The 2nd edition of The holistic Prevention, Management and Treatment of Dementia under The Microscope of Conventional Medicine: Treatment of Dementia associated to Creutzfeldt-Jakob disease

Kyle J. Norton (Scholar)

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Abstract
Dementia is defined as neuro degeneration syndrome among elder, affecting memory, thinking, orientation, comprehension, calculation, learning capacity, language, and judgement over 47 millions
of worldwide population, mostly in the West. The evaluation of the syndrome by holistic medicine has been lacking, especially through conventional medicine research and studies. The aim of this essay is to provide accurate information of how effective of holistic medicine in prevention, management and treatment of dementia through searching data base of PubMed.
This is the third time, a research paper has been written this way to general public that you will not find any where in the net.

Dementia is a neuropsychiatric disorder induced of cognitive impairment and behavioral disturbances. The behavioral and psychological symptoms of dementia (BPSD) are common, with a progressive loss of memory and other mental abilities, affecting a person's ability to perform usual tasks in everyday life.

Treatment in Conventional Medicine Perspective

D. Dementia associated to Creutzfeldt-Jakob disease
People who have eaten contaminated beef in a prolonged period of times may be infected by infectious agent prion(514) without even knowing it. Creutzfeldt-Jakob disease is a quickly progressing and fatal disease(513) inducing dementia(515), especially in elder(516), causing degeneration of skeletal muscle, peripheral nerves(517) linked to mutations in the PrP gene(518). CJD is characterized by rapidly progressive dementia(513)(519). Initially, individuals experience of epilepsy seizure(519), problems with muscular coordination(522); cognitive change (loss of motor planning, loss of motor functioning's, inability to speak)(519), such as impaired memory(521), loss of functional independence(523) and impaired vision(520). People with the disease also may experience insomnia(524)(525), depression(526)(527), or unusual sensations(522).

Treatments of Creutzfeldt-Jakob disease (CJD)
There is no treatment that can cure or control CJD. The available treatments are to relieve the symptoms and may help slow the disease.
1. Interleukins
a. Interleukins is defined as any group of naturally occurring proteins that mediate communication between cells(528), produced by while blood cells. The set of interleukins stimulated by a specific infectious agent in determined cells in responding to the infection and influences(528) through its modulated inflammation and immune response.(529).
According to University Hospital Göttingen, interleukin 10 levels, inflammatory cytokines(530) were significantly elevated in the cerebrospinal fluid of CJD, dementia, motoneuron disease patients through it inflammatory cytokines(529). Cyclooxygenase-2 (COX-2)(532) and prostaglandins (PGs)(533) are the most conventional medicine used to treat neurotoxiticy in acute conditions, including in inflammatory chronic diseases, such as Creutzfeldt-Jakob disease (CJD) and Alzheimer's disease (AD)(531).

b. Common side effects are not limit to
b.1. Cyclooxygenase-2 (COX-2)
b.1.1 Insomnia,
b.1.2 Abdominal pain,
b.1.3. Flatulence (gas),
b.1.4. Headache ,
b.1.5. Nausea and diarrhea.

b.2. Prostaglandins (PGs)
b.2. Dizziness
b.2.2. Fainting
b.2.3. Irregular heartbeat or pulse•
b.2.4. Slow heartbeat

2. Other medication
2.1. Quinacrine
a. Quinacrine used for treatment of giardiasis caused by Giardia lamblia(535) may be a potential medicine for treatment of Creutzfeldt-Jakob disease(CJD)(536)(537), according to a report in The Mail on Sunday 12 August 2001, entitled "Briton 'cured' in CJD drug trial"(534).
Although Quinacrine at a dose of 300 mg per day was reasonably tolerated, it did not induce significantly affect in course of prion diseases(537), including Creutzfeldt-Jakob disease (CJD(538)(539).
b. Most common side effects are not limit to
b.1. Abdominal and cramps
b.2. Diarrhea
b.3. Fever
b.4. Headache
b.5. loss of appetite
b.6. Changes in menstrual flow
b.7. Nausea and vomiting

2.2. Gamma-aminobutyric acid, dopamine and serotonin
a. Other medication used to control aggressive and uncontrolled behavior, such as gamma-aminobutyric acid(541)(542)(543) with functions of inhibitory neurotransmitter in the mammalian central nervous system(540), (541)(543). Dopamine and serotonin(542)(543) also functioning as a neurotransmitter may be helpful.
b. Common side effects are not limit to
b.1. Gamma-aminobutyric acid
b.1.1. Anxiety
b..2.2. Dizziness
b.1.3.Drowsiness
b.1.4 dry mouth
b.1.5. Blurred vision
b.1.6. Constipation
b.1.7. Irritation
b.1.8. Joint or muscle pain
b.1.9. Increased appetite

b.2. Dopamine
b.2.1. Fast heartbeat
b.2.2. Headache
b.2.3. Nausea
b.2.4. Vomiting

b.3.. Serotonin
b.3.1. Feeling agitated, shaky or anxious
b.3.2. Indigestion
b.3.3. Diarrhea or constipation
b.3.4. Loss of appetite
b.3.5. Weight loss
b.3.6. Dizziness
b.3.7. Blurred vision
b.3.8. Excessive sweating
b.3.9. Insomnia
b.3.10. Dry mouth

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References
(513) Human prion diseases: from Kuru to variant Creutzfeldt-Jakob disease by Sikorska B1, Liberski PP.(PubMed)
(514) An overview of human prion diseases by Imran M1, Mahmood S.(PubMed)
(515) Rapidly progressive dementia: prion diseases and other rapid dementias by Geschwind MD.(PubMed)
(516) Neuroimaging of rapidly progressive dementias, part 1: neurodegenerative etiologies by Degnan AJ1, Levy LM.(PubMed)
(517) Degeneration of skeletal muscle, peripheral nerves, and the central nervous system in transgenic mice overexpressing wild-type prion proteins by Westaway D1, DeArmond SJ, Cayetano-Canlas J, Groth D, Foster D, Yang SL, Torchia M, Carlson GA, Prusiner SB.(PubMed)
(518) Prion protein transgenes and the neuropathology in prion diseases by DeArmond SJ1, Prusiner SB.(PubMed)
(519) [Differential diagnosis of status epilepticus in intensive care: about one case of sporadic Creutzfeldt-Jakob].[Article in French] by Chauvin A1, Dubost JL2, Cleophax C2, Niclot P3, Thuong M2.(PubMed)
(520) Prion protein accumulation in eyes of patients with sporadic and variant Creutzfeldt-Jakob disease by Head MW1, Northcott V, Rennison K, Ritchie D, McCardle L, Bunn TJ, McLennan NF, Ironside JW, Tullo AB, Bonshek RE.(PubMed)
(521) Fast progressive memory loss in a 63-year-old man by De Smet K1, De Maeseneer M, Amir TY, De Mey J.(PubMed)
(522) Creutzfeldt-Jakob Disease Fact Sheet(NIH)
(523) Accuracy of diagnostic criteria for sporadic creutzfeldt-jakob disease among rapidly progressive dementia by Tagliapietra M1, Zanusso G, Fiorini M, Bonetto N, Zarantonello G, Zambon A, Ermani M, Monaco S, Manara R, Cagnin A.(PubMed)
(524) Hereditary Creutzfeldt-Jakob disease and fatal familial insomnia by Gambetti P1, Parchi P, Chen SG.(PubMed)
(525) Genetic Creutzfeldt-Jakob disease and fatal familial insomnia: insights into phenotypic variability and disease pathogenesis. by Capellari S1, Strammiello R, Saverioni D, Kretzschmar H, Parchi P.;(PubMed)
(526) Sporadic Creutzfeldt-Jakob disease presenting as major depression by Jiang TT1, Moses H, Gordon H, Obah E.(PubMed)
(527) [Course of anxiety, depression, and quality of life in relatives of patients with Creutzfeldt-Jakob-Disease][Article in German]by Riedemann C1, Zerr I, Kropp S, Otto A, Poser S, Herrmann C.(PubMed)
(528) Interleukin (IL) Protein Written by: The Editors of Encyclopædia Britannica
(529) Interleukin 4 and interleukin 10 levels are elevated in the cerebrospinal fluid of patients with Creutzfeldt-Jakob disease by Stoeck K1, Bodemer M, Ciesielczyk B, Meissner B, Bartl M, Heinemann U, Zerr I.(PubMed)
(530) The role of inflammatory cytokines as key modulators of neurogenesis by Borsini A1, Zunszain PA1, Thuret S2, Pariante CM3.(PubMed)

(531) Role of COX-2 in inflammatory and degenerative brain diseases. by Minghetti L1(PubMed)
(532) Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain diseases by Minghetti L1.(PubMed)
(533)  Prostaglandins and cyclooxygenases in glial cells during brain inflammation by Tzeng SF1, Hsiao HY, Mak OT.(PubMed)
(534) Briton cured in CJD drug trial by ANDREW CHAPMAN, (Mail on line)
(535) Treatment of Giardiasis by Timothy B. Gardner and David R. Hill(PMC)
(536) Quinacrine treatment trial for sporadic Creutzfeldt-Jakob disease by Geschwind MD1, Kuo AL, Wong KS, Haman A, Devereux G, Raudabaugh BJ, Johnson DY, Torres-Chae CC, Finley R, Garcia P, Thai JN, Cheng HQ, Neuhaus JM, Forner SA, Duncan JL, Possin KL, Dearmond SJ, Prusiner SB, Miller BL.(PubMed)
(537) Safety and efficacy of quinacrine in human prion disease (PRION-1 study): a patient-preference trial by Collinge J1, Gorham M, Hudson F, Kennedy A, Keogh G, Pal S, Rossor M, Rudge P, Siddique D, Spyer M, Thomas D, Walker S, Webb T, Wroe S, Darbyshire J.(PubMed)
(538) Quinacrine treatment trial for sporadic Creutzfeldt-Jakob disease by Geschwind MD1, Kuo AL, Wong KS, Haman A, Devereux G, Raudabaugh BJ, Johnson DY, Torres-Chae CC, Finley R, Garcia P, Thai JN, Cheng HQ, Neuhaus JM, Forner SA, Duncan JL, Possin KL, Dearmond SJ, Prusiner SB, Miller BL.(PubMed)
(539) Compassionate use of quinacrine in Creutzfeldt-Jakob disease fails to show significant effects by Haïk S1, Brandel JP, Salomon D, Sazdovitch V, Delasnerie-Lauprêtre N, Laplanche JL, Faucheux BA, Soubrié C, Boher E, Belorgey C, Hauw JJ, Alpérovitch A.(PubMed)
(540) gamma-Aminobutyric acid(Wikipedia)
(541) Alterations of neurotransmitter norepinephrine and gamma-aminobutyric acid correlate with murine behavioral perturbations related to bisphenol A exposure by Ogi H1, Itoh K2, Ikegaya H3, Fushiki S1.(PubMed)
(542) Social and neural determinants of aggressive behavior: pharmacotherapeutic targets at serotonin, dopamine and gamma-aminobutyric acid systems by Miczek KA1, Fish EW, De Bold JF, De Almeida RM.(PubMed)
(543) Escalated aggressive behavior: dopamine, serotonin and GABA by de Almeida RM1, Ferrari PF, Parmigiani S, Miczek KA.(PubMed)