Cause Of Alzheimer's Disease Research Articles

Diverse Heterocyclic Molecules Targeting Oxidative Stress as Therapeutic Effects Against Various Neurological Diseases

Abstract: Heterocyclic compounds are the most common and diverse group of organic substances. Heterocyclic compounds are rapidly increasing in number as a result of intensive synthetic research as well as their value in other synthetic procedures. More than 90% of medications contain heterocyclic rings, and a wide range of medicinal chemistry applications make use of these substances. There are always unique characteristics of an efficient approach for creating newly discovered heterocyclic compounds and their moieties. Due to their biological effects, including those that are anti-cancer, anti-inflammatory, anti-fungal, anti-allergic, antibacterial, antiviral, and anticonvulsant, heterocyclic compounds are crucial to medicinal chemistry. Today's world population is generally suffering from various neurodegenerative diseases. Out of that, the most prevailing disease is Alzheimer's. There are many causes of Alzheimer's disease-like acetylcholinesterase enzyme, tau protein, amyloid aggregation, oxidative stress, phosphodiesterase, and others. In these cases, oxidative stress plays a very important role in the progression of this disease. To combat this oxidative stress various antioxidant-derived drugs have been used but the problem is that Alzheimer's progression cannot be targeted with a single target drug because of the other factors that are involved in its progression. So to overcome that, a drug targeting multiple targets has been synthesized by using the antioxidant in previous reports. These drugs are more potent and efficacious than single-target drugs. This review focused on various multi-target ligands to target oxidative stress.

Patterning amyloid-β aggregation under the effect of acetylcholinesterase using a biological nanopore - an in vitro study

Aggregation of amyloid-β peptide (Aβ) is hypothesized to be the primary cause of Alzheimer's disease (AD) progression. Aβ aggregation has been widely studied using conventional sensing tools like emission fluorescence, electron microscopy, mass spectroscopy, and circular dichroism. However, none of these techniques can provide cost-efficient, highly sensitive quantification of Aβ aggregation kinetics at the molecular level. Among the influences on Aβ aggregation of interest to disease progression is the acceleration of Aβ aggregation by acetylcholinesterase (AChE), which is present in the brain and inflicts the fast progression of disease due to its direct interaction with Aβ. In this work, we demonstrate the ability of a biological nanopore to map and quantify AChE accelerated aggregation of Aβ monomers to mixed oligomers and small soluble aggregates with single-molecule precision. This method will allow future work on testing direct and indirect effects of therapeutic drugs on AChE accelerated Aβ aggregation as well as disease prognosis.

A Triterpenoid Lupeol as an Antioxidant and Anti-Neuroinflammatory Agent: Impacts on Oxidative Stress in Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common neurodegenerative disease illustrated by neuronal dysfunctions, leading to memory weaknesses and personality changes mostly in the aged population worldwide. The exact cause of AD is unclear, but numerous studies have addressed the involvement of oxidative stress (OS), induced by reactive oxygen species (ROS), to be one of the leading causes in developing AD. OS dysregulates the cellular homeostasis, causing abnormal protein and lipid metabolism. Nutrition plays a pivotal role in modulating the antioxidant system and decreases the neuronal ROS level, thus playing an important therapeutic role in neurodegenerative diseases, especially in AD. Hence, medicinal herbs and their extracts have received global attention as a commercial source of antioxidants Lupeol. Lupeol is a pentacyclic triterpenoid and has many biological functions. It is available in fruits, vegetables, and medicinal plants. It has shown effective antioxidant and anti-inflammatory properties, and higher blood–brain barrier permeability. Also, the binding and inhibitory potentials of Lupeol have been investigated and proved to be effective against certain receptor proteins and enzymes in AD studies by computational molecular docking approaches. Therefore, AD-related research has gained interest in investigating the therapeutic effects of Lupeol. However, despite its beneficial effects in AD, there is still a lack of research in Lupeol. Hence, we compiled in this analysis all preclinical research that looked at Lupeol as an antioxidant and anti-inflammatory agent for AD.

Synthesis and evaluation of curcumin-based near-infrared fluorescent probes for detection of amyloid β peptide in Alzheimer mouse models

The abnormal accumulation of amyloid β protein (Aβ) is one of the most important causes of Alzheimer's disease (AD) and is usually a detecting biomarker. Curcumin and its derivatives have potential Aβ aggregate targeting ability; we synthesized a series of curcumin-based near-infrared fluorescence probes in this study. By characterizing the excitation wavelength and emission wavelength, the imaging characteristics of the investigation in the near-infrared light region were determined; with an increase in the concentration of the probe compounds, the fluorescence intensity showed an upward trend, demonstrating ideal optical characteristics. In vivo, imaging results showed that the synthesized probe compounds could penetrate the blood–brain barrier (BBB) and specifically bind to Aβ in the brain of APP/PS1 mice. Especially for compound 3b, the maximum emission wavelength was around 667 nm, and the fluorescence signal intensity in the brain of the APP/PS1 mice model was more than twice that of the wild control group at 120 min after administration, which could display Aβ pathological changes. The fluorescent probes designed in this study can become an effective tool for early AD diagnosis and visual detection.

Relationship between the tau protein and choroid plexus volume in Alzheimer's disease.

Tau protein accumulation in the brain is thought to be one of the causes of Alzheimer's disease (AD). Recent studies found that the choroid plexus (CP) has a role in β-amyloid and tau protein clearance in the brain. We evaluated the relationships between CP volume and the ß-amyloid and tau protein depositions. Participants were 20 patients with AD and 35 healthy subjects who underwent MRI and PET scanning using the ß-amyloid tracer 11C-PiB and the tau/inflammatory tracer 18F-THK5351. We computed the volume of the CP and estimated the relationships between the CP volume and ß-amyloid and tau protein/inflammatory deposition by Spearman's correlation test. The CP volume was significantly positively correlated with both the standardized uptake value ratio (SUVR) of 11C-PiB and the SUVR of 18F-THK5351 in all participants. The CP volume was also significantly positively correlated with the SUVR of 18F-THK5351in patients with AD. Our data suggested that the volume of the CP was a good biomarker for the evaluation of tau deposition and neuroinflammation.

Brain reserve is associated with cognition in AD and MCI patients with different vascualr risk factors status

AbstractBackgroundDementia due to Alzheimer’s disease (AD) is the major type of dementias in the world. In addition to amyloid plaques and neurofibrillary tangles, cerebrovascular disease is another important pathophysiological cause of AD. Cerebrovascular disease is highly associated with vascular risk factors (VRFs). Well‐treated VRFs might decrease the risk and progression of AD. However, findings on the impact of VRFs treatment status on cognitive decline after the diagnosis of AD established are unclear, and there is no direct evidence supporting well‐treated VRFs can slow down the AD progression.MethodThis study recruited mild cognitive impairment (MCI) and mild AD patients (CDR = 0.5 or 1) with at least one VRF from at Taichung Veteran General Hospital. The treatment status of the VRFs was identified and all participants were evaluated by a standard neuropsychological test battery. We collected the participants’ brain MRI done within one year and performed Apolipoprotein E genotyping. FreeSurfer was used for structural MRI reconstruction and calculated total gray matter volume, hippocampus volume, and AD signature cortical thickness. Cerebrovascular lesions, including perivascular spaces in centrum semiovale, basal ganglia and presence of lobar cerebral microbleeds (LCMBs), and the volume of white matter hyperintensities were estimated by visual rating scales and Lesion Segmentation Tool for Statistical Parametric Mapping. We analyzed the relationships among the treatment status of VRFs, neuropsychological tests, and brain MRI.ResultWe recruited 61 patients in this study. Four patients refused to keep involving the study, 6 patients were not compatible with the criteria of MCI and AD after neuropsychiatric testing, and 4 patients’ brain MRI images cannot be analyzed after quality checked. The remaining 47 patients (15 MCI patients and 32 AD patients) constituted the final sample for analysis. The patients with well‐controlled VRFs present with similar cognitive function compared to the patients with partially‐controlled VRFs even though the more severe hippocampal atrophy was noted in the patients with well controlled VRFs. The severity of white matter hyperintensities and other cerebrovascular lesions are not correlated with the cognitive function in MCI and AD patients.ConclusionBrain reserve in the AD and MCI patients with well‐controlled VRFs might contribute cognitive function

Potential Alzheimer's disease therapeutic nano-platform: Discovery of amyloid-beta plaque disaggregating agent and brain-targeted delivery system using porous silicon nanoparticles.

There has been a lot of basic and clinical research on Alzheimer's disease (AD) over the last 100 years, but its mechanisms and treatments have not been fully clarified. Despite some controversies, the amyloid-beta hypothesis is one of the most widely accepted causes of AD. In this study, we disclose a new amyloid-beta plaque disaggregating agent and an AD brain-targeted delivery system using porous silicon nanoparticles (pSiNPs) as a therapeutic nano-platform to overcome AD. We hypothesized that the negatively charged sulfonic acid functional group could disaggregate plaques and construct a chemical library. As a result of the in vitro assay of amyloid plaques and library screening, we confirmed that 6-amino-2-naphthalenesulfonic acid (ANA) showed the highest efficacy for plaque disaggregation as a hit compound. To confirm the targeted delivery of ANA to the AD brain, a nano-platform was created using porous silicon nanoparticles (pSiNPs) with ANA loaded into the pore of pSiNPs and biotin-polyethylene glycol (PEG) surface functionalization. The resulting nano-formulation, named Biotin-CaCl2-ANA-pSiNPs (BCAP), delivered a large amount of ANA to the AD brain and ameliorated memory impairment of the AD mouse model through the disaggregation of amyloid plaques in the brain. This study presents a new bioactive small molecule for amyloid plaque disaggregation and its promising therapeutic nano-platform for AD brain-targeted delivery.

Assessing inflammasome activity in mouse models of Down syndrome and organotypic brain slice cultures

AbstractBackgroundDown syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is a leading genetic cause of Alzheimer’s disease. Neuroinflammation occurs in the DS brain, with altered microglial morphology and transcriptional profiles, and upregulated proinflammatory cytokines, including IL‐1β. IL‐1β is produced by inflammasome activity. We hypothesize that IL‐1β levels are raised in the DS brain via upregulation of inflammasome activity or heightened sensitivity to inflammasome stimuli, which persists when people with DS develop AD.MethodLevels of 10 cytokines, including IL‐1β, TNFα and IL‐6 were measured (MSD) in the 3‐month hippocampus of a panel of segmental duplication mouse models of DS; Dp1Tyb, Dp2Tyb, Dp3Tyb, Dp9Tyb, Dp10Yey and Dp17Yey. These models have a duplication on one chromosome of a number of orthologues for Hsa21 genes. Organotypic brain slice cultures (OBSCs) were prepared from Dp1Tyb mice and stimulated with LPS ± nigericin, to determine if they have an altered response to inflammasome stimuli, as measured by ELISA for cytokines and IHC for IBA1 and ASC.ResultRaised IL‐1β abundance was identified in the hippocampus of the Dp1Tyb mouse, which has an additional copy of 148 mouse orthologues for Hsa21 genes. No difference in IL‐1β or other cytokines measured were identified in the Dp3Tyb, Dp9Tyb, Dp2Tyb, Dp10Yey or Dp17Yey hippocampus, which have 37, 76, 33, 31 and 19 genes in three copies respectively. LPS + nigericin treatment does not affect the secretion of IL‐1β from Dp1Tyb OHSCs compared to WT controls, nor the number of ASC specks formed.ConclusionRaised IL‐1β in the Dp1Tyb brain is a multigenic phenotype, with three‐copies of more than one gene/region of Hsa21 required to drive the phenotype. This is not due to increased sensitivity to inflammasome stimuli in Dp1Tyb OBSCs. Next, we will determine what products are raised in the Dp1Tyb brain that have the potential to increase IL‐1β production, and Dp1Tyb OBSCs will be treated with these products, E.g. Aβ. Here, we are further understanding the mechanisms of neuroinflammation in DS, which is critical in determining how AD‐DS differs from AD, and if people with DS can be included in AD research and clinical trials.

Assessing farmer's exposure to pesticides and the risk for non-communicable diseases: A biomonitoring study

This cross-sectional study aimed to assess the adverse effects of pesticide use in humans, such as non-communicable diseases, using acetylcholinesterase (AChE) and pesticide concentrations in blood samples. A total of 353 samples (290 case and 63 control) were collected from participants with >20 years of experience in agricultural pesticide use. The pesticide and AChE concentrations were determined using Liquid Chromatography with tandem mass spectrometry (LC-MS/MS) and Reverse Phase High Performance Liquid Chromatography (RP-HPLC). Various health risks from pesticide exposure were assessed, including dizziness or headache, tension, anxiety, confusion, loss of appetite, loss of balance, concentration difficulties, irritability, anger, and depression. These risks may be influenced by the duration and intensity of exposure, the type of pesticide, and environmental factors in the affected areas. A total of 26 pesticides were detected in the blood samples from the exposed population, including 16 insecticides, three fungicides, and seven herbicides. Pesticide concentrations ranged from 0.20 to 12.12 ng/mL, and were statistically significant between the case and control groups (p < 0.05, p < 0.01, and p < 0.001). A correlation analysis was performed to determine statistically significance between pesticide concentration and symptoms of non-communicable diseases, such as Alzheimer's, Parkinson's, obesity, and diabetes. The estimated AChE levels in case and control blood samples were 21.58 ± 2.31 and 24.13 ± 1.08 U/mL, respectively (mean ± SD). The AChE levels were significantly lower in case samples than in controls (p < 0.001), which is considered to be an effect of long-term pesticide exposure, and is the cause of Alzheimer's disease (p < 0.001), Parkinson's disease (p < 0.001), and obesity (p < 0.01). Chronic exposure to pesticides and low levels of AChE are somewhat related to non-communicable diseases.

A Closer Look at Hearing Loss, Dementia, and Stigma

A Closer Look at Hearing Loss, Dementia, and Stigma

π-stacking interactions between curcumin and aromatic ring of amino acids in amyloid fibrils: A theoretical study

The aggregation of amyloid-β peptides into amyloid fibrils is considered as one of the possible causes of Alzheimer's disease. Curcumin is a well-known inhibitor for aggregation of Aβ1-42 peptides and has the ability to disintegrate preformed Aβ fibrils and amyloid plaques. This study provides an insight on the magnitude of π-stacking interactions between the aromatic AAs of Aβ and curcumin via quantum mechanical methods in gas phase and in water solvent. The results showed stacking interaction energies for CurK and amino acids are greater. The calculated charges on carbon atoms showed that B ring in CurE is more susceptible to π-stacking interaction. HOMO-LUMO energy gap showed that CurE is a better antioxidant than CurK. It was shown that the sum of electron densities, Ʃρ/n, calculated at BCPs and RCPs can be useful as descriptors for prediction of π-stacking interaction in the complexes.

Phenotype and imaging features associated with APP duplications

BackgroundAPP duplication is a rare genetic cause of Alzheimer disease and cerebral amyloid angiopathy (CAA). We aimed to evaluate the phenotypes of APP duplications carriers.MethodsClinical, radiological, and neuropathological features of 43 APP duplication carriers from 24 French families were retrospectively analyzed, and MRI features and cerebrospinal fluid (CSF) biomarkers were compared to 40 APP-negative CAA controls.ResultsMajor neurocognitive disorders were found in 90.2% symptomatic APP duplication carriers, with prominent behavioral impairment in 9.7%. Symptomatic intracerebral hemorrhages were reported in 29.2% and seizures in 51.2%. CSF Aβ42 levels were abnormal in 18/19 patients and 14/19 patients fulfilled MRI radiological criteria for CAA, while only 5 displayed no hemorrhagic features. We found no correlation between CAA radiological signs and duplication size. Compared to CAA controls, APP duplication carriers showed less disseminated cortical superficial siderosis (0% vs 37.5%, p = 0.004 adjusted for the delay between symptoms onset and MRI). Deep microbleeds were found in two APP duplication carriers. In addition to neurofibrillary tangles and senile plaques, CAA was diffuse and severe with thickening of leptomeningeal vessels in all 9 autopsies. Lewy bodies were found in substantia nigra, locus coeruleus, and cortical structures of 2/9 patients, and one presented vascular amyloid deposits in basal ganglia.DiscussionPhenotypes associated with APP duplications were heterogeneous with different clinical presentations including dementia, hemorrhage, and seizure and different radiological presentations, even within families. No apparent correlation with duplication size was found. Amyloid burden was severe and widely extended to cerebral vessels as suggested by hemorrhagic features on MRI and neuropathological data, making APP duplication an interesting model of CAA.

Advances in the Study of APOE and Innate Immunity in Alzheimer's Disease.

Alzheimer's disease (AD) is a progressive degenerative disease of the nervous system (CNS) with an insidious onset. Clinically, it is characterized by a full range of dementia manifestations including memory impairment, aphasia, loss of speech, loss of use, loss of recognition, impairment of visuospatial skills, and impairment of executive function, as well as changes in personality and behavior. The exact cause of AD has not yet been identified. Nevertheless, modern research indicates that genetic factors contribute to 70% of human's risk of AD. Apolipoprotein (APOE) accounts for up to 90% of the genetic predisposition. APOE is a crucial gene that cannot be overstated. In addition, innate immunity plays a significant role in the etiology and treatment of AD. Understanding the different subtypes of APOE and their interconnections is of paramount importance. APOE and innate immunity, along with their relationship to AD, are primary research motivators for in-depth research and clinical trials. The exploration of novel technologies has led to an increasing trend in the study of AD at the cellular and molecular levels and continues to make more breakthroughs and progress. As of today, there is no effective treatment available for AD around the world. This paper aims to summarize and analyze the role of APOE and innate immunity, as well as development trends in recent years. It is anticipated that APOE and innate immunity will provide a breakthrough for humans to hinder AD progression in the near future.

Amyloid- Signal Transduction Antagonist, A Possible Way to Relief Alzheimers Disease

As a well-known common neurodegenerative disease in aging, Alzheimers disease will cause the loss of the ability to talk, cognization and memorize. Amyloid beta is considered to be a major cause of Alzheimers disease. It will form many different types and accumulate in human brain and cause Alzheimers disease. However, a recent report about the plagiarism of the fundamental paper of this theory makes many people think that our research direction on Alzheimers disease is wrong. The author agrees that the plagiarism of the paper is terrible and should be punished, but the author does not think that this will waste everything we have done about amyloid beta. Amyloid beta is still a major reason that causes Alzheimers disease and find a way to stop the accumulation of amyloid beta in brain is a feasible way to cure Alzheimers disease. Research on the role of amyloid beta in Alzheimers disease, whether it is a major cause is the major purpose of the essay. Whats more a new method that aim to reduce amyloid beta in brain to cure and relief Alzheimers disease will be introduced in this article. This method aims to stop the signal transduction of amyloid beta to neuron cells, thus, stop amyloid beta from damaging our brain and cause Alzheimers disease. The reason this article is written is to confirm the importance of amyloid beta for Alzheimers disease. In addition, introduce a new cure method. Since this method is new, conclude the advantages and disadvantages of this method could inspire other researchers, and improve the performance of the drugs developed based on this method to reach the final goal, which is cure the Alzheimers disease.

Basic Concepts, Hypotheses and Drug Development of Alzheimer's Disease

Alzheimer's disease (AD) is a neurodegenerative disease that involves complicated pathogenesis and etiology that not entirely defined. As the most common form of dementia, AD is irreversibly progressive and aggravates, causing a great burden to global community. Meanwhile, the number of AD patients is growing annually with the global population aging. Unfortunately, there is currently no cure for the disease and the need for effective treatments of AD is urgent. Drug research and development for AD is a long-term and complicated process, which requires a deep understanding of the mechanisms of AD. At present, anti-Tau protein drugs as well as anti-inflammatory drugs are hot research topics. However, the clinical application of drugs still remains to improve various symptoms related to AD. This paper describes the basic concepts of pathology and gives an overview of the pathogenesis theories of AD, which include A hypothesis, Tau protein hyperphosphorylation theory, Cholinergic hypothesis and Inflammatory response. The final onset of AD is jointly caused by multiple mechanisms rather than a single one. In the paper, we summarizes the treatment strategies of AD and explores the status of drug development. This paper will help with understanding the causes of AD and provide insights into drug research and development for AD.

The Role of Mitochondrial Dysfunction in Alzheimer's: Molecular Defects and Mitophagy-Enhancing Approaches.

Alzheimer's disease (AD), a progressive and chronic neurodegenerative syndrome, is categorized by cognitive and memory damage caused by the aggregations of abnormal proteins, specifically including Tau proteins and β-amyloid in brain tissue. Moreover, mitochondrial dysfunctions are the principal causes of AD, which is associated with mitophagy impairment. Investigations exploring pharmacological therapies alongside AD have explicitly concentrated on molecules accomplished in preventing/abolishing the gatherings of the abovementioned proteins and mitochondria damages. Mitophagy is the removal of dead mitochondria by the autophagy process. Damages in mitophagy, the manner of diversified mitochondrial degeneracy by autophagy resulting in an ongoing aggregation of malfunctioning mitochondria, were also suggested to support AD. Recently, plentiful reports have suggested a link between defective mitophagy and AD. This treaty highlights updated outlines of modern innovations and developments on mitophagy machinery dysfunctions in AD brains. Moreover, therapeutic and nanotherapeutic strategies targeting mitochondrial dysfunction are also presented in this review. Based on the significant role of diminished mitophagy in AD, we suggest that the application of different therapeutic approaches aimed at stimulating mitophagy in AD would be beneficial for targeting or reducing the mitochondrial dysfunction induced by AD.

A global view of the genetic basis of Alzheimer disease.

The risk of Alzheimer disease (AD) increases with age, family history and informative genetic variants. Sadly, there is still no cure or means of prevention. As in other complex diseases, uncovering genetic causes of AD could identify underlying pathological mechanisms and lead to potential treatments. Rare, autosomal dominant forms of AD occur in middle age as a result of highly penetrant genetic mutations, but the most common form of AD occurs later in life. Large-scale, genome-wide analyses indicate that 70 or more genes or loci contribute to AD. One of the major factors limiting progress is that most genetic data have been obtained from non-Hispanic white individuals in Europe and North America, preventing the development of personalized approaches to AD in individuals of other ethnicities. Fortunately, emerging genetic data from other regions - including Africa, Asia, India and South America - are now providing information on the disease from a broader range of ethnicities. Here, we summarize the current knowledge on AD genetics in populations across the world. We predominantly focus on replicated genetic discoveries but also include studies in ethnic groups where replication might not be feasible. We attempt to identify gaps that need to be addressed to achieve a complete picture of the genetic and molecular factors that drive AD in individuals across the globe.

Basics of Alzheimer’s Disease and Dementia

Alzheimer’s Disease (AD) is a disorder that causes degeneration of the cells in the brain and it is the main cause of dementia, which is characterized by a decline Independence in an individual’s daily activities. AD is considered a multifactorial disease. Two main hypotheses have been proposed as the cause of AD. The cholinergic hypothesis and the amyloid hypothesis. In addition, several risk factors have been implicated in this disease, including aging, genetic factors, head trauma, vascular disease, infections, and environmental factors. Currently, there are only two classes of drugs approved for the treatment of AD, including cholinesterase enzyme inhibitors and N-Methyl-D-Aspartic Acid (NMDA) antagonists, which are not associated with AD symptoms or disease. Prevent. Today, research is focused on understanding the pathology of AD by targeting multiple mechanisms such as alteration of AD course. This review describes the drugs currently available and future theories for the development of new treatments for AD, including Disease-Modifying Therapies (DMTs), chaperones, and natural products.

Reactions

WOMEN IN SCIENCE Reactions ShareShare onFacebookTwitterWechatLinked InRedditEmail C&EN, 2023, 101 (11), p 3April 3, 2023Cite this:C&EN 101, 11, 3Letters to the editorShyamala RajenderThank you, Shyamala Rajender. Having been an undergraduate at Cornell University, class of 1967, with a group of 15 female chemistry majors, I had no idea that women were discriminated against in chemistry when I arrived at the Massachusetts Institute of Technology. In general we were treated well, but I learned that we were the first women in chemistry to be allowed to be classroom and lab teaching fellows. All of a sudden I realized that I had never had any female chemistry professors! I looked around, and few universities had even one female chemistry faculty member. Later, when applying for jobs, I was asked to promise not to get pregnant.So thank you, Dr. Rajender. Your case against the University of Minnesota had to be one of the first to detail and fight against discrimination against women in an academic science department. You are my heroine.Georgia WeinsteinLexington, MassachusettsCardiovascular disease and Alzheimer’s diseaseI was struck by the analogy between cholesterol/cardiovascular disease (CVD) and amyloid-β/Alzheimer’s disease in the excellent article in the March 13 issue of C&EN (page 20). The analogy is probably more apt than the rest of the article suggests. In the 1970s and ’80s, most people thought cholesterol caused CVD. While it is true that drugs that manipulate cholesterol have had some positive effects, it is now clear that inflammation may play a causal role in CVD. The plaques on arteries form after the inflammation, and there are multiple causes for this. Actual causes include bacteria in the bloodstream, insulin, tobacco, and stress hormones. The limited success with Alzheimer’s drugs, even when they reduce plaques in the brain, is interpreted by some researchers in the field as evidence there is an underlying cause of Alzheimer’s disease that has not yet been discovered. That idea was missing from this otherwise informative article.David E. HendersonHanover, New Hampshire CorrectionFeb. 20/27, 2023, page 40: The Newscripts article on Parafilm has an incorrect name for the current manufacturer of the material. It is Amcor, not Bemis Manufacturing Company.

Review Current and Emerging Treatment Options for Alzheimer's Disease

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects cognitive function, memory, and behavior. Currently, available treatments for AD primarily focus on managing symptoms, rather than addressing the underlying disease process. However, there is ongoing research and development in the field of AD treatment, with the hope of finding new and more effective therapies. Medications, such as cholinesterase inhibitors and NMDA receptor antagonists, are primarily used to treat cognitive symptoms of the disease. Non-pharmacological interventions, such as cognitive and memory training, occupational therapy, social and recreational activities, and environmental modifications, can also play a significant role in managing the symptoms of AD. Emerging treatments for AD include drugs that target beta-amyloid and tau protein, stem cell-based therapies, non-invasive brain stimulation techniques, and dietary and lifestyle interventions. The results of ongoing clinical trials will provide important information on the safety and efficacy of these treatments and will help to guide future research. It is important to note that while there are promising developments in the field, more research is needed to fully understand the underlying causes of AD and to develop effective treatments. This paper provides an overview of current and emerging treatments for AD. It discusses the role of medications, non-pharmacological interventions, and emerging treatments in managing the symptoms of AD. It also provides an update on the latest emerging treatments for AD, including drugs that target beta-amyloid and tau protein, stem cell-based therapies, non-invasive brain stimulation techniques, and dietary and lifestyle interventions. The paper concludes by emphasizing the need for further research and development in the field of AD treatment.