Holistic Health Articles and Research Related to Herbal Medicines, Foods and Phytochemicals

Monday 23 January 2017

The Conventional Treatment of Dementia associated to Creutzfeldt-Jakob disease - Dopamine

Kyle J. Norton (Scholar)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

Dementia

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.

Treatment of Dementia associated to Creutzfeldt-Jakob disease - Dopamine

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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)
(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)

Sunday 22 January 2017

The Conventional Treatment of Dementia Associated to Multi-infarct dementia - Plavix

Also known as vascular dementia, is the second most common form of dementia after Alzheimer's disease in older adults between ages of 60 and 75(571), caused by different mechanisms all resulting in vascular lesions in the brain(572)(573) with prevalence of major depression, depressed mood/anhedonia, and subjective and neurovegetative symptoms of depression(574).

1. Plavix
Plavix tablets is pescription-only medicine with function of keeping blood platelets from sticking together and forming clots(577) to prevent blood clotted causes of future stroke(579). In some cases, it is used conjunction with aspirin(578).

b. Side effects are not limit to
The most common side effects of Plavix (occurring in more than 2 percent of people and more often in the group taking Plavix) include:
b.1. Constipation
b.2. Diarrhea
b.3. Dizziness
b.4. Headache
b.5. Heartburn
b.6. Joint or muscle pain
b.7. Nausea and vomiting
b.8. Etc.
A sudden choking feeling, sore throat, difficulty swallowing and itchy mouth had been reported in patient taking clopidogrel 75 mg combined with 100 mg acetylsalicylic acid once daily, and metoprolol tartrate 50 mg twice daily(580)

(571) NINDS Multi-Infarct Dementia Information Page(NIH)
(572) Vascular dementia: different forms of vessel disorders contribute to the development of dementia in the elderly brain. by Thal DR1, Grinberg LT, Attems J.(PubMed)
(573) [Vascular dementia: big effects of small lesions].[Article in French]by Gold G1, Kövari E.(PubMed)
(574) Depressive Symptoms in Alzheimer's Disease and Multi-infarct Dementiaby William E. Reichman, MD.(Sagejournasl)
(577) Clopidogrel to prevent blood clots (Grepid, Plavix)(Patient)
(578) Aspirin plus clopidogrel as secondary prevention after stroke or transient ischemic attack: a systematic review and meta-analysis by Zhang Q1, Wang C, Zheng M, Li Y, Li J, Zhang L, Shang X, Yan C.(PubMed)
(579) [Antiplatelet agents in secondary prevention of stroke].[Article in French]by De Gautard G, Perrier A.(PubMed)

Saturday 21 January 2017

The Conventional Medicine: Treatment of Dementia associated to Creutzfeldt-Jakob disease - Gamma-aminobutyric acid

Treatment of Dementia associated to Creutzfeldt-Jakob disease - Gamma-aminobutyric acid

Friday 20 January 2017

The Conventional Medicine: Treatment of Dementia associated to Creutzfeldt-Jakob disease - Quinacrine

Treatment of Dementia associated to Creutzfeldt-Jakob disease - Quinacrine

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).

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

Thursday 19 January 2017

The Conventional Medicine: Treatment of Dementia associated to Creutzfeldt-Jakob disease - Interleukins

Treatment of Dementia associated to Creutzfeldt-Jakob disease - Interleukins

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).

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

(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)

Wednesday 18 January 2017

The Conventional Treatment of Dementia associated with Parkinson's disease Side Effects

Treatment of Dementia associated with Parkinson's disease side effects

Parkinson disease (PD) is a disabling, progressive condition induced symptoms of olfactory deficit, sleep problems such as rapid eye movement behaviour disorder, constipation and the more recently described male erectile dysfunction(456), due to the interruption of frontal-subcortical loops facilitated cognition and parallel the motor loop(457).
Contrary to common perception, many non-motor symptoms (NMS) also link to early onset of PD(459) and some may even predate the diagnosis of PD based on motor signs(458).

Most conventional medicine induced certain side effects. If you are taken any of these medicine, please consult your doctor. You also can search them from respectable sources. Here are some examples.
a, Macrogol(Allergic reaction (rash, itching, shortness of breath) changes in your body's fluid or electrolyte levels (swollenankles, other swelling, fatigue, dehydration, increased thirst with headache), Abdominal pain. Mild diarrhoea. Nausea. Vomiting. Swollen abdomen)(510).
b. Methylphenidate (stomach pain, nausea, vomiting, loss of appetite; vision problems, dizziness, mild headache; sweating, mild skin rash; numbness, tingling, or cold feeling in your hands or feet; nervous feeling, sleep problems (insomnia); or. weight loss)(511).
c. Modafinil (Black, tarry stools, blurred vision or other vision changes, chest pain, chills or fever, clumsiness or unsteadiness, confusion, dizziness or fainting, increased thirst and urination, mental depression, problems with memory, rapidly changing moods, shortness of breath, sore throat, trembling or shaking, trouble in urinating, uncontrolled movements of the face, mouth, or tongue unusual bleeding or bruising and unusual tiredness or weakness)(512).
d. Etc.

Tuesday 17 January 2017

The Conventional Treatment of Dementia associated for the motor symptoms of Parkinson's disease

Treatment of Dementia associated for the motor symptoms of Parkinson's disease

Parkinson disease (PD) is a disabling, progressive condition induced symptoms of olfactory deficit, sleep problems such as rapid eye movement behaviour disorder, constipation and the more recently described male erectile dysfunction(456), due to the interruption of frontal-subcortical loops facilitated cognition and parallel the motor loop(457).
Contrary to common perception, many non-motor symptoms (NMS) also link to early onset of PD(459) and some may even predate the diagnosis of PD based on motor signs(458).

According to the Movement Disorder Society (MDS) Task Force on Evidence-Based Medicine (EBM) Review of Treatments for Parkinson's Disease (PD) was first published in 2002 and updated in 2005 to cover clinical trial data up to January 2004 with the treatments on motor symptoms of PD(489), including

a. Piribedil(490)(491), pramipexole(491), pramipexole extended release(492)(493), ropinirole(491), rotigotine(494), cabergoline(491), and pergolide(491) were all efficacious as symptomatic monotherapy
b. Ropinirole prolonged release(495) was likely efficacious as a symptomatic adjunct therapy
c. Prevention/delay of motor fluctuations, pramipexole(496) and cabergoline(497) were efficacious
d. Prevention/delay of dyskinesia, pramipexole(498), ropinirole(499), ropinirole prolonged release(500), and cabergoline(501) were all efficacious, whereas pergolide(502) was likely efficacious.
e. Duodenal infusion of levodopa(502)(503) was likely efficacious in the treatment of motor complications, but the practice implication is investigational.
f. Rasagiline conclusions were revised to efficacious as a symptomatic adjunct(504), and as treatment for motor fluctuations(505).
g. Bilateral subthalamic nucleus deep brain stimulation(506), bilateral globus pallidus stimulation(507), and unilateral pallidotomy(508) were updated to efficacious for motor complications.
h. Physical therapy(509)was revised to likely efficacious as symptomatic adjunct therapy.

((457) Frontal-subcortical circuitry and behavior by Bonelli RM1, Cummings JL.(PubMed)
(458) Non-motor symptoms of Parkinson's disease: diagnosis and management by Salawu FK1, Danburam A, Olokoba AB.(PubMed)
(459) Early Parkinson's disease and non-motor issues by Chaudhuri KR1, Naidu Y.(PubMed)
(488) Practice Parameter: Treatment of nonmotor symptoms of Parkinson disease
Report of the Quality Standards Subcommittee of the American Academy of Neurology by T. A.Zesiewicz, MD, FAAN, K. L. Sullivan, MSPH, I. Arnulf, MD, K. R. Chaudhuri, MD, J. C.Morgan, MD, PhD, G. S. Gronseth, MD, FAAN, J. Miyasaki, MD, MEd, FAAN, D. J. Iverson, MD, FAAN and W. J. Weiner, MD(Neurology)
(489) The Movement Disorder Society Evidence-Based Medicine Review Update: Treatments for the motor symptoms of Parkinson's disease by Fox SH1, Katzenschlager R, Lim SY, Ravina B, Seppi K, Coelho M, Poewe W, Rascol O, Goetz CG, Sampaio C.(PubMed)
(490) Transdermal administration of piribedil reverses MPTP-induced motor deficits in the common marmoset by Smith LA1, Jackson MG, Bonhomme C, Chezaubernard C, Pearce RK, Jenner P.(PubMed)
(491) Clinical pharmacokinetic and pharmacodynamic properties of drugs used in the treatment of Parkinson's disease by Deleu D1, Northway MG, Hanssens Y.(PubMed)
(492) Role and clinical utility of pramipexole extended release in the treatment of early Parkinson's disease by Hametner EM1, Seppi K, Poewe W.(PubMed)
(493) Pramipexole extended-release: a review of its use in patients with Parkinson's disease by Frampton JE1.(PubMed)
(494) Role of dopamine receptor agonists in the treatment of early Parkinson's disease. by Bonuccelli U1, Del Dotto P, Rascol O.(PubMed).
(495) Long-term, open-label, safety study of once-daily ropinirole extended/prolonged release in early and advanced Parkinson's disease by Makumi CW1, Asgharian A, Ellis J, Shaikh S, Jimenez T, VanMeter S.(PubMed)
(496) Pramipexole and its extended release formulation for Parkinson's disease by Fishman PS1.(PubMed)
(497) [Dopamine agonists in the treatment of motor complications in advanced Parkinson's disease].[Article in Polish] by Sławek J1.(PubMed)
(498) Long-term safety and sustained efficacy of extended-release pramipexole in early and advanced Parkinson's disease by Hauser RA, Schapira AH, Barone P, Mizuno Y, Rascol O, Busse M, Debieuvre C, Fraessdorf M, Poewe W; Pramipexole ER Studies Group.(PubMed)
(499) A five-year study of the incidence of dyskinesia in patients with early Parkinson's disease who were treated with ropinirole or levodopa by Rascol O1, Brooks DJ, Korczyn AD, De Deyn PP, Clarke CE, Lang AE.(PubMed)
(500) Economic evaluation of ropinirole prolonged release for treatment of Parkinson's disease in the Netherlands by van Boven JF1, Novak A, Driessen MT, Boersma C, Boomsma MM, Postma MJ.(PubMed)
(501) Risk of heart failure following treatment with dopamine agonists in Parkinson's disease patients by Perez-Lloret S1, Rey MV, Crispo J, Krewski D, Lapeyre-Mestre M, Montastruc JL, Rascol O.(PubMed)
(502) Interaction of pergolide with central dopaminergic receptors. by Goldstein M, Lieberman A, Lew JY, Asano T, Rosenfeld MR, Makman MH.(PubMed)
(503) Medical management of levodopa-associated motor complications in patients with Parkinson's disease by Jankovic J1, Stacy M.(PubMed)
(504) [Rasagiline in monotherapy in patients with early stages of Parkinson's disease and in combined and adjunct therapy to levodopa with moderate and advanced stages].[Article in Spanish] by Pagonabarraga J1, Rodríguez-Oroz MC.(PubMed)
(505) Rasagiline: a review of its use in the treatment of idiopathic Parkinson's disease. by McCormack PL1.(PubMed)
(506) Subthalamic nucleus deep brain stimulation for Parkinson's disease: evidence for effectiveness and limitations from 12 years' experience. by Movement Disorder Group, Chan AY1, Yeung JH2, Mok VC1, Ip VH1, Wong A1, Kuo SH3, Chan DT4, Zhu XL4, Wong E4, Lau CK4, Wong RK5, Tang V6, Lau C1,Poon WS4.(PubMed)
(507) Deep brain stimulation for the treatment of Parkinson's disease: subthalamic nucleus versus globus pallidus internus by Krause M1, Fogel W, Heck A, Hacke W, Bonsanto M, Trenkwalder C, Tronnier V.(PubMed)
(508) Bilateral pallidotomy for treatment of Parkinson's disease induced corticobulbar syndrome and psychic akinesia avoidable by globus pallidus lesion combined with contralateral stimulation by Merello M1, Starkstein S, Nouzeilles MI, Kuzis G, Leiguarda R.(PubMed)
(509) Maintenance ECT in the treatment of PD. Therapy improves psychotic symptoms, physical function by Shulman RB1.(PubMed)