or slow down the disease process of AD. Lack of effective pharmacological interventions has led the community to reconsider alternatives [14].There is increased evidence indicating that cerebral vascular dysfunction plays an important role in the development of dementia and AD. A vascular pathogenesis has thus been proposed which comprises cerebral hypoperfusion, blood-brain barrier (BBB) dysfunction [14,20,21] and impaired cerebral microcirculation [22,23]. Diabetics with AD have increased numbers of beta amyloid plaques, tau-positive cells, advanced glycation end products and more activated microglia than the brains of AD patients without diabetes. These effects are markedly seen in the hippocampus [24]. The proposed mechanisms include insulin resistance [25], inflammation [26] and impaired glucose transporters [27]. However, there is additional impairment in cerebral autoregulation [28] resulting in microinfarction, hemorrhages, and eventual neuronal loss.

High Cerebral Autoregulation

Cerebral autoregulation was first described by Lassen in 1959, where he reported clinical studies assessing cerebral blood flow [29]. Since then, cerebral autoregulation has been broadly used to describe the local circulatory changes as well the global perfusion related changes in the brain [30]. For this review, we will use the cerebral autoregulation as blanket definition which encompasses both mechanoregulation as well chemoregulation. Perfusion related change occurring in large vessels has been described else where as mechanoregulation, where as, vascular changes occurring in response to changes in arterial CO2 is described as chemoregulation or metabolic regulation [30,31]. Furthermore, changes occurring locally around neurovascular junction are referred to as neurovascular coupling [30]. Cerebral autoregulation is an inherent mechanism where by the cerebral vasculature maintains constant cerebral blood flow by responding to systemic changes in blood pressure and thus maintaining neurovascular homeostasis [32-34]. Impaired cerebral autoregulation has been reported with advancing ageing [35-37], hypoxemia/ischemia [35] and hyperglycemia [38], suggesting these conditions are related to dysfunction at the autoregulatory pathway. Thus, it is important to understand the pathophysiology of cerebral autoregulation. The vessel’s ability to autoregulate with rise and drop in blood pressure is achieved mainly through myogenic response, and additional enhancement is achieved through metabolic activators [39]. Vascular smooth muscle cells (VSMC) are the main contractile vascular structures and are predominantly located in the wall of cerebral arteries as well pial and penetrating arterioles. These cells respond to pressure elevation by a constriction mechanism using Bayliss myogenic response [40]. Such response has been observed [33,34,41] in the middle cerebral artery territory (MCA) of the rats, where large diameter arteries (202μm) display greater myogenic response between 60-100 mmHg, whereas penetrating arterioles (58μm) show greater response between 20-16mmHg [42]. The myogenic response is enhanced by vasoconstrictors, e.g. Angiotensin II, ET1, and 20 HETE [33,43]. In contrast, during drop in blood pressure, vessels dilate in response to metabolic active vasodilators, e.g. Nitric Oxide (NO), endothelial derived hyperpolarizing factor, adenosine, extracellular K+, hydrogen ion, lactate, and carbon monoxide (CO) [44]. These metabolites are released at the level of neurovascular couplingfrom endothelial cells, and glial cells [45], including astrocytes [46], due to hypoxemia (reactive hyperemia) [47,48] or neuron activation (functional hyperemia) [45,49]. Thus, any dysfunction of these smooth muscles, endothelial and glial cells could result in autoregulatory dysfunction. Furthermore, the degree of vascular remodeling also contributes to the regulation of cerebral mechanoautoregulation. Increased vascular wall thickness and perivascular fibrosis could affect vascular compliance and decrease the ability of a blood vessel wall to expand in response to changes in blood pressure [50,51]. Enhanced vascular remodeling and decreased compliance has been reported in DM [52,53] as well in AD[54-56].

Cerebral autoregulation, DM and AD

Aging results in impairment of autoregulation which increases the risk of cerebral pathology including stroke, vascular cognitive impairment [57-60], and AD [60-62]. The risk isincreased with coexistence of hypertension and diabetes [63]. With ageing, there is increased rarefaction of small penetrating arteries to deeper structures of the brain especially the basal ganglia and periventricular white matter [59,62,64]. This results in compromised regional blood flow and formation of lacunar infarctions, as well microbleeds, all of which are correlated with decline in cognitive function [62,65,66]. As ageing advances, there is BBB breakdown, vascular remodeling, glial cell activation, and inflammation further exacerbating the neurodegeneration [51,58-60,67,68]. Evidence suggests that the myogenic response of the MCA is impaired in AD [44] and DM [69]. Persistent hyperglycemia is associated with cerebral vascular dysfunction, BBB leakage, and inflammation that may contribute to the development of neurodegeneration and eventually dementia. In AD, there is reduction in number of microvessels, VSMCs and flattening of endothelial cells [70], suggesting AD may be linked to impaired cerebral autoregulation. The Atherosclerosis Risk in Communities-Neurocognitive Study (ARIC-NCS) population, especially the diabetic population, was noted to have mild cognitive impairment (the early stage of AD) [12]. Two-hit hypothesis was first described by Zlokovic, BV. According to this hypothesis, there are vascular medicated injuries occurring from DM, Hypertension, and Stroke, which ensue a non-amyloidogenic pathway resulting in dementia [21]. In DM, arteriosclerosis occurs due to glycosylation, and as a result, vessels lose the stretch reflex, transferring the arterial pressure to the capillaries which in turn results in vascular leakage through breakdown of the BBB and oligemia (local reduction in blood flow): this last step is described as first hit [21]. consequently, the breakdown of BBB results in microinfarction, microbleeds, toxic accumulation and less clearance of Aβ proteins. Whereas, oligemia leads to APP expression and increased AB production which result in excess of Aβ: this step is described as second hit [21]. This furthers the cascade and thus perpetuates neuronal dysfunction and injury resulting in cognitive decline, and neurodegeneration [21,62,65].

Indeed, insulin resistance and glucose transporter dysfunction in the brain play important roles in T2D related AD. In a recent cohort study of about 1500 patients with T2D, researchers treated patients with Metformin vs. other hypoglycemic agents in order to observe change in cognition. They found that metformin intervention significantly reduced the risk of developing dementia by 20% when compared other diabetic therapies [71]. In another study, the use of sulfonylureas and metformin over 8 years, resulted in a decreased risk of dementia by 35% [72]. In addition, the amyloid precursor protein (APP) gene, which is associated with some cases of AD, has been shown to be involved in the insulin pathway. Therefore, impairment of this pathway can result in T2D [73]. On the other hand, impaired glucose utilization in mice via overexpression APP has been reported to cause derangement of CBF [74]. Furthermore, reduced expression of the glucose transporter GLUT1 [75,76] and GLUT3 [75,77] exacerbates AD, thus exacerbating the risk of dementia with each severe hypoglycemic episode in elderly diabetic patients [78-80].

Ideal Animal Models for Future Studies

To further elucidate the common pathology in AD and DM, there is need for an ideal animal model. A mixed mice model of T2D and AD has been generated by crossing APP/PS1 mice (AD model) with db/db mice (T2D model) [81]. This model exhibits microglia activation, BBB leakage, brain atrophy, and tau pathology. More recently, our group used a rat T2D model- T2DN, and found that it is associated with impaired autoregulation of CBF, glial activation, inflammation and Alzheimer-like cognitive deficits [82,83]. The T2DN rats closely mimic changes in diabetic patients and develops diabetic nephropathy at 6 months of age due to impaired renal autoregulation [84-86]. Nevertheless, both animal models exhibit cerebral vascular dysfunction suggesting a greater need to explore their common ground of vascular pathology.

Conclusion

AD and T2D are age dependent diseases. There are several potential mechanisms that have been proposed to be involved in the pathogenesis of AD including classical Aβ protein deposition, tau associated neurofibrillary tangles as well as the acetylcholine deficiency. Previous generations of treatment focusing on these mechanisms have failed to prevent the progression of AD, giving rise to the need for alternative therapeutic approaches. Recent studies have suggested that insulin resistance and cerebral autoregulation could be responsible for common pathogenesis in comorbid AD and DM. It is possible that impaired autoregulation is occurring very early before the onset of dementia. Whether this cerebral vascular dysfunction precedes neurodegeneration or whether it is simply an outcome of amyloid and tau deposition has yet to be validated. In order to identify this pathology and even to develop therapeutic interventions there is a great need for the development of an ideal animal model. The recent data on mixed T2D and AD mice and T2DN rat models are promising, however, further research is required to validate whether these models are ideal for mechanisms involved in “type 3 DM,’ especially starting from the cerebral vascular function aspect.

Acknowledgement

This study was supported by grants AG050049 (FF), P20GM104357 (FF) from the National Institutes of Health, and 16GRNT31200036 (FF) from the American Heart Association. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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medical-library202 · 6 years ago

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Abdullah bin Zayed presides over virtual meetings of Education and Human Resources Council

ABU DHABI, 6th April, 2020 (WAM) — H.H. Sheikh Abdullah bin Zayed Al Nahyan, Minister of Foreign Affairs and International Cooperation, and Chairman of the Education and Human Resources Council, EHRC, said the UAE boasts qualified cadres at the federal and local levels who are capable of coming up with innovative solutions to ensure a successful national development drive.

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daryljdugdale · 5 years ago

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IMPOWER 150-AT LAST IT BEGINS - pt1

So after six weeks and one day since notification my treatment plan must change, and after a series of blunders by both of my consultants, I got the go ahead my treatment would begin on the 6th July. I had to wait until the morning and a series of phone calls to and from the oncology department to check for bed availability, but we got the green light 9.45 am. TC and I dashed straight to the hospital determined our slot would not be taken by some one else whose priority was determined during our transit. It is an awful thing and a sad indictment on our politicians that there are not enough resources available within our health services that even those in acute need receive a service that in lots of cases adds to the stress and pain they might already be suffering. Having been closely connected to the health service in various ways since my diagnosis I know how much the majority of nurses and doctors care about their work. There are always going to be a small number of rotten apples like there are in any large organisation. I have to say my experience with one or two exceptions has been fantastic and extremely person centred. Now I am involved with more intrusive intervention it will be interesting to see how this changes if at all. After arriving in a busy department we are met by the staff in charge who explains she is on the phone to pharmacology to check where my drugs are! Not a great start. Then they realise I not had bloods taken for more than 3 weeks, a necessity before chemo starts. This delays things by a further hour or so as they await results. I’m happy enough though sat in a chair reading through the large ruck sack of books and papers I have to keep me occupied. Comedy moment whilst waiting for my bloods they wheel a rather life like dummy into the room followed by a lot of students preparing for a training simulation. TC who wasn’t wearing her glasses suddenly froze and squeezing my hand tightly said “ he doesn’t look well at all” she genuinely thought it was a real patient. We then spent the next half hour listening to what felt like an episode from casualty. The staff and trainers were very courteous in apologising for the noise and imposition but it was genuinely interesting. I was left with questions as to how much was learnt by the participants and how the training was evaluated. My previous role as trainer and educator coming to the fore. After a nearly two hour wait the first drugs were infused. Now impower 150 sounds a bit like an isotonic sports drink, but it is anything but. It’s a treatment plan that combines two traditional chemo drugs with a targeted therapy drug and an immunotherapy drug. Each is given sequentially and the total infusion lasts about 8 hours. I had been warned by my consultants and in the literature given to me that this was a complex blend of toxic drugs with potentially challenging side effects. This was something TC and I had to consider before consenting. Being relatively young and healthy and apart from the cancer ingressing my hip pain free, I thought it was worth a shot. Twelve hours after arriving we were free to leave the process completed. I had no side effects during the infusion save a little bit of heart burn and a small pain for about 20 minutes in my left arm where the infusion was entering, but neither were significant enough for me to inform the nurses. As we drove home, greeted before we did by Ede and her friend Izzy who had travelled across from London for St. Paul’s carnival which we were all planning on going to, we decided to stop off at the chippy for a fish and chip supper. It was a special treat after the days medical interventions and probably not what my consultants would have recommended. As I went to sleep I remember feeling a sense of satisfaction that I had finally gotten through the next stage of treatment. That battle was now over the next battle was dealing with the toxicity of the drugs and trying to keep myself healthy and exercised.

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Test Bank for Essentials of Pharmacology for Health Occupations 6th Edition by Woodrow Colbert and Smith

This is completed downloadable of Test Bank for Essentials of Pharmacology for Health Occupations 6th Edition by Ruth Woodrow,‎ Bruce Colbert and David M. Smith

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Product Descriptions

Essentials of Pharmacology for Health Occupations, 6th Edition provides an extensive framework of drug information in a concise format for learners studying licensed practical nursing, medical assisting and other allied health professions. Learn calculations quickly through a simplified step-by-step process. Discover key drug information by classifications, such as their purpose, side effects, cautions, and interactions, or utilize this resource to refresh your knowledge of drugs. The accompanying CD-ROM helps learners master pharmacology through quizzes, games, and case studies with immediate feedback and medication administration techniques and safety video clips. Open this resource now and see how easy learning pharmacology can be.

Test Bank for Essentials of Pharmacology for Health Occupations 6th Edition by Woodrow Colbert and Smith

Table of Contents

PART 1: INTRODUCTION 1. Consumer Safety and Drug Regulations 2. Drug Names and References 3. Sources and Bodily Effects of Drugs 4. Medication Preparations and Supplies 5. Abbreviations and Systems of Measurement 6. Safe Dosage Preparation 7. Responsibilities and Principles of Drug Administration 8. Administration by the Gastrointestinal Route 9. Administration by the Parenteral Route 10. Poison Control

PART II: DRUG CLASSIFICATIONS 11. Vitamins, Minerals, and Herbs 12. Skin Medications 13. Autonomic Nervous System Drugs 14. Antineoplastic Drugs 15. Urinary System Drugs 16. Gastrointestinal Drugs 17. Anti-infective Drugs 18. Eye Medications 19. Analgesics, Sedatives, and Hypnotics 20. Psychotropic Medications, Alcohol, and Drug Abuse 21. Musculoskeletal and Anti-inflammatory Drugs 22. Anticonvulsants, Antiparkinsonian Drugs, and Agents for Alzheimer’s Disease 23. Endocrine System Drugs 24. Reproductive System Drugs 25. Cardiovascular Drugs 26. Respiratory System Drugs and Antihistamines 27. Drugs and Older Adults

Product Details

Language: English ISBN-10: 1435480333 ISBN-13: 978-1435480339 ISBN-13: 9781435480339