Details of Alzheimer's Disease and Etiology of Protein.
Under the guidance of
Mr. Nilanjan Adhikari
Assistant professor,Department of Pharmacology
P.G INSTITUTE OF MEDICAL SCIENCES
19. Alzemer's Diseases in bsc nursing student PPT.pptxJagdishDalvi4
Alzheimer's disease is a progressive neurodegenerative disease that causes problems with memory, thinking, and behavior. It is the most common cause of dementia. The disease is characterized by amyloid plaques and tau tangles in the brain that damage neurons. Risk factors include age, family history, and genetic factors. There is no cure for Alzheimer's, but medications and lifestyle changes can temporarily improve symptoms. As the disease worsens, patients require full-time care.
1) Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It was first described by Alois Alzheimer in 1906 and is the most common form of dementia.
2) The disease is characterized by beta-amyloid plaques and tau protein tangles that build up in the brain, resulting in the loss of connections between neurons and death of brain cells. This leads to the symptoms of impaired memory, thinking, and behavior.
3) While the causes of Alzheimer's are not fully known, genetic and environmental factors are believed to play a role. Risk increases significantly with age, though early-onset Alzheimer's can occur much earlier. There is currently no cure for the disease.
This document discusses Alzheimer's disease, including its causes, symptoms, stages of progression, diagnosis, current treatments, and potential new treatments in development. Specifically, it describes how Alzheimer's is characterized by beta-amyloid plaque and tau protein tangle buildup in the brain, outlines the four stages of the disease and their symptoms, and discusses several FDA-approved medications commonly used to treat symptoms, including Aricept, Exelon, Razadyne, and Namenda. It also mentions two new compounds in clinical trials, a beta-secretase inhibitor and NIC5-15, that may help slow the disease's progression.
This document discusses Alzheimer's disease (AD), including its causes, symptoms, stages of progression, diagnosis, and treatment options. Some key points:
- AD is characterized by amyloid plaques and neurofibrillary tangles in the brain that are associated with loss of neurons and cognitive decline. It is generally diagnosed in those over 65 and causes memory loss and impaired thinking.
- Symptoms progress from mild memory loss to severe cognitive impairment. Stages include mild, moderate and severe.
- Risk factors include age, family history and genetic factors like the APOE gene. Diagnosis involves cognitive tests and brain imaging.
- Current treatments aim to slow progression but do not stop or cure the disease
The document discusses Alzheimer's disease (AD), including its causes, symptoms, diagnosis, and treatment. It provides details on:
- AD is characterized by beta-amyloid plaques and tau neurofibrillary tangles in the brain that lead to nerve cell death. Genetic and lifestyle factors may contribute to causes.
- Symptoms progress from mild memory loss to severe cognitive decline and inability for self-care. Stages include mild, moderate, and severe.
- Diagnosis involves assessing cognitive impairment and ruling out other conditions. Imaging and neurological tests are also used.
- Current treatments aim to slow progression and manage symptoms. These include cholinesterase inhibitors and memantine which increase
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It is the most common form of dementia. There is no cure for Alzheimer's, but medications and lifestyle interventions can temporarily slow the worsening of symptoms. The disease is caused by plaques and tangles that build up in the brain, resulting in the loss of connections between neurons. Early symptoms include memory loss and problems with thinking and language, while later stages involve the loss of motor skills and ability to communicate. Current treatments approved by the FDA include cholinesterase inhibitors and memantine, which can temporarily slow cognitive decline.
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It results from abnormal buildup of proteins in the brain that cause nerve cell death. Risk increases with age and family history. Symptoms start with mild memory loss and worsen over time, eventually causing severe brain damage. The only way to definitively diagnose is through brain autopsy. Currently, there is no cure and treatment focuses on managing symptoms and slowing progression.
Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. Alzheimer's disease is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.
Symptoms: Amnesia; Dementia
Diseases or conditions caused: Dementia
Pathophysiology
Pathology
BPharm 2nd Semester
MPharm
Therapeutics
MBBS
19. Alzemer's Diseases in bsc nursing student PPT.pptxJagdishDalvi4
Alzheimer's disease is a progressive neurodegenerative disease that causes problems with memory, thinking, and behavior. It is the most common cause of dementia. The disease is characterized by amyloid plaques and tau tangles in the brain that damage neurons. Risk factors include age, family history, and genetic factors. There is no cure for Alzheimer's, but medications and lifestyle changes can temporarily improve symptoms. As the disease worsens, patients require full-time care.
1) Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It was first described by Alois Alzheimer in 1906 and is the most common form of dementia.
2) The disease is characterized by beta-amyloid plaques and tau protein tangles that build up in the brain, resulting in the loss of connections between neurons and death of brain cells. This leads to the symptoms of impaired memory, thinking, and behavior.
3) While the causes of Alzheimer's are not fully known, genetic and environmental factors are believed to play a role. Risk increases significantly with age, though early-onset Alzheimer's can occur much earlier. There is currently no cure for the disease.
This document discusses Alzheimer's disease, including its causes, symptoms, stages of progression, diagnosis, current treatments, and potential new treatments in development. Specifically, it describes how Alzheimer's is characterized by beta-amyloid plaque and tau protein tangle buildup in the brain, outlines the four stages of the disease and their symptoms, and discusses several FDA-approved medications commonly used to treat symptoms, including Aricept, Exelon, Razadyne, and Namenda. It also mentions two new compounds in clinical trials, a beta-secretase inhibitor and NIC5-15, that may help slow the disease's progression.
This document discusses Alzheimer's disease (AD), including its causes, symptoms, stages of progression, diagnosis, and treatment options. Some key points:
- AD is characterized by amyloid plaques and neurofibrillary tangles in the brain that are associated with loss of neurons and cognitive decline. It is generally diagnosed in those over 65 and causes memory loss and impaired thinking.
- Symptoms progress from mild memory loss to severe cognitive impairment. Stages include mild, moderate and severe.
- Risk factors include age, family history and genetic factors like the APOE gene. Diagnosis involves cognitive tests and brain imaging.
- Current treatments aim to slow progression but do not stop or cure the disease
The document discusses Alzheimer's disease (AD), including its causes, symptoms, diagnosis, and treatment. It provides details on:
- AD is characterized by beta-amyloid plaques and tau neurofibrillary tangles in the brain that lead to nerve cell death. Genetic and lifestyle factors may contribute to causes.
- Symptoms progress from mild memory loss to severe cognitive decline and inability for self-care. Stages include mild, moderate, and severe.
- Diagnosis involves assessing cognitive impairment and ruling out other conditions. Imaging and neurological tests are also used.
- Current treatments aim to slow progression and manage symptoms. These include cholinesterase inhibitors and memantine which increase
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It is the most common form of dementia. There is no cure for Alzheimer's, but medications and lifestyle interventions can temporarily slow the worsening of symptoms. The disease is caused by plaques and tangles that build up in the brain, resulting in the loss of connections between neurons. Early symptoms include memory loss and problems with thinking and language, while later stages involve the loss of motor skills and ability to communicate. Current treatments approved by the FDA include cholinesterase inhibitors and memantine, which can temporarily slow cognitive decline.
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It results from abnormal buildup of proteins in the brain that cause nerve cell death. Risk increases with age and family history. Symptoms start with mild memory loss and worsen over time, eventually causing severe brain damage. The only way to definitively diagnose is through brain autopsy. Currently, there is no cure and treatment focuses on managing symptoms and slowing progression.
Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. Alzheimer's disease is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.
Symptoms: Amnesia; Dementia
Diseases or conditions caused: Dementia
Pathophysiology
Pathology
BPharm 2nd Semester
MPharm
Therapeutics
MBBS
This document discusses Alzheimer's disease including its causes, symptoms, diagnosis and treatment. It is a neurodegenerative disease that causes memory loss and cognitive decline. The main pathologies involved are beta-amyloid plaques and neurofibrillary tangles composed of tau proteins. Diagnosis involves assessing cognitive impairment and ruling out other conditions, while treatments can help symptoms but currently there is no cure as brain cells continue to be lost.
- Alzheimer's disease (AD) is a progressive dementia characterized by cognitive decline and behavioral changes. It is the most common type of dementia and risk increases with age.
- The pathology of AD involves beta-amyloid plaques and tau neurofibrillary tangles in brain regions critical for memory and cognition. This leads to deficits in the neurotransmitter acetylcholine.
- While the exact causes are unknown, genetic and environmental factors likely contribute. Treatment focuses on managing symptoms with cholinesterase inhibitors or memantine, which target acetylcholine and glutamate pathways respectively. Currently there is no cure for AD.
An 80-year-old man presented with symptoms of Alzheimer's disease including memory loss, disorientation, difficulty completing tasks, and mood changes. Brain scans and examination of brain tissue confirmed Alzheimer's disease. Alzheimer's is caused by abnormal accumulation of tau and amyloid-beta proteins in the brain, which form plaques and tangles that damage neurons. It is diagnosed based on symptoms, cognitive tests, and brain imaging, and progresses from mild to severe impairment over time. There are medications to temporarily improve symptoms but no cure for the underlying disease process.
A presentation about Alzheimer's disease, it's definition, it's etiology, its mechanism of development as well as actual treatment and developing treatments.
This document summarizes information about Alzheimer's disease from a student paper, including descriptions of symptoms, causes, pathophysiology and treatment options. It discusses how Alzheimer's is a progressive neurodegenerative disorder causing dementia. Key pathological features are amyloid plaques and neurofibrillary tangles in the brain. Current treatments aim to improve cognitive symptoms and include cholinesterase inhibitors such as donepezil for mild-moderate cases and memantine for moderate-severe cases. Several drug trials are also mentioned.
This document discusses Alzheimer's disease (AD), including its definition, etiology, risk factors, pathophysiology, clinical symptoms, diagnosis, and treatment. Some key points include:
- AD is the most common cause of dementia and is characterized by cognitive and behavioral impairment. While the exact cause is unknown, risk factors include age, family history, and genetics such as the APOE E4 allele.
- Pathologically, AD is defined by amyloid plaques and neurofibrillary tangles in the brain. It results from the death of brain cells, affecting processes like memory, thinking, and behavior.
- Diagnosis involves assessing symptoms, ruling out other conditions through tests, and structural imaging of the brain
Ms. Ritika Soni presented on Alzheimer's disease. Alzheimer's is a progressive brain disorder that causes memory loss and cognitive decline. It was first described by Dr. Alois Alzheimer in 1906 from examining a patient with unusual brain abnormalities. The causes are not fully known but risk factors include age, family history, and head injuries. Diagnosis involves cognitive assessments and brain imaging. Currently, there is no cure, but medications and caregiving can temporarily improve symptoms.
Are elderly with schizophrenia more or less likely to (docx) (1)Adonis Sfera, MD
This document discusses whether elderly patients with schizophrenia are more or less likely to develop Alzheimer's disease. While schizophrenia is associated with accelerated cognitive decline in elderly patients, most studies have failed to find increased amyloid deposits or cerebrospinal fluid markers of Alzheimer's pathology in elderly schizophrenia patients. Some potential protective factors for Alzheimer's in schizophrenia patients are discussed, such as effects of antipsychotic medications, tobacco smoking, and abnormalities in brain insulin signaling and glucose metabolism. The cognitive deficits seen in elderly schizophrenia differ from those in Alzheimer's, and structural brain imaging also shows different patterns of tissue loss between the two conditions. In conclusion, while cognitive impairment is common in elderly schizophrenia, they do not appear to have an increased risk of progressive Alzheimer's
This document discusses a student research project aimed at developing new drug leads for Alzheimer's disease by targeting beta-secretase, an enzyme involved in the production of amyloid beta peptides. It provides background on Alzheimer's disease mechanisms and treatments. The project will use rational drug design methods to develop small molecule beta-secretase inhibitors, which will then be patented and licensed to a company for further development as a potential pharmaceutical.
The document discusses Alzheimer's disease and dementia. It defines Alzheimer's as a degenerative brain disease caused by complex brain changes that damage brain cells. Dementia can have various reversible causes while Alzheimer's is currently irreversible. The stages of Alzheimer's are described from mild to severe. Medical treatments aim to boost brain chemicals but do not stop decline. New treatments focus on amyloid plaques, tau tangles, inflammation and insulin resistance. Non-drug therapies aim to maintain cognitive function and quality of life.
the feathers of the disease and It is histology
For downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
This document provides an overview of Alzheimer's disease including its causes, symptoms, stages, diagnosis, and treatment approaches. It discusses how Alzheimer's is characterized by plaques and tangles in the brain made up of beta-amyloid and tau proteins. Current treatment aims to improve cognitive function and behaviors through cholinesterase inhibitors and memantine, though none can stop or reverse the disease. Non-pharmacological interventions like education, communication, and stimulation therapies may provide additional support.
Alzheimer's disease is the most common cause of dementia. It is a progressive, degenerative brain disease that causes deterioration of brain cells and ultimately death. It starts with damage to the hippocampus, making it harder to form new memories over time. Plaques and tangles then spread throughout the brain, killing cells and compromising function. While there is no cure, medications can help slow cognitive decline. Support from family caregivers is also important for managing the condition.
Alzheimer's disease - A detailed case study Uzair Ahmed
This case study describes a 63-year-old woman diagnosed with Alzheimer's disease and a novel presenilin 2 mutation. She was referred to a memory clinic at age 58 with a 2-year history of repetitiveness, memory loss, and executive dysfunction. Neurocognitive testing revealed poor performance in multiple domains. Her condition progressed over several years despite treatment with cholinesterase inhibitors and memantine. She developed additional neurological symptoms including rigidity, apraxia, and worsening cognition. Genetic testing later identified a novel presenilin 2 mutation, which may have contributed to her early-onset and rapidly progressive form of Alzheimer's disease.
Alzheimer's disease is characterized by the abnormal build-up of amyloid and tau proteins in the brain, which is believed to cause neuronal death and loss of brain function. Symptoms appear as brain cells become affected and include memory loss, cognitive decline, and issues with language and visuospatial abilities. While there is no cure for Alzheimer's, some drugs can temporarily reduce symptoms by targeting amyloid plaques or preserving acetylcholine levels. The strongest genetic risk factor is an APOE allele. Recent treatments focus on reducing amyloid production and preventing tau hyperphosphorylation to improve neuronal connectivity and function.
Alzheimer's disease is a neurodegenerative disorder with severe dementia. Due to the accumulation of Beta-Amyloid proteins acetyl-choline producing neurons are getting degenerated. Alzheimer's disease is one of the most devastating brain disorders of elderly humans. It is an under-treated and under-recognized disease that is becoming a major public health problem.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
This document discusses Alzheimer's disease including its causes, symptoms, diagnosis and treatment. It is a neurodegenerative disease that causes memory loss and cognitive decline. The main pathologies involved are beta-amyloid plaques and neurofibrillary tangles composed of tau proteins. Diagnosis involves assessing cognitive impairment and ruling out other conditions, while treatments can help symptoms but currently there is no cure as brain cells continue to be lost.
- Alzheimer's disease (AD) is a progressive dementia characterized by cognitive decline and behavioral changes. It is the most common type of dementia and risk increases with age.
- The pathology of AD involves beta-amyloid plaques and tau neurofibrillary tangles in brain regions critical for memory and cognition. This leads to deficits in the neurotransmitter acetylcholine.
- While the exact causes are unknown, genetic and environmental factors likely contribute. Treatment focuses on managing symptoms with cholinesterase inhibitors or memantine, which target acetylcholine and glutamate pathways respectively. Currently there is no cure for AD.
An 80-year-old man presented with symptoms of Alzheimer's disease including memory loss, disorientation, difficulty completing tasks, and mood changes. Brain scans and examination of brain tissue confirmed Alzheimer's disease. Alzheimer's is caused by abnormal accumulation of tau and amyloid-beta proteins in the brain, which form plaques and tangles that damage neurons. It is diagnosed based on symptoms, cognitive tests, and brain imaging, and progresses from mild to severe impairment over time. There are medications to temporarily improve symptoms but no cure for the underlying disease process.
A presentation about Alzheimer's disease, it's definition, it's etiology, its mechanism of development as well as actual treatment and developing treatments.
This document summarizes information about Alzheimer's disease from a student paper, including descriptions of symptoms, causes, pathophysiology and treatment options. It discusses how Alzheimer's is a progressive neurodegenerative disorder causing dementia. Key pathological features are amyloid plaques and neurofibrillary tangles in the brain. Current treatments aim to improve cognitive symptoms and include cholinesterase inhibitors such as donepezil for mild-moderate cases and memantine for moderate-severe cases. Several drug trials are also mentioned.
This document discusses Alzheimer's disease (AD), including its definition, etiology, risk factors, pathophysiology, clinical symptoms, diagnosis, and treatment. Some key points include:
- AD is the most common cause of dementia and is characterized by cognitive and behavioral impairment. While the exact cause is unknown, risk factors include age, family history, and genetics such as the APOE E4 allele.
- Pathologically, AD is defined by amyloid plaques and neurofibrillary tangles in the brain. It results from the death of brain cells, affecting processes like memory, thinking, and behavior.
- Diagnosis involves assessing symptoms, ruling out other conditions through tests, and structural imaging of the brain
Ms. Ritika Soni presented on Alzheimer's disease. Alzheimer's is a progressive brain disorder that causes memory loss and cognitive decline. It was first described by Dr. Alois Alzheimer in 1906 from examining a patient with unusual brain abnormalities. The causes are not fully known but risk factors include age, family history, and head injuries. Diagnosis involves cognitive assessments and brain imaging. Currently, there is no cure, but medications and caregiving can temporarily improve symptoms.
Are elderly with schizophrenia more or less likely to (docx) (1)Adonis Sfera, MD
This document discusses whether elderly patients with schizophrenia are more or less likely to develop Alzheimer's disease. While schizophrenia is associated with accelerated cognitive decline in elderly patients, most studies have failed to find increased amyloid deposits or cerebrospinal fluid markers of Alzheimer's pathology in elderly schizophrenia patients. Some potential protective factors for Alzheimer's in schizophrenia patients are discussed, such as effects of antipsychotic medications, tobacco smoking, and abnormalities in brain insulin signaling and glucose metabolism. The cognitive deficits seen in elderly schizophrenia differ from those in Alzheimer's, and structural brain imaging also shows different patterns of tissue loss between the two conditions. In conclusion, while cognitive impairment is common in elderly schizophrenia, they do not appear to have an increased risk of progressive Alzheimer's
This document discusses a student research project aimed at developing new drug leads for Alzheimer's disease by targeting beta-secretase, an enzyme involved in the production of amyloid beta peptides. It provides background on Alzheimer's disease mechanisms and treatments. The project will use rational drug design methods to develop small molecule beta-secretase inhibitors, which will then be patented and licensed to a company for further development as a potential pharmaceutical.
The document discusses Alzheimer's disease and dementia. It defines Alzheimer's as a degenerative brain disease caused by complex brain changes that damage brain cells. Dementia can have various reversible causes while Alzheimer's is currently irreversible. The stages of Alzheimer's are described from mild to severe. Medical treatments aim to boost brain chemicals but do not stop decline. New treatments focus on amyloid plaques, tau tangles, inflammation and insulin resistance. Non-drug therapies aim to maintain cognitive function and quality of life.
the feathers of the disease and It is histology
For downloading the presentation, more presentations , infographics and blogs visit :
studyscienceblog.wordpress.com
This document provides an overview of Alzheimer's disease including its causes, symptoms, stages, diagnosis, and treatment approaches. It discusses how Alzheimer's is characterized by plaques and tangles in the brain made up of beta-amyloid and tau proteins. Current treatment aims to improve cognitive function and behaviors through cholinesterase inhibitors and memantine, though none can stop or reverse the disease. Non-pharmacological interventions like education, communication, and stimulation therapies may provide additional support.
Alzheimer's disease is the most common cause of dementia. It is a progressive, degenerative brain disease that causes deterioration of brain cells and ultimately death. It starts with damage to the hippocampus, making it harder to form new memories over time. Plaques and tangles then spread throughout the brain, killing cells and compromising function. While there is no cure, medications can help slow cognitive decline. Support from family caregivers is also important for managing the condition.
Alzheimer's disease - A detailed case study Uzair Ahmed
This case study describes a 63-year-old woman diagnosed with Alzheimer's disease and a novel presenilin 2 mutation. She was referred to a memory clinic at age 58 with a 2-year history of repetitiveness, memory loss, and executive dysfunction. Neurocognitive testing revealed poor performance in multiple domains. Her condition progressed over several years despite treatment with cholinesterase inhibitors and memantine. She developed additional neurological symptoms including rigidity, apraxia, and worsening cognition. Genetic testing later identified a novel presenilin 2 mutation, which may have contributed to her early-onset and rapidly progressive form of Alzheimer's disease.
Alzheimer's disease is characterized by the abnormal build-up of amyloid and tau proteins in the brain, which is believed to cause neuronal death and loss of brain function. Symptoms appear as brain cells become affected and include memory loss, cognitive decline, and issues with language and visuospatial abilities. While there is no cure for Alzheimer's, some drugs can temporarily reduce symptoms by targeting amyloid plaques or preserving acetylcholine levels. The strongest genetic risk factor is an APOE allele. Recent treatments focus on reducing amyloid production and preventing tau hyperphosphorylation to improve neuronal connectivity and function.
Alzheimer's disease is a neurodegenerative disorder with severe dementia. Due to the accumulation of Beta-Amyloid proteins acetyl-choline producing neurons are getting degenerated. Alzheimer's disease is one of the most devastating brain disorders of elderly humans. It is an under-treated and under-recognized disease that is becoming a major public health problem.
Similar to Etiology of TAU & PLAQUE protein in Alzheimer's Disease (20)
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...
Etiology of TAU & PLAQUE protein in Alzheimer's Disease
1. Etiology of TAU and
PLAQUE protein in
Alzheimer’s
Ansar Laskar
B.pharm, Final Year
Under the Guidance of
Mr. Nilanjan Adhikari
Assistant Professor
Department of Pharmacology of P.G. Institute of Medical Sciences
Presented by
2. 1. Alzheimer’s Disease
Introduction
Changes in Brain
Causes of AD
Diagnosis & Treatment of AD
2. Aim
3. Objective
Clinical Hallmark of AD
Beta amyloid Plaque
Neurofibrillary Tangles
4. Conclusion
5. Reference
Contents:
3. Introduction:
Alzheimer’s Disease:
Alzheimer’s Disease is a progressive neurodegenerative disease
discovered by Alois Alzheimer, in 1906.
Brain cell are progressively damaged leading to loss of memory,
thinking skills, etc.
Disease was identified more than 100 years ago, which associated with
dementia like symptoms.
Dementia ????
So in this disease a person might forget where he kept his car keys, the
way of his home, impaired reasoning of judgement, difficulty in facial
recognition.
4. Changes in Brain:
Gyri become narrower.
Sulci get widened.
Ventricles get severely enlarged.
Figure 1: Progression of Alzheimer’s Disease[8]
5. Causes of AD:
Alzheimer’s disease is caused by a combinational of genetic
lifestyle and environmental factors that affect the brain over time.
At a fundamental level, brain protein fail to function normally.
Which disrupts the work of brain cells(neurons) and trigger a series
of harmful events.
Causes of Alzheimer’s disease are focused on the role of two
protein that is:
β-amyloid protein- Beta-amyloid is a fragment of a larger protein.
When these fragments cluster together, they appear to have a toxic
effect on neurons and to disrupt cell-to-cell communication.
TAU Protein- Tau proteins play a part in a neuron's internal support
and transport system to carry nutrients and other essential
materials.
Another causes is dysfunctional cholinergic neurons and they
release less acetylcholine in the synaptic cleft and because of these
there reduce cholinergic transmission, due to reduce cholinergic
transmission neuronal death occurs.
6. Doctors will look at the signs and symptoms take a medical history and rule out
other conditions before making a diagnosis.
Check the person’s neurological function for example by testing their balance,
senses and reflexes other assessments may includes a blood and urine test.
Perform brain scans such as : CT, MRI, PET etc.
Diagnosis of AD
Treatment of AD
Currently there is no cure for Alzheimer’s. Treatments aim to slow down the
process of destruction and relieve symptoms to improve quality of life for
patients.
Alzheimer’s medications can help for a time with memory symptoms and other
cognitive changes .
Two types of drugs are currently used to treat cognitive symptoms
Cholinesterase inhibitors.
Memantine(Namenda).
Clozapine, Haloperidol are used to treat non-cognitive Symptoms.
7. Aim:
Objective:
Clinical hallmarks of Alzheimer’s Disease:
clinical hallmarks involve Beta amyloid plaques and neurofibrillary
tangles.
Beta amyloid plaque:
Amyloid precursor protein(APP) is a part of nerve cell membrane which
required for nerve growth and repaired, this APP is broken into fragments and
these fragments removed from the body by two pathways-
Non-amyloidogenic pathway : Responsible enzymes are α-secretase
and γ-secretase.
Amyloidogenic pathway : the two enzymes named β-secretase and γ-
secretase.
In amyloidogenic pathway β-secretase enzymes breaks APP in such a way that
a comparatively larger fragment, which is called as beta amyloid protein.
In questing the hypothesis on clinical establishment in the etiology of
plaque and TAU proteins in Alzheimer’s.
8. This β-amyloid protein is made up of 36 to 43 amino acid, due to larger in size
this protein is also very sticky.
In Alzheimer’s Disease:
Excessive formation of β-amyloid protein
Reduced removal of β-amyloid protein
Accumulation of these protein in the neuronal junction
Form plaques which resulting in progressive neurodegeneration.
Neurofibrillary Tangles:
The function of microtubules is the intracellular transportation.
Tau protein is responsible for the stabilization of microtubules in nerve cells.
In Alzheimer’s there is excessive formation of beta amyloid protein, now this
protein activate intracellular kinase which causes phosphorylation of tau
protein.
After phosphorylation it detached itself from microtubules.
They aggregates together to form neurofibrillary tangles because of the
formation of tangles there is de-stabilization of microtubules.
Which disrupts the normal intracellular transport mechanism.
10. Alzheimer’s disease is the most common form of dementia in older adults. The
etiology of the disease is too much fishy yet. The procurements of AD with
drug developments need further assessment to layout the hypothetically
establishment of the disorder.
Remarkable progress is going on, but needs to more exploration for
questing advanced treatment sustaining many more miles to go.
Conclusion:
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neuroscience. 2020 Oct;23(10):1183-93.
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8. Figure 1: https://www.thehelperbees.com/individuals/healthy-hive/alzheimers-and-the-importance-of-
brain-health/ Date: 15.05.2022 Time: 11:25 am.
9. Figure 3: https://www.molecularcloud.org/p/il3-in-astrocyte-and-microglia-communication-a-potential-
therapeutic-target Date:20.05.2022Time:07:00pm.
Reference: