Pick Disease Medication

Updated: Nov 18, 2019
  • Author: Monica Saini, MD, MBBS, MRCP(UK); Chief Editor: Jasvinder Chawla, MD, MBA  more...
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Medication Summary

Unfortunately, no available drugs arrest or reverse Pick disease. Currently, practitioners use a combination of neuroprotective and symptomatic therapies—including the administration of vitamins, antidepressants, cholinergic agents, and/or dopaminergic agents—in patients with the disorder.

Research studies suggest that a number of agents may actively inhibit neurodegeneration in animals, cellular models, or other disorders (see Scott and Barrett for a review [53] ), but none of these drugs are currently standard for use in Pick disease.



Class Summary

These are cofactors that are needed in metabolic reactions and that are essential for normal deoxyribonucleic acid (DNA) synthesis, with some vitamins providing antioxidant effects.

Vitamin E (E-Gem, Gamma-E-Gems, Aqua Gem-E, Aquasol E)

Vitamin E may protect polyunsaturated acid in membranes from attack by free radicals.


Thiamine is an essential coenzyme that combines with adenosine triphosphate (ATP) to form thiamine pyrophosphate.



Class Summary

Although selective serotonin reuptake inhibitors (SSRIs) have been suggested for behavioral symptoms (eg, a craving for sweets, hypersexual behavior) in these patients, [54, 55] exercise care in using these agents in patients with parkinsonism, who may develop adverse effects of akathisia or dyskinesias.

Agents with mixed noradrenergic and serotonergic action may be helpful in treating patients with depression and frontal cognitive disorder.

Mirtazapine (Remeron)

Mirtazapine may be sedating, especially at the lower 15mg dose, and may be useful for patients with agitation or disinhibition and depression.

Venlafaxine (Effexor, Effexor XR)

Venlafaxine may be helpful for abulic patients who also have symptoms of depression or decreased initiative.

Trazodone (Oleptro)

Trazodone is a 5-HT2–receptor antagonist that inhibits the reuptake of 5-HT. It has a negligible affinity for cholinergic, adrenergic, dopaminergic, or histaminic receptors. Trazodone has good hypnotic properties and is effective in reducing agitation in patients with head trauma or dementia. This agent is also useful for sleep disturbances. It is structurally unrelated to tricyclic antidepressants (TCAs), tetracyclics, or monoamine oxidase inhibitors (MAOIs). The cardiac conduction effects of trazodone are qualitatively dissimilar to and quantitatively less pronounced than those of TCAs and so are less toxic in cases of trazodone overdose. [29]


Acetylcholinesterase Inhibitors, Central

Class Summary

Cholinergic therapy may be helpful for patients with aphasia, [56] and preliminary studies indicate that cholinesterase inhibitors may be useful for aphasia in Pick disease, [57] as well as for other dementia-related symptoms in this disorder. [58]

Donepezil (Aricept)

Donepezil is an acetylcholinesterase inhibitor that is used in dementia of the Alzheimer type. Cholinergic stimulation may improve naming [30] and increase neuronal plasticity [33] ; thus, it is reasonable to attempt therapy in patients with primary progressive aphasia. Unfortunately, no clinical studies are available on the effect of donepezil in patients with Pick disease.


Ergot Derivatives

Class Summary

Although these agents may worsen sexual or behavioral disinhibition, they may improve executive function, perseveration, and abulia. [59, 60, 61]

Bromocriptine (Parlodel, Cycloset)

Bromocriptine is a semisynthetic ergot alkaloid derivative. It is a strong dopamine D2-receptor agonist and a partial dopamine D1-receptor agonist. Bromocriptine inhibits prolactin secretion, with no effect on other pituitary hormones. It may be given with food to minimize the possibility of gastrointestinal (GI) irritation.

Approximately 28% of this agent is absorbed from the GI tract and metabolized in liver. Bromocriptine's approximate elimination half-life is 50 hours, with 85% excreted in feces and 3-6% eliminated in urine.

Initiate this drug at a low dosage; slowly increase the dosage to individualize therapy. Assess the dosage titration every 2 weeks. Gradually reduce the dose in 2.5-mg decrements if severe adverse reactions occur.


Antiparkinson Agents, Dopamine Agonists

Class Summary

Although these agents may worsen sexual or behavioral disinhibition, they may improve executive function, perseveration, and abulia.


Amantadine inhibits N-methyl-D-aspartic acid (NMDA) receptor–mediated stimulation of acetylcholine release in rat striatum. It may enhance dopamine release, inhibit dopamine reuptake, stimulate postsynaptic dopamine receptors, or enhance dopamine receptor sensitivity.