1. Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. The main pathologies are amyloid plaques and neurofibrillary tangles in the brain.
2. There are three stages of Alzheimer's: mild, moderate, and severe. Symptoms worsen over time and include memory loss, impaired judgment, and changes in mood and personality.
3. Risk factors include age, family history, and genetics. The disease causes cell damage and loss in areas of the brain involved in memory and cognition.
Definition
Statistics of AD
A brief introduction
Signs and symptoms of AD
NMDA receptors
Classification
Causes
Risk Factors
Pathophysiology
AD… The great unknown
Treatment Options
Future Trends
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, imagination and speaking skills, and behavioural changes. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older.
This presentation was delivered to students at UC San Diego on May 2, 2012 by Dawn DeStefani, BSW, who is the director of programs and services for The Glenner Memory Care Centers in San Diego. Learn more at www.glenner.org.
Definition
Statistics of AD
A brief introduction
Signs and symptoms of AD
NMDA receptors
Classification
Causes
Risk Factors
Pathophysiology
AD… The great unknown
Treatment Options
Future Trends
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, imagination and speaking skills, and behavioural changes. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older.
This presentation was delivered to students at UC San Diego on May 2, 2012 by Dawn DeStefani, BSW, who is the director of programs and services for The Glenner Memory Care Centers in San Diego. Learn more at www.glenner.org.
Describes about the major neurodegenerative disorders such as Dementia,Alzhimers disease,Parkinsons disease,Amyotrophic lateral sclerosis,etc.Their causes,symptoms and preventative measures.
Circulating Biomarkers for Alzheimer's Disease: Neurodegenerative Disorders ...QIAGEN
Alzheimer's disease (AD) is a complex neurodegenerative disorder. Circulating miRNAs hold great promise in the discovery of non-invasive and novel biomarkers for AD diagnosis and prognosis. This slideshow presents the role of miRNAs in AD and details current progress in biomarker discovery. Various tools for pathway-focused and genome-wide miRNA expression profiling, miRNA functional studies and target identification are also included.
Pharmacotherapy of Alzheimer's disease
Introduction
History
Risk factors
Pathophysiology
Symptoms
Diagnosis
Non pharmacological treatment
Drugs used in treatment of Alzheimer`s
Recent advances
Screening methods
Summary
References
Alzheimer's disease is a neurological disorder that destroys memory "dementia" and other important mental functions. Learn the Causes, Symptoms & Treatment for Alzheimer’s Disease here.
Molecular Mechanisms of Neurodegeneration: Neurodegenerative Disorders Webin...QIAGEN
Common molecular mechanisms and pathways leading to neurodegeneration, such as Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease or Multiple Sclerosis, are presented in this slideshow. Learn more about research and therapeutic strategies as well as how these discoveries and tools can be used to facilitate your neurodegeneration research.
Describes about the major neurodegenerative disorders such as Dementia,Alzhimers disease,Parkinsons disease,Amyotrophic lateral sclerosis,etc.Their causes,symptoms and preventative measures.
Circulating Biomarkers for Alzheimer's Disease: Neurodegenerative Disorders ...QIAGEN
Alzheimer's disease (AD) is a complex neurodegenerative disorder. Circulating miRNAs hold great promise in the discovery of non-invasive and novel biomarkers for AD diagnosis and prognosis. This slideshow presents the role of miRNAs in AD and details current progress in biomarker discovery. Various tools for pathway-focused and genome-wide miRNA expression profiling, miRNA functional studies and target identification are also included.
Pharmacotherapy of Alzheimer's disease
Introduction
History
Risk factors
Pathophysiology
Symptoms
Diagnosis
Non pharmacological treatment
Drugs used in treatment of Alzheimer`s
Recent advances
Screening methods
Summary
References
Alzheimer's disease is a neurological disorder that destroys memory "dementia" and other important mental functions. Learn the Causes, Symptoms & Treatment for Alzheimer’s Disease here.
Molecular Mechanisms of Neurodegeneration: Neurodegenerative Disorders Webin...QIAGEN
Common molecular mechanisms and pathways leading to neurodegeneration, such as Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease or Multiple Sclerosis, are presented in this slideshow. Learn more about research and therapeutic strategies as well as how these discoveries and tools can be used to facilitate your neurodegeneration research.
This presentation illustrates the various pathways of development of AD ,including the recent molecular pathways , and their implication in early diagnosis and therapy .
There is increasing evidence that free radical-induced oxidative damage may play a role in the pathogenesis of Alzheimer's disease. Free radicals are reactive oxygen compounds that may attack and damage lipids, proteins, and DNA. The brain is especially sensitive to oxidative damage because of its high content of readily oxidized fatty acids, high use of oxygen, and low levels of antioxidants. Evidence for oxidative damage has been obtained from postmortem brain tissue as well as from living patients with Alzheimer's disease. Antioxidants such as vitamin E show promise that they may help in treating the disease.
Etiology of TAU & PLAQUE protein in Alzheimer's Disease PintuLaskar
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
16. Vaccination Dale Schenk, Michael Hagen, Peter Seubert. Current progress in beta-amyloid immunotherapy. Current Opinion in Immunology , Volume 16, Issue 5 , October 2004 , Pages 599-606
29. Depletion of Neurotrophin Neurotrophins are a family of proteins that induce the survival, development and function of neurons. learning memory behavior
41. Mitochondrial Dysfunction Oxidative Stress Amany Mohamed , et. al., Int J Alzheimers Dis . 2011 , 127984. A can be translocated to the cell via interacting with RAGE
42. Mitochondrial Dysfunction Oxidative Stress A can be translocated to mt via TOM Inhibit cyt. c oxidase lead to ROS and oxidative stress Renato X. Santos , et. al., Int J Clin Exp Pathol 2010;3(5):570-581
56. Some components of the inflammatory to CNS degeneration http://www.gladstone.ucsf.edu/wp/2009/10/inflammationalzheimers/
57. Inflammatory responses and neurodegeneration http://www.gladstone.ucsf.edu/wp/2009/10/inflammationalzheimers/
58. Neurotoxic and neurotrophic action of microglia and astrocytes McNally L, Bhagwager Z, Hannestad J, CNS Spectr, Vol 13 NO.6. 2008.
59. Using the inflammatory response against AD http://www.gladstone.ucsf.edu/wp/2009/10/inflammationalzheimers/
60.
61. Calcium Presenilin mutation Disrupt calcium homeostasis Calcium in endoplasmic reticulum Release calcium into cytoplasm Alzheimer’s disease A β level
62.
63.
64. Axonal – transport deficit Impairment of transport Amyloid precursor protein, vesicle and kinesin Exonal swelling, A β deposition and neurodegeneration
Although amyloid plaques or senile plaques may be classified further according to their composition, all contain forms of β-amyloid protein (Aβ). Aβ is a 39- to 42-amino acid peptide that is formed by the proteolytic cleavage of β-amyloid precursor protein (APP) and is found in extracellular deposits throughout the central nervous system (CNS). 9 Aβ is believed to interfere with neuronal activity because of its stimulatory effect on production of free radicals, resulting in oxidative stress and neuronal cell death. In AD, the amyloid deposits are largely spherical, reaching up to 200 μm in diameter, and are prevalent throughout the cortex and hippocampus of brains from affected individuals. Neurofibrillary tangles are paired helical filaments composed of tau protein, which in normal cells is essential for axonal growth and development. However, when hyperphosphorylated, the tau protein forms tangles that are deposited within neurons located in the hippocampus and medial temporal lobe, the parietotemporal region, and the frontal association cortices, leading to cell death.
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The biggest risk factor for Alzheimer's disease is increased age. The likelihood of developing Alzheimer's disease After age 65, and rises sharply after age 75 Genetics==== Family history of AD Sex=====Women are more likely to develop AD than men Having Down syndrome
Proteolytic processing of amyloid precursor protein (APP) by the secretases. APP is a type-I transmembrane glycoprotein. The majority of APP is processed in the nonamyloidogenic pathway (thick arrow); APP is first cleaved by a-secretase within the amyloid-b peptide (Ab) domain (darker shaded region), leading to APPsa secretion and precluding Ab generation. Membrane-anchored a-carboxy terminal fragment (CTF) is then cleaved by g-secretase within the membrane, releasing the p3 peptide and APP intracellular domain (AICD). Alternatively, amyloidogenesis (thin arrow) takes place when APP is first cleaved by b-secretase, producing APPsb. Ab and AICD are generated upon cleavage by g-secretase of the b-CTF fragment retained in the membrane. Scissors indicate the cleavage sites of a-, b- and g–secretase.
The neocortex is part of the cerebral cortex . It is involved in higher functions such as sensory perception , generation of motor commands , spatial reasoning, conscious thought and language .
Beta-amyloid (Ab) immunotherapy strategies. Immunotherapy can be achieved through either active immunization with full length Ab or an Ab immunoconjugate, or passive administration of monoclonal anti-Ab antibodies. After active immunization with Ab1–42, the peptide is processed by antigen-presenting cells and Ab fragments are presented to T cells. Subsequently, various B-cells that can recognize epitopes on Ab1–42 are engaged, proliferate and produce polyclonal anti-Ab antibodies. The second type of active immunization approach involves the administration of small fragments of Ab conjugated to an unrelated carrier protein. The immunological response after immunization of an Ab peptide-carrier protein conjugate is similar to the first strategy, with the exception that the T cells are stimulated by the carrier protein rather than the Ab fragment (which lacks T-cell epitopes). The third strategy involves direct administration of monoclonal antibodies directed against Ab and, as such, does not require any type of immunological response from the host.
Aging: synapse loss
Figure 4 . Oxidative Stress and Mitochondrial Failure.A [beta]-amyloid peptide (A[beta])-centric scheme depicts production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Their peroxidative attack on cell and organelle membrane lipids yields the mitochondrial toxins hydroxynonenal (HNE) and malondialdehyde. Oxidative damage to membrane-bound, ion-specific ATPases and stimulation of calcium (Ca2+) entry mechanisms - for example, glutamate (N-methyl-d-aspartate [NMDA]) receptors (NMDAr), membrane-attack complex (MAC) of complement, and ion-selective amyloid pore formation - cause cytosolic and mitochondrial Ca2+ overload. Cellular A[beta] directly attacks electron transport complex IV (cytochrome c oxidase) and key Krebs-cycle enzymes ([alpha]-ketoglutarate and pyruvate dehydrogenase) and damages mitochondrial DNA (mtDNA), leading to fragmentation. Lipid peroxidation products also promote tau phosphorylation and aggregation, which in turn inhibit complex I. Exaggerated amounts of ROS and RNS are generated at complexes I and III. As the mitochondrial membrane potential (MPP) collapses and permeability-transition pores ([psi]m) open, caspases are activated. A[beta] also induces the stress-activated protein kinases p38 and c-jun N-terminal kinase (JNK), as well as p53, which are further linked with apoptosis. Substrate deficiencies, notably NADH and glucose, combine with electron transport uncoupling to further diminish ATP production. Alcohol dehydrogenase was recently identified as the mitochondrial-binding target for A[beta]. Endoplasmic reticulum contributions are shown. GLUT1, 4 denotes glucose transporter 1, 4.
Long-term potentiation involved in memory
However, there’s no single linear chain of events and matters are complicating
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