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Presented by
K.SAIKRISHNAM.PHARM
(Pharmacology)
Under the Guidance of
Dr. K. PRASAD
M.PHARM., PhD
Shri Vishnu College of Pharmacy, Dept. of pharmacology , Vishnupur, Bhimavaram -2.
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AD STATISTICS INSIDE THE HUMAN BRAIN MECHANISM OF ACTION
TYPES OF AD
SEARCH FOR CAUSES
DIAGNOSIS
TREATMENT
RECENT DEVELOPMENTS CONCLUSION REFERENCES
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The Impact ofAlzheimer's Disease(AD)
Once considered a rare
disorder, Alzheimers diseaseis now seen as a major publichealth problem that isseriously affecting millions of
older People and their families.
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Although the risk of developing AD increases with
age in most people with AD, symptoms firstappear after age 60 AD is not a part of normalaging. AD is the most common cause of dementiaamong people age 65 and older.[2]
This incurable, degenerative, and terminal diseasewas first described by German psychiatrist andneuropathologist Alois Alzheimer in 1906 and was
named after him.[1]
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The World Health Organizationestimated that in 2005, 0.379% ofpeople worldwide had dementia,and that the prevalence wouldincrease to 0.441% in 2015 and to0.556% in 2030.[3]
Scientists estimate that around4.5 million people now have AD.
AD Statistics.
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To understandAlzheimersdisease, itsimportant toknow a bit about
the brainThe Brains Vital Statistics
Adult weight:about 3 pounds
Adult size:
a medium cauliflower Number of neurons:
100,000,000,000(100 billion)
Number of synapses(the gap between neurons):100,000,000,000,000
(100 trillion)Slide 8
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The Three Main layers
1. Cerebral Hemispheres
2. Cerebellum
3. Brain Stem
Other Crucial Parts Hippocampus: where short-term memories are converted
to long-term memories
Thalamus: receives sensory and limbic information andsends to cerebral cortex
Hypothalamus: monitors certain activities and controlsbodys internal clock
Limbic system: controls emotions and instinctive behavior(includes the hippocampus and parts of the cortex)
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The Brain in Action
Hearing Words Speaking Words Seeing Words Thinking about Words
Different mental activities take place in different parts
of the brain. Positron emission tomography (PET)scans can measure this activity. Chemicals taggedwith a tracer light up activated regions shown in redand yellow.
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Neurons
The brain has billionsof neurons, each withan axon and manydendrites.
To stay healthy,neurons mustcommunicate witheach other, carry out
metabolism, andrepair themselves.
AD disrupts all threeof these essential jobs.
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Plaques and Tangles[4]: The Hallmarks of AD
The brains of people with AD have an abundance oftwo abnormal structures:
An actual AD plaque An actual AD tangle
Beta-amyloid plaques[5] [6], which are densedeposits of protein and cellular material that
accumulate outside and around nerve cells Neurofibrillary tangles [7], which are twisted fibers
that build up inside the nerve cell
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Beta-Amyloid Plaques
Amyloid precursor protein (APP) isthe precursor to Amyloid plaque [8] [9].
1. APP sticks through the neuronmembrane.
2. Enzymes cut the APP intofragments of protein, includingbeta-Amyloid.
3. Beta-Amyloid fragments cometogether in clumps to form plaques.
1.
2.
3.
In AD, many of these clumps form,disrupting the work of neurons.This affects the hippocampus andother areas of the cerebral cortex.
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NeurofibrillaryTangles
Neurons have an internal support structure partly made up ofmicrotubules. A protein called tauhelps stabilize microtubules.In AD, tauchanges, causing microtubules to collapse, and tau
proteins clump together to form neurofibrillary tangles[10].
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Preclinical AD[10] [11] Signs of AD are firstnoticed in the entorhinalcortex, then proceed to thehippocampus.
Affected regions begin to
shrink as nerve cells die.
Changes can begin 10-20years before symptomsappear.
Memory loss is the firstsign of AD.
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Mild to Moderate AD[12] [113]
AD spreads through thebrain. The cerebral cortexbegins to shrink as more andmore neurons stop workingand die.
Mild AD signscan includememory loss, confusion,
trouble handling money,poor judgment, moodchanges, and increasedanxiety.
Moderate AD signscaninclude increased memoryloss and confusion, problemsrecognizing people, difficultywith language and thoughts,
restlessness, agitation,
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Severe AD [14] [15] In severe AD, extreme
shrinkage occurs in thebrain. Patients arecompletely dependent onothers for care.
Symptoms can includeweight loss, seizures, skininfections, groaning,moaning, or grunting,increased sleeping, loss of
bladder and bowel control. Death usually occurs from
aspiration pneumonia orother infections. Caregiverscan turn to a hospice for helpand palliative care.
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AD develops when genetic, lifestyle, and
environmental factors work together to causethe disease process to start.
In recent years, scientists have discoveredgenetic links [16] to AD. They are alsoinvestigating other factors that may play a rolein causing AD.
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Genetic Studies [17]
The two main types ofAD are early-onset andlate-onset:
Early-onset AD is rare,usually affecting people
aged 30 to 60 and usuallyrunning in families.Researchers haveidentified mutations inthree genes that causeearly-onset AD.
Late-onset AD is morecommon. It usually affectspeople over age 65.
Researchers have identified a gene that produces a protein calledapolipoprotein E (ApoE). Scientists believe this protein is involved in
the formation of beta-amyloid plaques.
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Studies at the Cellular and Molecular
Level
Homocysteine, an amino acid, is a risk factor for heartdisease. A study shows that an elevated level ofhomocysteine is associated with increased risk of AD.
Scientists are also looking at inflammation in certainregions of the brain and strokes as risk factors for AD.
Oxidative damage fromfree radical moleculescan injure neurons.
P t S f
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Physicians today use a
number of tools todiagnose AD:
a detailed patient history
physical and neurological
exams and lab tests
Advanced medical imaging withcomputed tomography (CT) ormagnetic resonance imaging(MRI), and with single photonemission computed tomography(SPECT) or positron emissiontomography (PET) can be usedto help exclude other cerebralpathology or subtypes of
dementia.[18]
Normal & AD MRI SCAN
Pet Scan ofNormal Brain
Pet Scan ofAlzheimers
Disease Brain
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TREATMENTFOR
Alzheimer'sDisease
DRUG
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DRUG
NAMEDRUG TYPE AND USE HOW IT WORKS COMMON SIDE EFFECTS
Namenda
(memantin
e)[19][20][21]
N-methyl D-aspartate
(NMDA) antagonist
prescribed to treat
symptoms of moderate tosevere Alzheimers
Blocks the toxic effects
associated with excess
glutamate and regulates
glutamate activation
Dizziness, headache,
constipation, confusion[22]
Razadyne
(galantami
ne)[23]
Cholinesterase inhibitor
prescribed to treat
symptoms of mild to
moderate Alzheimers
Prevents the breakdown of
acetylcholine and stimulates
nicotinic receptors to release
more acetylcholine in the brain
Nausea, vomiting,
diarrhea, weight loss, loss
of appetite
Exelon
(rivastigmi
ne)[24]
Cholinesterase inhibitor
prescribed to treat
symptoms of mild to
moderate Alzheimers
Prevents the breakdown of
acetylcholine and butyrylcholine
(a brain chemical similar to
acetylcholine) in the brain
Nausea, vomiting,
diarrhea, weight loss, loss
of appetite, muscle
weakness
Aricept
(donepezil)[25]
Cholinesterase inhibitor
prescribed to treat
symptoms of mild to
moderate, and moderate
to severe Alzheimers
Prevents the breakdown of
acetylcholine in the brain
Nausea, vomiting, diarrhea
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Dietary supplements[26]The following are the supplements to take:
Supplement Purpose
------------------- -----------------------------------------------
Vitamins C & E provides antioxidants to prevent Alzheimer'sCurcumin prevent Alzheimer's
Aspirin keeps blood thin - helps prevent heart attacks
Omega-3 (fish oil) prevent Alzheimer's
Iron pills maintain healthy red blood cells
Glucosamine sulfate prevents arthritisVitamin B complex prevent Alzheimer's
Sage leaf prevent Alzheimer's
DHEA hormone supplement
Blueberries prevent Alzheimer's
Citrical provides calcium for strong bonesDMAE active ingredient of skin care creams
Phosphatidyl choline prevent Alzheimer's - help retain acetylcholine in the brai
Lemonade prevent kidney stones
Huperzine-A prevent Alzheimer's (* NEW *)
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1. Scientists discover way to reverse loss of memory : It seems that in some
cases electrical stimulation of the brain can reverse memory loss. I guess thequestion is how many people can afford this type of treatment.?
2. Within 5 years there could be a vaccine which will break up the sticky globesof amyloid proteins which cause Alzheimer's disease, Known as CAD106, it isthe brainchild of scientists at Zurich-based biotechnology firm Cytos.
3. PBT2 - Australian doctors have produced a drug , PBT2, which not onlyprevents build up of the amyloid protein linked to the disease, but actuallyclears it out of the brain. Phase II clinical trails are beginning.
4. Huperzine A - It is an extract from a club moss (Huperzia serrata) that has
been used for centuries in Chinese folk medicine. Huperzine's action has beenattributed to its ability to strongly inhibit acetylcholinesterase, the enzyme thatbreaks down acetylcholine in the synaptic cleft. Acetylcholine is involved inmemory and learning.
RECENT DEVELOPMENTS
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1. By doing physical exercise like.
Walk, run, dance, swim, pump iron, whatever you can handle.
2. Bydoing mental exercise like.
Learn a new language. Play bridge, or chess. Do crossword
puzzles, Read.
3. By change your diet like.
The above mentioned diet have been found to be beneficial.
By doing these steps it will reduce risk of
suffering from this fatal disease.
CONCLUSION
REFERENCES
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1. Berchtold NC, Cotman CW (1998). "Evolution in the conceptualization of dementia and Alzheimer's
disease: Greco-Roman period to the 1960s". Neurobiol. Aging 19 (3): 17389. doi:10.1016/S0197-
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4. Tiraboschi P, Hansen LA, Thal LJ, Corey-Bloom J (June 2004). "The importance of neuritic plaques and
tangles to the development and evolution of AD".Neurology 62 (11): 19849. PMID 15184601
5. Hardy J, Allsop D (October 1991). "Amyloid deposition as the central event in the aetiology of
Alzheimer's disease". Trends Pharmacol. Sci. 12 (10): 38388. doi:10.1016/0165-6147(91)90609-V.
PMID 1763432.
6. Mudher A, Lovestone S (January 2002). "Alzheimer's disease-do tauists and baptists finally shakehands".Trends Neurosci. 25 (1): 2226. doi:10.1016/S0166-2236(00)02031- 2. PMID 11801334.
7. Mudher A, Lovestone S (January 2002). "Alzheimer's disease-do tauists and baptists finally shake
hands". Trends Neurosci. 25 (1): 2226. doi:10.1016/S0166- 2236(00)02031-2. PMID 11801334.
REFERENCES
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8. Priller C, Bauer T, Mitteregger G, Krebs B, Kretzschmar HA, Herms J (July 2006). "Synapse formation
and function is modulated by the amyloid precursor protein".J. Neurosci. 26 (27): 721221.
doi:10.1523/JNEUROSCI.1450-06.2006. PMID 16822978.
9. Turner PR, O'Connor K, Tate WP, Abraham WC (May 2003). "Roles of amyloid precursor protein and
its fragments in regulating neural activity, plasticity and memory". Prog. Neurobiol. 70 (1): 132.
doi:10.1016/S0301-0082(03)00089-3. PMID 12927332.
10. Hernndez F, Avila J (September 2007). "Tauopathies". Cell. Mol. Life Sci. 64 (17): 221933.
doi:10.1007/s00018-007-7220-x. PMID 17604998.
11. Frstl H, Kurz A (1999). "Clinical features of Alzheimer's disease".European Archives of
Psychiatry and Clinical Neuroscience 249 (6): 288290. doi:10.1007/s004060050101.
PMID 10653284.
12. Carlesimo GA, Oscar-Berman M (June 1992). "Memory deficits in Alzheimer's patients: a
comprehensive review".Neuropsychol Rev 3 (2): 11969. doi:10.1007/BF01108841.
PMID 1300219.
13. Jelicic M, Bonebakker AE, Bonke B (1995). "Implicit memory performance of patients with
Alzheimer's disease: a brief review".International Psychogeriatrics 7 (3): 385
392.
doi:10.1017/S1041610295002134. PMID 8821346.
14. Taler V, Phillips NA (Jul 2008). "Language performance in Alzheimer's disease and mild
cognitive impairment: a comparative review".J Clin Exp Neuropsychol 30 (5): 50156.
doi:10.1080/13803390701550128. PMID 1856925.
15. Frank EM (September 1994). "Effect of Alzheimer's disease on communication function".J S C MedAssoc 90 (9): 41723. PMID 7967534.
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16. Blennow K, de Leon MJ, Zetterberg H (July 2006). "Alzheimer's disease".Lancet368 (9533): 387403.
doi:10.1016/S0140-6736(06)69113-7. PMID 16876668.
17. Waring SC, Rosenberg RN (March 2008). "Genome-wide association studies in Alzheimer disease".Arch
Neurol 65 (3): 32934. doi:10.1001/archneur.65.3.329. PMID 18332245.
18. "Dementia: Quick reference guide" (PDF). London: (UK) National Institute for Health and Clinical
Excellence. November 2006. http://www.nice.org.uk/nicemedia/pdf/CG042quickrefguide.pdf. Retrieved 2008-
02-22.
19. Lipton SA (2006). "Paradigm shift in neuroprotection by NMDA receptor blockade: memantine and
beyond".Nat Rev Drug Discov 5 (2): 160170. doi:10.1038/nrd1958. PMID 16424917.
20."Memantine". US National Library of Medicine (Medline). 2004-01-04.
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a604006.html. Retrieved 2010-02-03.21. Areosa Sastre A, McShane R, Sherriff F (2004). "Memantine for dementia". Cochrane Database Syst Rev (4):
CD003154. doi:10.1002/14651858.CD003154.pub2. PMID 15495043.
22. "Namenda Prescribing Information" (PDF). Forest Pharmaceuticals. http://www.frx.com/pi/namenda_pi.pdf.
Retrieved 2008-02-19.
23. "Galantamine".Medline Plus. US National Library of Medicine. 2007-01-08.
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a699058.html. Retrieved 2010-02-03
24. "Rivastigmine".Medline Plus. US National Library of Medicine. 2007-01-08.
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a602009.html. Retrieved 2010-02-03.
25. "Donepezil".Medline Plus. US National Library of Medicine. 2007-01-08.
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a697032.html. Retrieved 2010-02-03
26. www.fatsforhealth.com
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