Cholinesterase Inhibitors
Phenylcarbamates
Galantamine
Tacrine
Physostigmine
Acetylcholinesterase
Memantine
Neostigmine
Nootropic Agents
Pyridostigmine Bromide
Edrophonium
Trichlorfon
Alzheimer Disease
Parathion
Organothiophosphorus Compounds
Chlorpyrifos
Sarin
Insecticides
Soman
Echothiophate Iodide
Acetylcholine
Carbamates
Muscarinic Antagonists
Dementia
Chemical Warfare Agents
Parasympathomimetics
Cholinesterase Reactivators
Organophosphorus Compounds
Reality Therapy
Thiocholine
Neurotoxicity Syndromes
Aminacrine
Atropine
Choline
Dibucaine
Dopamine Agents
Muscarinic Agonists
Receptors, Muscarinic
Tetraisopropylpyrophosphamide
Dose-Response Relationship, Drug
Lewy Body Disease
Cholinergic Antagonists
Organophosphate Poisoning
Mental Status Schedule
Bradycardia
Cholinergic Agents
Pralidoxime Compounds
Succinylcholine
Parasympathetic Nervous System
Brain
Carbaryl
Receptors, Cholinergic
Neuropsychological Tests
Dementia, Vascular
Butyrylthiocholine
Cognition Disorders
Acetylthiocholine
Alkaloids
Isoflurophate
Rats, Sprague-Dawley
Double-Blind Method
Excitatory Amino Acid Antagonists
Phosphoramides
Receptors, Nicotinic
Neuroprotective Agents
Nicotinic Antagonists
Treatment Outcome
Drug Interactions
Pesticides
Antipsychotic Agents
Nicotine
Synaptic Transmission
Metrifonate increases neuronal excitability in CA1 pyramidal neurons from both young and aging rabbit hippocampus. (1/1796)
The effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal neurons from hippocampal slices of young and aging rabbits using current-clamp, intracellular recording techniques. Bath perfusion of metrifonate (10-200 microM) dose-dependently decreased both postburst afterhyperpolarization (AHP) and spike frequency adaptation (accommodation) in neurons from young and aging rabbits (AHP: p < 0.002, young; p < 0.050, aging; accommodation: p < 0.024, young; p < 0.001, aging). These reductions were mediated by muscarinic cholinergic transmission, because they were blocked by addition of atropine (1 microM) to the perfusate. The effects of chronic metrifonate treatment (12 mg/kg for 3 weeks) on CA1 neurons of aging rabbits were also examined ex vivo. Neurons from aging rabbits chronically treated with metrifonate had significantly reduced spike frequency accommodation, compared with vehicle-treated rabbits. Chronic metrifonate treatment did not result in a desensitization to metrifonate ex vivo, because bath perfusion of metrifonate (50 microM) significantly decreased the AHP and accommodation in neurons from both chronically metrifonate- and vehicle-treated aging rabbits. We propose that the facilitating effect of chronic metrifonate treatment on acquisition of hippocampus-dependent tasks such as trace eyeblink conditioning by aging subjects may be caused by this increased excitability of CA1 pyramidal neurons. (+info)Comparison of two in vitro activation systems for protoxicant organophosphorous esterase inhibitors. (2/1796)
In order to perform in vitro testing of esterase inhibition caused by organophosphorous (OP) protoxicants, simple, reliable methods are needed to convert protoxicants to their esterase-inhibiting forms. Incubation of parathion or chlorpyrifos with 0.05% bromine solution or uninduced rat liver microsomes (RLM) resulted in production of the corresponding oxygen analogs of these OP compounds and markedly increased esterase inhibition in SH-SY5Y human neuroblastoma cells. Neither activation system affected cell viability or the activity of AChE or NTE in the absence of OP compounds. Although parathion and chlorpyrifos were activated by RLM, bromine activation required fewer steps and produced more esterase inhibition for a given concentration of chlorpyrifos. However, RLM activation of OP protoxicants produced metabolites other than oxygen analogs and may, therefore, be more relevant as a surrogate for OP biotransformation in vivo. This methodology makes the use of intact cells for in vitro testing of esterase inhibition caused by protoxicant organophosphate compounds a viable alternative to in vivo tests. (+info)Anaphylactic bronchoconstriction in BP2 mice: interactions between serotonin and acetylcholine. (3/1796)
1. Immunized BP2 mice developed an acute bronchoconstriction in vivo and airway muscle contraction in vitro in response to ovalbumin (OA) and these contractions were dose dependent. 2. Methysergide or atropine inhibited OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro. 3. Neostigmine potentiated the OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro of BP2 mice. This potentiation was markedly reduced by the administration of methysergide or atropine and when the two antagonists were administered together, the responses were completely inhibited. 4. Neostigmine also potentiated the serotonin (5-HT)- and acetylcholine (ACh)-induced bronchoconstriction and this potentiation was significantly reversed by atropine. 5. These results indicate that OA provokes a bronchoconstriction in immunized BP2 mice by stimulating the release of 5-HT, which in turn acts via the cholinergic mediator, ACh. (+info)Efficacy and safety of rivastigmine in patients with Alzheimer's disease: international randomised controlled trial. (4/1796)
OBJECTIVES: To assess the effects of rivastigmine on the core domains of Alzheimer's disease. DESIGN: Prospective, randomised, multicentre, double blind, placebo controlled, parallel group trial. Patients received either placebo, 1-4 mg/day (lower dose) rivastigmine, or 6-12 mg/day (higher dose) rivastigmine. Doses were increased in one of two fixed dose ranges (1-4 mg/day or 6-12 mg/day) over the first 12 weeks with a subsequent assessment period of 14 weeks. SETTING: 45 centres in Europe and North America. PARTICIPANTS: 725 patients with mild to moderately severe probable Alzheimer's disease diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, and the criteria of the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association. OUTCOME MEASURES: Cognitive subscale of the Alzheimer's disease assessment scale, rating on the clinician interview based impression of change incorporating caregiver information scale, and the progressive deterioration scale. RESULTS: At the end of the study cognitive function had deteriorated among those in the placebo group. Scores on the Alzheimer's disease assessment scale improved in patients in the higher dose group when compared with patients taking placebo (P<0.05). Significantly more patients in the higher dose group had improved by 4 points or more than had improved in the placebo group (24% (57/242) v 16% (39/238)). Global function as rated by the clinician interview scale had significantly improved among those in the higher dose group compared with those taking placebo (P<0.001), and significantly more patients in the higher dose group showed improvement than did in the placebo group (37% (80/219) v 20% (46/230)). Mean scores on the progressive deterioration scale improved from baseline in patients in the higher dose group but fell in the placebo group. Adverse events were predominantly gastrointestinal, of mild to moderate severity, transient, and occurred mainly during escalation of the dose. 23% (55/242) of those in the higher dose group, 7% (18/242) of those in the lower dose group, and 7% (16/239) of those in the placebo group discontinued treatment because of adverse events. CONCLUSIONS: Rivastigmine is well tolerated and effective. It improves cognition, participation in activities of daily living, and global evaluation ratings in patients with mild to moderately severe Alzheimer's disease. This is the first treatment to show compelling evidence of efficacy in a predominantly European population. (+info)The cholinergic hypothesis of Alzheimer's disease: a review of progress. (5/1796)
Alzheimer's disease is one of the most common causes of mental deterioration in elderly people, accounting for around 50%-60% of the overall cases of dementia among persons over 65 years of age. The past two decades have witnessed a considerable research effort directed towards discovering the cause of Alzheimer's disease with the ultimate hope of developing safe and effective pharmacological treatments. This article examines the existing scientific applicability of the original cholinergic hypothesis of Alzheimer's disease by describing the biochemical and histopathological changes of neurotransmitter markers that occur in the brains of patients with Alzheimer's disease both at postmortem and neurosurgical cerebral biopsy and the behavioural consequences of cholinomimetic drugs and cholinergic lesions. Such studies have resulted in the discovery of an association between a decline in learning and memory, and a deficit in excitatory amino acid (EAA) neurotransmission, together with important roles for the cholinergic system in attentional processing and as a modulator of EAA neurotransmission. Accordingly, although there is presently no "cure" for Alzheimer's disease, a large number of potential therapeutic interventions have emerged that are designed to correct loss of presynaptic cholinergic function. A few of these compounds have confirmed efficacy in delaying the deterioration of symptoms of Alzheimer's disease, a valuable treatment target considering the progressive nature of the disease. Indeed, three compounds have received European approval for the treatment of the cognitive symptoms of Alzheimer's disease, first tacrine and more recently, donepezil and rivastigmine, all of which are cholinesterase inhibitors. (+info)Comparison between huperzine A, tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. (6/1796)
AIM: To compare the effects of huperzine A (Hup A), tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. METHODS: The isolated mouse phrenic nerve-hemidiaphragm preparations were used with the conventional intracellular recording technique. The miniature end-plate potentials (MEPP), the mean quantal content of end-plate potentials (EPP), and the resting membrane potentials of muscle fiber were recorded. RESULTS: Hup A, tacrine, and E2020 at the concentration of 1.0 mumol.L-1 increased the amplitude, time-to-peak, and half-decay time of MEPP in the potencies of E2020 > Hup A > tacrine. Hup A did not significantly change the frequency of MEPP, the appearance of giant MEPP or slow MEPP, the resting membrane potentials, and the mean quantal content of EPP. CONCLUSION: Hup A is a selective and potent cholinesterase inhibitor, by which activity it facilitates the cholinergic transmission at mouse neuromuscular junction, and devoid of pre- and post-synaptic actions. (+info)Central nervous system-mediated hyperglycemic effects of NIK-247, a cholinesterase inhibitor, and MKC-231, a choline uptake enhancer, in rats. (7/1796)
We investigated the effects of intracerebroventricular administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclo-penta(b)-quinoline monohydrate hydrochloride; a cholinesterase inhibitor) or MKC-231 (2-(2-oxypyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofur o[2,3-b]quinolin-4-yl) acetoamide; a choline uptake enhancer) on plasma glucose level in comparison with that of neostigmine administration in rats. The extents of NIK-247- and MKC-231-induced hyperglycemia were considerably less than that by neostigmine, suggesting that the potencies of the drugs to produce the peripheral hyperglycemia may be pharmacologically negligible. (+info)Electron paramagnetic resonance reveals altered topography of the active center gorge of acetylcholinesterase after binding of fasciculin to the peripheral site. (8/1796)
Fasciculin, a peptidic toxin from snake venom, inhibits mammalian and fish acetylcholinesterases (AChE) by binding to the peripheral site of the enzyme. This site is located at the rim of a narrow, deep gorge which leads to the active center triad, located at its base. The proposed mechanisms for AChE inhibition by fasciculin include allosteric events resulting in altered conformation of the AChE active center gorge. However, a fasciculin-induced altered topography of the active center gorge has not been directly demonstrated. Using electron paramagnetic resonance with the spin-labeled organophosphate 1-oxyl-2,2,6, 6-tetramethyl-4-piperidinylethylphosphorofluoridate (EtOSL) specifically bound to the catalytic serine of mouse AChE (mAChE), we show that bound fasciculin on mAChE slows down, but does not prevent phosphorylation of the active site serine by EtOSL and protects the gorge conformation against thermal denaturation. Most importantly, a restricted freedom of motion of the spin label bound to the fasciculin-associated mAChE, compared to mAChE, is evidenced. Molecular models of mAChE and fasciculin-associated mAChE with tethered EtOSL enantiomers indicate that this restricted motion is due to greater proximity of the S-EtOSL nitroxide radical to the W86 residue in the fasciculin-associated enzyme. Our results demonstrate a topographical alteration indicative of a restricted conformation of the active center gorge of mAChE with bound fasciculin at its rim. (+info)The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.
There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.
Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.
There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.
Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.
There are several types of dementia, each with its own set of symptoms and characteristics. Some common types of dementia include:
* Alzheimer's disease: This is the most common form of dementia, accounting for 50-70% of all cases. It is a progressive disease that causes the death of brain cells, leading to memory loss and cognitive decline.
* Vascular dementia: This type of dementia is caused by problems with blood flow to the brain, often as a result of a stroke or small vessel disease. It can cause difficulty with communication, language, and visual-spatial skills.
* Lewy body dementia: This type of dementia is characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. It can cause a range of symptoms, including memory loss, confusion, hallucinations, and difficulty with movement.
* Frontotemporal dementia: This is a group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.
The symptoms of dementia can vary depending on the underlying cause, but common symptoms include:
* Memory loss: Difficulty remembering recent events or learning new information.
* Communication and language difficulties: Struggling to find the right words or understand what others are saying.
* Disorientation: Getting lost in familiar places or having difficulty understanding the time and date.
* Difficulty with problem-solving: Trouble with planning, organizing, and decision-making.
* Mood changes: Depression, anxiety, agitation, or aggression.
* Personality changes: Becoming passive, suspicious, or withdrawn.
* Difficulty with movement: Trouble with coordination, balance, or using utensils.
* Hallucinations: Seeing or hearing things that are not there.
* Sleep disturbances: Having trouble falling asleep or staying asleep.
The symptoms of dementia can be subtle at first and may progress slowly over time. In the early stages, they may be barely noticeable, but as the disease progresses, they can become more pronounced and interfere with daily life. It is important to seek medical advice if you or a loved one is experiencing any of these symptoms, as early diagnosis and treatment can help improve outcomes.
The different types of Neurotoxicity Syndromes include:
1. Organophosphate-induced neurotoxicity: This syndrome is caused by exposure to organophosphate pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
2. Heavy metal neurotoxicity: Exposure to heavy metals, such as lead, mercury, and arsenic, can damage the nervous system and cause symptoms such as tremors, muscle weakness, and cognitive impairment.
3. Pesticide-induced neurotoxicity: This syndrome is caused by exposure to pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
4. Solvent-induced neurotoxicity: Exposure to solvents, such as toluene and benzene, can damage the nervous system and cause symptoms such as memory loss, difficulty with concentration, and mood changes.
5. Medication-induced neurotoxicity: Certain medications, such as antidepressants and antipsychotics, can damage the nervous system and cause symptoms such as tremors, muscle rigidity, and cognitive impairment.
6. Environmental neurotoxicity: Exposure to environmental toxins, such as air pollution and pesticides, can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
7. Neurodegenerative disease-induced neurotoxicity: Neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, can cause neurotoxicity and lead to symptoms such as cognitive decline, memory loss, and motor dysfunction.
8. Traumatic brain injury-induced neurotoxicity: Traumatic brain injury can cause neurotoxicity and lead to symptoms such as cognitive impairment, memory loss, and mood changes.
9. Stroke-induced neurotoxicity: A stroke can cause neurotoxicity and lead to symptoms such as weakness or paralysis on one side of the body, difficulty with speech and language, and memory loss.
10. Neurodevelopmental disorder-induced neurotoxicity: Neurodevelopmental disorders, such as autism spectrum disorder, can cause neurotoxicity and lead to symptoms such as cognitive impairment, social withdrawal, and repetitive behaviors.
It is important to note that these are just a few examples of the many different types of neurotoxicity that can occur, and that each type may have its own unique set of causes, symptoms, and treatments. If you suspect that you or someone you know may be experiencing neurotoxicity, it is important to seek medical attention as soon as possible in order to receive an accurate diagnosis and appropriate treatment.
The symptoms of Lewy body disease can vary from person to person, but they often include:
1. Cognitive problems, such as difficulty with memory, attention, and decision-making.
2. Slowness of movement, rigidity, and tremors, similar to those seen in Parkinson's disease.
3. Visual hallucinations and sleep disturbances.
4. Balance problems and falls.
5. Mood changes, such as depression and anxiety.
Lewy body disease can be difficult to diagnose, as it can resemble other conditions such as Alzheimer's disease or Parkinson's disease. A definitive diagnosis is usually made through an autopsy after death, but a clinical diagnosis can be made based on a combination of symptoms and medical imaging studies.
There is no cure for Lewy body disease, but medications and therapies can help manage its symptoms. Treatment options may include cholinesterase inhibitors, dopamine agonists, and antidepressants, as well as physical, occupational, and speech therapy. In some cases, surgery may be recommended to regulate medication or improve cognitive function.
Lewy body disease is a relatively rare condition, affecting about 1% of people over the age of 65. It is more common in men than women, and the risk of developing the disease increases with age. There is currently no known cause for Lewy body disease, but research suggests that it may be linked to genetic factors and exposure to certain environmental toxins.
In summary, Lewy body disease is a progressive neurodegenerative disorder that affects the brain and nervous system, characterized by abnormal protein deposits called Lewy bodies. It can cause a range of cognitive and motor symptoms, and diagnosis can be challenging. There is no cure for the disease, but medications and therapies can help manage its symptoms.
The symptoms of organophosphate poisoning can vary depending on the severity of exposure and individual sensitivity, but may include:
1. Respiratory problems: Difficulty breathing, wheezing, coughing, and shortness of breath
2. Nervous system effects: Headache, dizziness, confusion, tremors, and muscle weakness
3. Eye irritation: Redness, itching, tearing, and blurred vision
4. Skin irritation: Redness, itching, and burns
5. Gastrointestinal effects: Nausea, vomiting, diarrhea, and abdominal pain
6. Cardiovascular effects: Rapid heart rate, low blood pressure, and cardiac arrhythmias
7. Neurological effects: Seizures, coma, and memory loss
Organophosphate poisoning can be caused by ingestion of contaminated food or water, inhalation of pesticides, or absorption through the skin. Treatment typically involves supportive care, such as fluids and oxygen, as well as medications to counteract the effects of organophosphates on the nervous system. In severe cases, hospitalization may be necessary to monitor and treat the patient.
Prevention is key in avoiding organophosphate poisoning, which can be achieved by using protective clothing and equipment when handling pesticides, keeping products away from food and children, and following the recommended dosage and application instructions carefully. Regular testing of soil and water for organophosphate residues can also help prevent exposure.
In conclusion, organophosphate poisoning is a serious health hazard that can result from exposure to pesticides and insecticides. Prompt recognition of symptoms and proper treatment are essential in preventing long-term health effects and reducing the risk of fatalities. Prevention through safe handling practices and regular testing of soil and water for organophosphate residues can also help minimize the risks associated with these chemicals.
* Heart block: A condition where the electrical signals that control the heart's rhythm are blocked or delayed, leading to a slow heart rate.
* Sinus node dysfunction: A condition where the sinus node, which is responsible for setting the heart's rhythm, is not functioning properly, leading to a slow heart rate.
* Medications: Certain medications, such as beta blockers, can slow down the heart rate.
* Heart failure: In severe cases of heart failure, the heart may become so weak that it cannot pump blood effectively, leading to a slow heart rate.
* Electrolyte imbalance: An imbalance of electrolytes, such as potassium or magnesium, can affect the heart's ability to function properly and cause a slow heart rate.
* Other medical conditions: Certain medical conditions, such as hypothyroidism (an underactive thyroid) or anemia, can cause bradycardia.
Bradycardia can cause symptoms such as:
* Fatigue
* Weakness
* Dizziness or lightheadedness
* Shortness of breath
* Chest pain or discomfort
In some cases, bradycardia may not cause any noticeable symptoms at all.
If you suspect you have bradycardia, it is important to consult with a healthcare professional for proper diagnosis and treatment. They may perform tests such as an electrocardiogram (ECG) or stress test to determine the cause of your slow heart rate and develop an appropriate treatment plan. Treatment options for bradycardia may include:
* Medications: Such as atropine or digoxin, to increase the heart rate.
* Pacemakers: A small device that is implanted in the chest to help regulate the heart's rhythm and increase the heart rate.
* Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.
It is important to note that bradycardia can be a symptom of an underlying condition, so it is important to address the underlying cause in order to effectively treat the bradycardia.
The symptoms of vascular dementia can vary depending on the location and severity of the damage to the brain, but common symptoms include:
* Memory loss, such as difficulty remembering recent events or learning new information
* Confusion and disorientation
* Difficulty with communication, including trouble finding the right words or understanding what others are saying
* Difficulty with problem-solving, decision-making, and judgment
* Mood changes, such as depression, anxiety, or agitation
* Personality changes, such as becoming more passive or suspicious
* Difficulty with coordination and movement, including trouble walking or balance
Vascular dementia can be caused by a variety of conditions that affect the blood vessels in the brain, including:
* Stroke or transient ischemic attack (TIA, or "mini-stroke")
* Small vessel disease, such as tiny strokes or changes in the blood vessels that occur over time
* Moyamoya disease, a rare condition caused by narrowing or blockage of the internal carotid artery and its branches
* Cerebral amyloid angiopathy, a condition in which abnormal protein deposits build up in the blood vessels of the brain
* Other conditions that can cause reduced blood flow to the brain, such as high blood pressure, diabetes, or cardiovascular disease
There is no cure for vascular dementia, but there are several treatment options available to help manage its symptoms and slow its progression. These may include medications to improve memory and cognitive function, physical therapy to maintain mobility and strength, and lifestyle changes such as a healthy diet and regular exercise. In some cases, surgery or endovascular procedures may be recommended to treat the underlying cause of the dementia, such as a stroke or blocked blood vessel.
It is important for individuals with vascular dementia to receive timely and accurate diagnosis and treatment, as well as ongoing support and care from healthcare professionals, family members, and caregivers. With appropriate management, many people with vascular dementia are able to maintain their independence and quality of life for as long as possible.
Types of Cognition Disorders: There are several types of cognitive disorders that affect different aspects of cognitive functioning. Some common types include:
1. Attention Deficit Hyperactivity Disorder (ADHD): Characterized by symptoms of inattention, hyperactivity, and impulsivity.
2. Traumatic Brain Injury (TBI): Caused by a blow or jolt to the head that disrupts brain function, resulting in cognitive, emotional, and behavioral changes.
3. Alzheimer's Disease: A progressive neurodegenerative disorder characterized by memory loss, confusion, and difficulty with communication.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to cognitive impairment and other symptoms.
5. Parkinson's Disease: A neurodegenerative disorder that affects movement, balance, and cognition.
6. Huntington's Disease: An inherited disorder that causes progressive damage to the brain, leading to cognitive decline and other symptoms.
7. Frontotemporal Dementia (FTD): A group of neurodegenerative disorders characterized by changes in personality, behavior, and language.
8. Post-Traumatic Stress Disorder (PTSD): A condition that develops after a traumatic event, characterized by symptoms such as anxiety, avoidance, and hypervigilance.
9. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not severe enough to interfere with daily life.
Causes and Risk Factors: The causes of cognition disorders can vary depending on the specific disorder, but some common risk factors include:
1. Genetics: Many cognitive disorders have a genetic component, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Age: As people age, their risk of developing cognitive disorders increases, such as Alzheimer's disease, vascular dementia, and frontotemporal dementia.
3. Lifestyle factors: Factors such as physical inactivity, smoking, and poor diet can increase the risk of cognitive decline and dementia.
4. Traumatic brain injury: A severe blow to the head or a traumatic brain injury can increase the risk of developing cognitive disorders, such as chronic traumatic encephalopathy (CTE).
5. Infections: Certain infections, such as meningitis and encephalitis, can cause cognitive disorders if they damage the brain tissue.
6. Stroke or other cardiovascular conditions: A stroke or other cardiovascular conditions can cause cognitive disorders by damaging the blood vessels in the brain.
7. Chronic substance abuse: Long-term use of drugs or alcohol can damage the brain and increase the risk of cognitive disorders, such as dementia.
8. Sleep disorders: Sleep disorders, such as sleep apnea, can increase the risk of cognitive disorders, such as dementia.
9. Depression and anxiety: Mental health conditions, such as depression and anxiety, can increase the risk of cognitive decline and dementia.
10. Environmental factors: Exposure to certain environmental toxins, such as pesticides and heavy metals, has been linked to an increased risk of cognitive disorders.
It's important to note that not everyone with these risk factors will develop a cognitive disorder, and some people without any known risk factors can still develop a cognitive disorder. If you have concerns about your cognitive health, it's important to speak with a healthcare professional for proper evaluation and diagnosis.
Cholinesterase inhibitor
Vascular dementia
Dementia
Medicinal plants
Galantamine
Leucojum aestivum
Leucojum vernum
Selenophos
BW284C51
Phenserine
Tetraethyl pyrophosphate
Nucleus basalis
Organophosphate-induced delayed neuropathy
Carbophenothion
Rivastigmine
Beta-secretase 1
Methamidophos
Malaoxon
Enzyme inhibitor
Mark Cushman
Phosphamidon
Fazio-Londe disease
Acetylcholinesterase inhibitor
Lars-Erik Tammelin
Soman
Cholinesterase reactivator
Alex Karczmar
Cyclobuxine
Neuron
RIC3
Tacrine
Chlorphoxim
Parathion S
Diethyl phosphorochloridate
Cyanotoxin
TMTFA
Xerostomia
NeuroAiD
V-sub x
Rhipicephalus microplus
Cyanophos
Donepezil
Naled
Nostocarboline
Physostigma venenosum
Legalization of non-medical cannabis in the United States
Bungarus
IPTBO
List of MeSH codes (D27)
Echothiophate
Amphibian
Eseroline
Indigestion
Cholinesterase Inhibitors: Initial Check | Environmental Medicine | ATSDR
Atropine Dosing for Cholinesterase Inhibitor Toxicity - MDCalc
Results of search for 'su:{Cholinesterase inhibitors}'
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WHO HQ Library catalog
Latest Developments in Dementia 2008, Alzheimer's Disease: From Cholinesterase Inhibitors to Stem Cell Treatment | HYGEIA...
Alzheimer disease Information | Mount Sinai - New York
CDC - NIOSH Worker Health Charts
BI 409306 in Patients With Cognitive Impairment Due to Alzheimer's Disease. - Full Text View - ClinicalTrials.gov
Honokiol improves learning and memory impairments induced by scopolamine in mice
F 50 Pill Pink Round - Pill Identifier
Myasthenia Gravis (MG) Treatment Market Size, Share & Trends Analysis, By Drug Class (Cholinesterase Inhibitors,...
Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral...
CMU Intellectual Repository: Simple colorimetric method for cholinesterase-inhibitor screening in gastric content by using...
NIOSHTIC-2 Search Results - Full View
Exelon Oral Solution - Uses, Side Effects, Interactions - MedBroadcast.com
The EPA National Library Catalog | EPA National Library Network | US EPA
Heptopargil (Ref: GL-1016)
CDC Nerve Agents | Emergency Preparedness & Response
Rivastigmine Transdermal Patch: MedlinePlus Drug Information
Alzheimer Disease in Down Syndrome: Overview, Pathophysiology/Risk Factors, Epidemiology
Phospholine Iodide, (echothiophate iodide) dosing, indications, interactions, adverse effects, and more
Black People Less Likely to Receive Dementia Meds
Browsing Pharmacy by Title
CONICET | Buscador de Institutos y Recursos Humanos
Monitoring Therapy for Patients with Alzheimer's Disease | AAFP
Sergeant's GUARDIAN® Flea & Tick Collar for Cats, Fresh Scent | Sergeant's®
Learn Something - Hazardous Substance Continuing Education | Blogs | CDC
Alzheimer's Disease7
- A Meeting on the topic "Latest Developments in Dementia - Alzheimer's Disease: From Cholinesterase Inhibitors to Stem Cell Treatment" was held at King George Hotel on February 22-23, 2008. (hygeia.gr)
- Galantamine is used in the treatment of alzheimer's disease and belongs to the drug class cholinesterase inhibitors . (drugs.com)
- How do you monitor patients with Alzheimer's disease to determine if they are benefiting from receiving a cholinesterase inhibitor? (aafp.org)
- Of the many assessment tools validated for use in patients with Alzheimer's disease, there are several that demonstrate the effectiveness of cholinesterase inhibitors versus placebo in randomized controlled trials ( Table 1 11 , 12 ) . (aafp.org)
- For Alzheimer's Disease associated memory loss cholinesterase inhibitors, such as tacrine (Cognex®), donepezil (Aricept®), rivastigmine (Exelon®) and galantamine (Reminyl®), have been beneficial. (clevelandclinicmeded.com)
- Studies currently underway include evaluating the role of health specialists in treating depressed patients, looking at bereavement and its effects on patients, and the role of estrogen, vitamin E, NSAIDs and COX-2 inhibitors in preventing and treating Alzheimer's disease. (psychiatrictimes.com)
- Cholinesterase inhibitors for Alzheimer's disease. (bvsalud.org)
Insecticides2
- Doses atropine for cholinesterase inhibitor toxicity (prescribed drugs, nerve gas, insecticides). (mdcalc.com)
- Data are given for cholinesterase (9001085) levels of affected persons, symptoms, and details of dermatitis resulting from the insecticides and allergic reactions from celery juice and sunlight. (cdc.gov)
Acetylcholinesterase1
- The treatment options for MG include medications such as acetylcholinesterase inhibitors, immunosuppressive drugs, and monoclonal antibodies that target the immune system. (marketresearchcommunity.com)
Toxicity2
Pesticides1
- Do not use this product on animals simultaneously or within 30 days before or after treatment with or exposure to cholinesterase inhibiting drugs, pesticides, or chemicals. (sergeants.com)
Symptoms1
- What are the major classifications of signs and symptoms characteristic of cholinesterase inhibitor poisoning? (cdc.gov)
Medications3
- Rivastigmine belongs to a family of medications known as cholinesterase inhibitors . (medbroadcast.com)
- Rivastigmine is in a class of medications called cholinesterase inhibitors. (medlineplus.gov)
- Patients are treated with medications, such as cholinesterase inhibitors, that are approved by the U.S. Food and Drug Administration for memory impairment. (psychiatrictimes.com)
Organophosphate1
- Dichlorvos, an organophosphate, is a direct-acting cholinesterase (ChE)l inhibitor. (unep.org)
NMDA3
- These included cholinesterase inhibitors, N -methyl D -aspartate (NMDA) receptor antagonists, selective serotonin reuptake inhibitors (SSRIs), antipsychotics, and benzodiazepines. (medscape.com)
- The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists at rates comparable to White patients. (medscape.com)
- There are currently three cholinesterase inhibitors and one N-methyl-D-aspartate (NMDA) antagonist indicated in the treatment of AD as monotherapy or in combination. (bvsalud.org)
Cholinergic1
- When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. (bvsalud.org)
Drugs1
- Drugs that inhibit cholinesterases. (bvsalud.org)
Acute4
- What are the major treatment strategies recommended in acute cholinesterase inhibitor poisoning? (cdc.gov)
- What is the usual cause of death from acute cholinesterase inhibitor poisoning? (cdc.gov)
- Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral alpha 2-adrenoceptors. (bvsalud.org)
- Acute (12 h), short-term (4 days) or chronic (7-18 days) treatment with the cholinesterase inhibitors neostigmine (0.1 mg/kg), physostigmine (0.1 mg/kg) and diisopropylfluorophosphate (2 mg/kg) and with the muscarinic receptor agonist pilocarpine (10 mg/kg) did not alter the density of brain alpha 2- adrenoceptors . (bvsalud.org)
Exposure2
- What aspects of this situation suggest toxic exposure to a cholinesterase inhibitor? (cdc.gov)
- Recommendations include monitoring of pre- exposure cholinesterase levels, checking of red blood cell or plasma decrease, provision of protective equipment and facilities for maintaining good personal hygiene, and informing farm ers of safety measures. (cdc.gov)
Clinical4
- What is the pathophysiology underlying the clinical findings in cholinesterase inhibitor poisoning? (cdc.gov)
- The clinical findings of eye pain, blurred or dim vision, respiratory distress, diaphoresis and seizures are all consistent with cholinesterase inhibitor poisoning. (cdc.gov)
- There are no clinical trials directly assessing the best way to monitor patients on a cholinesterase inhibitor. (aafp.org)
- The Mini-Mental State Examination (MMSE) also has been used in clinical trials of cholinesterase inhibitors, and although it is familiar to most physicians, it lacks specificity. (aafp.org)
Cognitive1
- Cholinesterase inhibitors remain the first-line therapy in patients with mild to moderate AD, which may stabilise the symptomatic cognitive and functional decline. (bvsalud.org)
Patients1
- 2 , 4 Over the first six to 12 months, patients treated with cholinesterase inhibitors showed improvement by an average of 2.7 points. (aafp.org)
Effects1
- Behavioral and Physiological Effects of the Cholinesterase Inhibitor Carbaryl (1-Naphthyl Methylcarbamate). (epa.gov)
Include1
- Other pharmacotherapy options include the use of memantine which may be used by itself or in combination with cholinesterase inhibitors. (bvsalud.org)
Rivastigmine7
- Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase. (nih.gov)
- All 4 currently approved ChEIs (ie, donepezil, rivastigmine, galantamine) inhibit acetylcholinesterase (AChE) at the synapse (specific cholinesterase). (medscape.com)
- Rivastigmine is a potent, selective inhibitor of brain AChE and BChE. (medscape.com)
- Rivastigmine is considered a pseudo-irreversible inhibitor of AChE. (medscape.com)
- The cholinesterase inhibitors (ChEIs) donepezil and rivastigmine are used to ease the symptoms of dementia associated with AD. (nih.gov)
- Galantamine, rivastigmine, and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimer's symptoms. (nih.gov)
- Rivastigmine is in a class of medications called cholinesterase inhibitors. (medlineplus.gov)
Donepezil1
- Donepezil transdermal is a reversible acetylcholinesterase inhibitor. (medscape.com)
ChEIs1
- Cholinesterase inhibitors (ChEIs) are used to palliate cholinergic deficiency. (medscape.com)
Alzheimer's1
- Because cholinesterase inhibitors work in a similar way, switching from one to another may not produce significantly different results, but a person living with Alzheimer's may respond better to one drug versus another. (nih.gov)
Acetylcholine3
- The mainstay of therapy for patients with Alzheimer disease (AD) is the use of centrally acting cholinesterase inhibitors to attempt to compensate for the depletion of acetylcholine (ACh) in the cerebral cortex and hippocampus. (medscape.com)
- This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase. (medscape.com)
- Cholinesterase inhibitors prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking . (nih.gov)
Consistent1
- The clinical findings of eye pain, blurred or dim vision, respiratory distress, diaphoresis and seizures are all consistent with cholinesterase inhibitor poisoning. (cdc.gov)
Adverse effects1
- What are the three major delayed adverse effects that can follow recovery from the acute cholinesterase toxicity? (cdc.gov)