{"id":696,"date":"2020-02-17T20:56:27","date_gmt":"2020-02-17T15:26:27","guid":{"rendered":"https:\/\/medicineplexus.com\/?p=696"},"modified":"2020-02-17T20:56:27","modified_gmt":"2020-02-17T15:26:27","slug":"drugs-for-parkinsons-disease","status":"publish","type":"post","link":"https:\/\/medicineplexus.com\/drugs-for-parkinsons-disease\/","title":{"rendered":"Drugs for Parkinson\u2019s Disease"},"content":{"rendered":"\n<p><strong>Parkinson\u2019s Disease<\/strong><\/p>\n\n\n\n<ul><li>First described in modern medicine in &#8220;An Essay on the Shaking Palsy,&#8221; published in 1817 by a London physician named James Parkinson<\/li><li>Parkinson\u2019s Disease is a neurological disease affecting over four million patients worldwide.<\/li><li>While it can affect individuals at any age, it is <strong>most common in the elderly.<\/strong><\/li><li>The average age of <strong>onset is 55 years,<\/strong> although <strong>approximately 10 percent<\/strong> of cases affect those <strong>under age 40.<\/strong><\/li><\/ul>\n\n\n\n<p><strong>Parkinson\u2019s Disease is characterized by the clinical picture of<\/strong><\/p>\n\n\n\n<ul><li><strong><u>Bradykinesia<\/u><\/strong><strong> <\/strong>&#8211; Slowness in Initiation and Execution of Voluntary Movements<\/li><li><strong><u>Rigidity<\/u><\/strong> &#8211; Increase Muscle Tone and Increase Resistance to Movement (Arms and Legs Stiff)<\/li><li><strong><u>Tremor<\/u><\/strong> &#8211; Usually Tremor at Rest, When Person Sits, Arm Shakes, Tremor Stops When Person Attempts to Grab Something<\/li><li><strong><u>Postural Instability<\/u><\/strong> &#8211; abnormal fixation of posture (stoop when standing), equilibrium, and righting reflex<\/li><li><strong><u>Gait Disturbance<\/u><\/strong> &#8211; Shuffling Feet<\/li><\/ul>\n\n\n\n<p>Accompanied Autonomic Deficits Seen Later in Disease Process:<\/p>\n\n\n\n<ul><li>Orthostatic Hypotension,<\/li><li>Dementia<\/li><li>Dystonia<\/li><li>Ophthalmoplegia<\/li><li>Affective Disorders<strong><\/strong><\/li><\/ul>\n\n\n\n<p><strong>Neurological basis of Parkinson\u2019s Disease<\/strong><\/p>\n\n\n\n<ul><li><strong>Loss of Dopaminergic (DA) Cells Located in Basal Ganglia;<\/strong> most symptoms do not appear until <strong>striata DA<\/strong> levels <strong>decline by at least 70-80%.<\/strong>&nbsp;<\/li><li><strong>Imbalance<\/strong><strong> <\/strong>primarily between the <strong>excitatory<\/strong> neurotransmitter <strong>Acetylcholine<\/strong> and i<strong>nhibitory <\/strong>neurotransmitter <strong>Dopamine<\/strong> in the Basal Ganglia<\/li><li>Though the cholinergic system is not primarily affected. its suppression (by anticholinergics) tends to restore balance.<\/li><li>The Dopaminergic Neurons in the Basal Ganglia are mainly affected.<\/li><li>GABA neuron has an inhibitory action on the substantia nigra. From substantia nigra, there is a dopaminergic feed back to striatum which gets lost giving signs and symptoms of Parkinson disease.<\/li><li>Drug-induced reversible parkinsonism due to neuroleptics, metoclopramide (dopaminergic blockers) is now fairly common<\/li><li><strong>Two major strategies for the treatment of Parkinsonism<\/strong> are to increase brain dopaminergic activity or to decrease central cholinergic activity.<\/li><\/ul>\n\n\n\n<p><strong>Anti Parkinson\u2019s Disease Drugs<\/strong><\/p>\n\n\n\n<p><strong>Drugs affecting brain dopaminergic system<\/strong><\/p>\n\n\n\n<p>Dopamine Precursor: Levodopa (l-dopa)<\/p>\n\n\n\n<p>Peripheral decarboxylase inhibitors: Carbidopa, Benserazide<\/p>\n\n\n\n<p>Dopaminergic Agonists: Non ergot derivatives: Ropinirole, Pramipexole, Ergot derivatives: Bromocriptine, Pergolide<\/p>\n\n\n\n<p>MAO- B inhibitors: Selegiline, Rasagiline<\/p>\n\n\n\n<p>Dopamine facilitator: Amantadine<\/p>\n\n\n\n<p>COMT inhibitors: Entacapone, Tolcapone<\/p>\n\n\n\n<p><strong>Drugs affecting brain cholinergic system<\/strong><\/p>\n\n\n\n<p>Central anticholinergics: Trihexyphenidyl (Benzhexol), Procyclidine, Biperiden<\/p>\n\n\n\n<p>Antihistaminics: Orphenadrine, Promethazine<\/p>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"684\" height=\"318\" src=\"https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-278.png?w=684\" alt=\"\" class=\"wp-image-738\" srcset=\"https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-278.png 684w, https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-278-300x139.png 300w\" sizes=\"(max-width: 684px) 100vw, 684px\" \/><\/figure>\n\n\n\n<p><strong><u>Levodopa<\/u><\/strong><\/p>\n\n\n\n<ul><li><strong>Mechanism of Action:<\/strong> <strong>Converted to dopamine by decarboxylation primarily within the presynaptic terminals of dopaminergic neurons in the striatum.<\/strong> The dopamine produced is responsible for the therapeutic effectiveness of the drug in PD; after release, it is either transported back into dopaminergic terminals by the presynaptic uptake mechanism <strong>or metabolized by the actions of MAO and catechol-<em>O<\/em>-methyltransferase (COMT)<\/strong><\/li><li>It is inactive by itself, but is the immediate precursor of the transmitter DA. More than 95% of an oral dose is decarboxylated in the peripheral tissues (mainly gut and liver).<\/li><li>About 1\u20132% of administered levodopa crosses to the brain, is taken up by the surviving dopaminergic neurones, converted to DA which is stored and released as a transmitter.<\/li><li>Concentrations of the drug in plasma usually peak between 0.5 and 2 hours after an oral dose.<\/li><li>The <strong>half-life in plasma is short (1 to 3 hours)<\/strong><\/li><li>The <strong>rate and extent of absorption of levodopa depends on the rate of gastric emptying, the pH of gastric juice, and the length of time the drug is exposed to the degradative enzymes<\/strong> of the gastric and intestinal mucosa<\/li><li><strong>Adverse Effects:<br>At the initiation of therapy:<\/strong><ul><li>Nausea and vomiting \u00e0 DA action on CTZ \u00e0 tolerance gradually develops \u00e0 <strong>Domperidone<\/strong> but not metoclopramide can be used for the treatment of this vomiting <strong>\u00e0<\/strong><strong> because domperidone does not cross blood-brain barrier, but reaches CTZ.<\/strong><\/li><\/ul><ul><li>The peripherally formed DA can cause tachycardia by acting on \u03b2 adrenergic receptors.<\/li><\/ul><ul><li>Postural hypotension<\/li><\/ul><ul><li>Cardiac arrhythmias and angina<\/li><\/ul><ul><li>Alteration of taste sensation<\/li><\/ul><\/li><li><strong>After prolonged therapy:<\/strong><ul><li><strong>Abnormal movements<\/strong> \u00e0 (dyskinesias) Facial tics, grimacing, tongue thrusting, choreoathetoid movements of limbs \u00e0 no tolerance to adverse effects.<\/li><\/ul><ul><li><strong>Behavioral effects<\/strong> \u00e0 mild anxiety, nightmares, etc. to severe depression, mania, hallucinations, mental confusion or frank psychosis.<\/li><\/ul><ul><li><strong>Fluctuation in motor performance <\/strong><strong>\u00e0<\/strong><strong> <\/strong>\u2018End of dose\u2019 deterioration (wearing off) which is initially gradual, develops into rapid \u2018switches\u2019 or \u2018on-off\u2019 effect. With time \u2018all or none\u2019 response develops \u00e0 reflection of progression of the disorder<\/li><\/ul><ul><li>On\/off phenomenon<\/li><\/ul><ul><li>Embarrassingly disproportionate increase in sexual activity has also been noted.<\/li><\/ul><ul><li>Abrupt withdrawal of levodopa may precipitate <strong>neurolept malignant syndrome.<\/strong><\/li><\/ul><\/li><\/ul>\n\n\n\n<p><strong>Interactions<\/strong><\/p>\n\n\n\n<ol type=\"1\"><li><strong>Pyridoxine:<\/strong> Abolishes the therapeutic effect of levodopa (not combined with carbidopa) by enhancing its peripheral decarboxylation so that less of it remains available to cross to the brain.<\/li><li><strong>Antihypertensive drugs:<\/strong> postural hypotension caused by levodopa is accentuated<\/li><\/ol>\n\n\n\n<figure class=\"wp-block-image size-large\"><img loading=\"lazy\" decoding=\"async\" width=\"618\" height=\"220\" src=\"https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-279.png?w=618\" alt=\"\" class=\"wp-image-739\" srcset=\"https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-279.png 618w, https:\/\/medicineplexus.com\/wp-content\/uploads\/2020\/02\/image-279-300x107.png 300w\" sizes=\"(max-width: 618px) 100vw, 618px\" \/><\/figure>\n\n\n\n<p><strong>Dopamine Decarboxylase Inhibitors<\/strong><\/p>\n\n\n\n<ul><li>These are the drugs <strong>that inhibit peripheral metabolism of levodopa<\/strong> by inhibiting enzyme <em>Dopa decarboxylase<\/em><\/li><li><strong>Do not cross blood brain barrier<\/strong><\/li><li>Drugs included in this category are:<ul><li>Carbidopa and Benserazide<\/li><\/ul><\/li><li><strong>Plasma t<sub>1\/2 <\/sub>of levodopa is prolonged and its dose is reduced to 1\/ 4<sup>th<\/sup><\/strong><\/li><li><strong>Systemic conc. of DA is reduced, nausea and vomiting are not prominent<\/strong> \u2013 therapeutic doses of levodopa can be attained quickly<\/li><li><strong>Cardiac complications are minimized<\/strong><\/li><li><strong>On-off effect is minimized<\/strong> since cerebral DA level are more sustained<\/li><li>Pyridoxine reversal of levodopa effect does not occur.<\/li><li>Degree of improvement may be higher<\/li><\/ul>\n\n\n\n<p><strong>Problems not resolved or accentuated are\u2014<\/strong><\/p>\n\n\n\n<p>1. Involuntary movements<\/p>\n\n\n\n<p>2. Behavioural abnormalities<\/p>\n\n\n\n<p>3. Excessive day time sleepiness in some patients.<\/p>\n\n\n\n<p>4. Postural hypotension.<\/p>\n\n\n\n<p><strong>Bromocriptine<\/strong><\/p>\n\n\n\n<ul><li>A <strong>D2 agonist<\/strong><\/li><li>Bromocriptine is absorbed to a variable extent from the gastrointestinal tract;<\/li><li><strong>Peak plasma levels are reached within 1-2 hours<\/strong> after an oral dose<\/li><li>It is excreted in the <strong>bile and feces.<\/strong><\/li><li>The usual daily dose of bromocriptine in the treatment of parkinsonism is between <strong>7.5 and 30 mg, depending on response and tolerance.<\/strong><\/li><li>To minimize adverse effects, the dose is built up slowly over 2 or 3 months from a starting level of 1.25 mg twice daily after meals; the daily dose is then increased by 2.5 mg every 2 weeks depending on the response or the development of adverse reactions.<\/li><\/ul>\n\n\n\n<p><strong>Pergolide<\/strong><\/p>\n\n\n\n<ul><li><strong>Ergot derivative<\/strong><\/li><li>Directly <strong>stimulates both D1 and D2 receptors<\/strong><\/li><li>Has been widely used for parkinsonism<\/li><li>Comparative studies suggest that it is <strong>more effective than bromocriptine in relieving the symptoms and signs of the disease, increasing &#8220;on-time&#8221; among response<\/strong> fluctuators, and permitting the levodopa dose to be reduced.<\/li><li>Because the <strong>use of pergolide has recently been associated with clinical or subclinical valvular heart disease<\/strong> in about one third of patients, one of the newer non-ergot agents is preferred when a dopamine agonist is required.<\/li><\/ul>\n\n\n\n<p><strong>Pramipexole<\/strong><\/p>\n\n\n\n<ul><li>Preferential affinity for the <strong>D3 family<\/strong> of receptors<\/li><li>It <strong>is effective when used as monotherapy for mild parkinsonism<\/strong><\/li><li>It is also <strong>helpful in patients with advanced disease<\/strong>, permitting the dose of levodopa to be reduced and smoothing out response fluctuations<\/li><li>It may ameliorate affective symptoms<\/li><\/ul>\n\n\n\n<p><strong>Ropinirole<\/strong><\/p>\n\n\n\n<ul><li>Nonergoline derivative<\/li><li>Relatively <strong>pure D2 receptor agonist<\/strong> that is <strong>effective as monotherapy in patients with mild disease and as a means of smoothing the response to levodopa in patients with more advanced disease<\/strong> and response fluctuations<\/li><li>longer acting than levodopa, useful in the management of motor fluctuations and reducing frequency of on-off effects<\/li><li>also used for Restless leg syndrome.<\/li><li>It is introduced at 0.25 mg three times daily, and the total daily dose is then increased by 0.75 mg at weekly intervals until the fourth week and by 1.5 mg thereafter. In most instances, a dose of between 2 and 8 mg three times daily is necessary<\/li><\/ul>\n\n\n\n<p><strong>COMT inhibitors: Entacapone, Tolcapone<\/strong><\/p>\n\n\n\n<ul><li>As an<strong> adjuvants<\/strong> to levodopa-carbidopa for advanced PD<\/li><li><strong>Inhibit<\/strong> enzyme <strong><em>Catechol-O-methyl transferase<\/em><\/strong>which is <strong>responsible for degradation of levodopa when peripheral Dopa decarboxylase<\/strong> is inhibited by Carbidopa.<\/li><li>It also <strong>inhibits COMT in brain, thereby increasing t<sub>1\/2 <\/sub>of levodopa.<\/strong><\/li><li><strong>Entacapone has peripheral<\/strong> effect whereas <strong>Tolcapone has peripheral as well as central effect<\/strong><\/li><li><strong>Worsen the adverse effects of levodopa<\/strong> (nausea, vomiting, dyskinesias, etc.)<\/li><li><strong>Not indicated early in the disease<\/strong><\/li><li><strong>Used to smoothen \u2018wearing off\u2019, increase \u2018on\u2019 time and decrease \u2018off\u2019 time<\/strong> in response fluctuators<\/li><li><strong>Tolcapone: Hepatotoxic and rhabdomyolysis<\/strong><\/li><li>Entacapone is not hepatotoxic<\/li><\/ul>\n\n\n\n<p><strong>MAO-B inhibitors: Selegiline, Rasagiline<\/strong><\/p>\n\n\n\n<ul><li><strong>Selective, irreversible MAO-B inhibitor<\/strong><\/li><li><strong>Mild antiparkinsonian activity<\/strong>, decreases motor fluctuations and wearing off effects.<\/li><li>Permits reduction in dose of levodopa.<\/li><li>Clinical benefits are short lived (6 \u2013 26 months)<\/li><li><strong>Postural hypotension, nausea, accentuation of levodopa induced involuntary movements and psychosis<\/strong><\/li><li>Interaction with tricyclic antidepressants and SSRIs.<\/li><\/ul>\n\n\n\n<p><strong>Safinamide \u00e0 <\/strong>new MAO-B inhibitor \u00e0 used with levodopa\/carbidopa in patients of PD experiencing \u2018off\u2019 episodes.<\/p>\n\n\n\n<p><strong>Amantadine<\/strong><\/p>\n\n\n\n<ul><li>An <strong>antiviral agent<\/strong>, found to have anti-parkinsonism properties<\/li><li>It increases synaptic dopamine level by increasing presynaptic release and decreasing its reuptake.<\/li><li>It also possesses anticholinergic and antiglutaminergic (NMDA blocking) activity.<\/li><li>It is indicated for\u00e0 dyskinesia associated with chronic levo-dopa therapy.<\/li><li>The plasma half-life is between <strong>2 and 4 hours<\/strong><\/li><li>Excreted unchanged in the <strong>urine<\/strong><\/li><li>Amantadine is <strong>less potent than levodopa, and its benefits may be short-lived<\/strong>, often disappearing after only a few weeks of treatment. Nevertheless, during that time it may favorably influence the bradykinesia, rigidity, and tremor of parkinsonism<\/li><li><strong>Number of undesirable central nervous system effects:<\/strong> restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion<\/li><li><strong>Livedo reticularis <\/strong>(bluish discolouration) and edema of ankles.<\/li><li>Amantadine should be used with <strong>caution in patients with a history of seizures or heart failure<\/strong><\/li><\/ul>\n\n\n\n<p><strong>Rotigotine transdermal patch <\/strong><strong>\u00e0<\/strong><strong> <\/strong>dopamine agonist \u00e0 discontinued due to crystal formation on the patches.<\/p>\n\n\n\n<p><strong>Apomorphine<\/strong> can be given subcutaneously for temporary relief of off-periods. However, it cause troublesome nausea.<\/p>\n\n\n\n<p><strong>Central Anticholinergics<\/strong><\/p>\n\n\n\n<ul><li>certain H1 antihistaminics have significant central anticholinergic proper<\/li><li>Act by <strong>reducing unbalanced cholinergic activity in striatum<\/strong><\/li><li><strong>Produce 10 \u2013 25 % improvement<\/strong> in clinical features<\/li><li>Sialorrhoea is controlled by their peripheral action.<\/li><li><strong>Tremor is more benefited<\/strong> than rigidity<\/li><li>Overall efficacy is less than levodopa<\/li><li>Used in mild cases OR in patients in whom levodopa is contraindicated<\/li><li>Anticholinergics are the <strong>only drugs effective in drug (phenothiazine) induced parkinsonism<\/strong><\/li><li><strong>Trihexyphenidyl <\/strong>It is the most commonly used drug. 2\u201310 mg\/day.<\/li><\/ul>\n\n\n\n<p><strong>\u2018Drug holiday\u2019 <\/strong>(withdrawal of levodopa for 4\u201321 days) to reestablish striatal sensitivity to DA by increasing dopaminergic receptor population is<strong> no longer practiced.<\/strong><\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><strong>RA in Parkinson drugs<\/strong><\/h2>\n\n\n\n<ol type=\"1\"><li>Need for new drugs:<ol start=\"1\" type=\"a\"><li>Current therapies <strong>do not prevent neuro-degeneration.<\/strong><\/li><li>The <strong>motor and behavioral s\/e<\/strong> of levodopa decrease the QOL of patients.<\/li><\/ol><\/li><\/ol>\n\n\n\n<ol type=\"1\" start=\"2\"><li>Recent advances in current t\/t.<\/li><\/ol>\n\n\n\n<ul><li><strong>Orally disintegrating selegiline:<\/strong><ul><li>Bypasses the FPM. Therefore achieves Tmax faster. Also Cmax is 4 times higher than IR.<\/li><\/ul><ul><li>Lower dose is given (1.25 to 2.5 mg).<\/li><\/ul><ul><li>Also selegiline is metabolized to amphetamine which is a\/w s\/e; this is prevented by ODT.<\/li><\/ul><ul><li>Approved in 2006 as add on to Levodopa in patients who show deterioration in therapeutic response.<\/li><\/ul><\/li><li><strong>Rotigotine transdermal patch:<\/strong> 2,4,6 mg TDP. The primary outcome parameter was the change in baseline score of UPDRS II and III. a\/w application site reaction, somnolesence etc. Approved in 2007 by EMEA for all stages of PD while in 2007 was approved by USFDA for mild PD.<\/li><\/ul>\n\n\n\n<ul><li><strong>Sustained release ropirinole<\/strong>: Advantage is OD dosing a\/c\/t TDS of the IR preparation. Approved in 2008 by USFDA.<\/li><\/ul>\n\n\n\n<ul><li><strong>Safinamide:<\/strong> March 2017 \u00e0 (MAO-B) inhibitor.<ul><li>inhibits the calcium, sodium channels, inhibits glutamate secretion and inhibits the MAO-B reversibly.<\/li><\/ul><ul><li>add on the dopamine agonist in early PD and add on the levodopa in PD with motor dysfunction<\/li><\/ul><\/li><\/ul>\n\n\n\n<ul><li><strong>Duodopa (Levodopa 20 mg\/mL and Carbidopa 5 mg\/mL gel). &nbsp;(Jan 2015)<\/strong><\/li><li>Supplied in 100 mL cassettes. The cassette is attached to an external pump which is connected to a percutaneous endoscopic gastrostomy tube which releases the gel in the proximal jejunum.<\/li><li>Duopa is supplied as a solution for enteral infusion.<\/li><li>Duopa is administered over a 16-hour infusion period. The maximum recommended daily dose of Duopa is 2000 mg of levodopa (i.e., one cassette per day) administered over 16 hours.<\/li><li>Prior to initiating Duopa, convert patients from all forms of levodopa to oral immediate-release carbidopa-levodopa tablets. Titrate total daily dose based on clinical response for the patient.<\/li><li>Improvement in motor fluctuation in 96% and dyskinesia in 95%. But was a\/w technical problems in 63%.<\/li><li>Drawbacks: Surgical intervention necessary, device malfunction can occur. Inconvenient<\/li><li>Alternative to DBS to treat motor fluctuations and dyskinesia.<\/li><\/ul>\n\n\n\n<ul><li><strong>Extended release formulation of Carbidopa\/levodopa<\/strong>. (2015)<\/li><li>Increased time spent in the ON phase a\/c\/t IR formulation.<\/li><\/ul>\n\n\n\n<p><strong>Pimavanserin (April 2016) <\/strong><strong>\u00e0<\/strong><strong> <\/strong>atypical antipsychotic.<\/p>\n\n\n\n<ul><li>specifically indicated for&nbsp;the treatment of hallucinations and delusions associated with Parkinson\u2019s disease.<\/li><li>the effect of pimavanserin could be mediated through a combination of inverse agonist and antagonist activity at serotonin 5-HT2A receptors and to a lesser extent at serotonin 5-HT2C receptors.<\/li><li>s\/e \u00e0 peripheral edema, confusional state<\/li><\/ul>\n\n\n\n<ul><li><strong>New drugs in pipeline<\/strong><\/li><li><strong>A2a antagonists<\/strong>: A2a receptors are co-llocated with D2 receptors in the striatal neurons. Inhibition of these receptors is a\/w decreased activity of the striatopallidal pathway.<\/li><\/ul>\n\n\n\n<ul><li><strong>Istradefylline<\/strong>: redcued the OFF time significantly a\/c\/t placebo.<\/li><li><strong>Preladenan<\/strong>t: Decreased time spent on OFF period when preladenant was added to levodopa. Phase 3 is on-going<\/li><\/ul>\n\n\n\n<p><strong>Neuroprotective agents<\/strong>: Agents that have been tried are: Cogane, Ubiquinone, Ultra-pure creatine, Pioglitazone.<\/p>\n\n\n\n<ul><li>Pioglitazone: Furthest along development. Inhibits the neuro-inflammation involving reactive microglia, activation of genes involved in cellular bioenergertics and inhibition of MAO-B.<\/li><li>Stem cell therapy: Aims at modifying neuronal action to relieve symptoms.<\/li><li>AAV2\/GAD: glutamic acid decarboxylase: increases synthesis of GABA<\/li><li>AAV2\/AADC: aromatic acid decarboxylase: increases synthesis of dopamine<\/li><li>AAV2\/GDNF<\/li><\/ul>\n\n\n\n<ul><li>Drugs for Levodopa induced dyskinesia: Targets. mGluR5 antagonist. Fipamizole: Selective alpha 2 receptor antagonist.<\/li><li>Drugs for Parkinsons dementia: Rivastigmine is approved. Capsule: 2006 and transdermal patch: 2013.<\/li><\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Parkinson\u2019s Disease First described in modern medicine in &#8220;An Essay on the Shaking Palsy,&#8221; published in 1817 by a London physician named James Parkinson Parkinson\u2019s Disease is a neurological disease affecting over four million patients worldwide. While it can affect individuals at any age, it is most common in the elderly. The average age of[&#8230;]\n","protected":false},"author":3,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_seopress_robots_primary_cat":"","_seopress_titles_title":"","_seopress_titles_desc":"","_seopress_robots_index":"","footnotes":""},"categories":[3],"tags":[],"_links":{"self":[{"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/posts\/696"}],"collection":[{"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/users\/3"}],"replies":[{"embeddable":true,"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/comments?post=696"}],"version-history":[{"count":0,"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/posts\/696\/revisions"}],"wp:attachment":[{"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/media?parent=696"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/categories?post=696"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/medicineplexus.com\/wp-json\/wp\/v2\/tags?post=696"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}