L-Deprenyl Therapy Improves Verbal Memory in Amnesic Alzheimer Patients

Finali, Giancarlo; Piccirilli, Massimo; Oliani, C; Piccinin, Gian Luigi

doi:10.1097/00002826-199112000-00005

Cited by 47 publications

(16 citation statements)

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“…Pharmacological studies have demonstrated that MAO inhibitors exert neuroprotective effects in patients with AD (21,52,53) through the following mechanisms: Improvement of cognitive impairment (50,54,55); antioxidant and enhancement of iron chelating activities (56-59); regulation of APP and Aβ expression processing (56,60), involving the activation of certain signaling pathways, including the p42/44 mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) signaling pathways (61); and inhibition of cholinesterase (ChE) activity (62-64).…”

Section: Involvement Of Mao In Neurodegenerationmentioning

confidence: 99%

“…The main neuroprotective mechanisms of MAO inhibitors in AD include the following: i) Improvement of cognitive impairment (50,54,55), where MAO inhibitors correct chemical imbalances in the brain; ii) antioxidant activities and enhancement of iron-chelating activities (56)(57)(58)(59), where chelators can modulate Aβ accumulation, protect against tau hyperphosphorylation and block metal-associated oxidative stress, thereby holding considerable promise as effective anti-AD drugs (145,146); iii) regulation of APP and Aβ expression processing (56,60), for example ladostigil (TV3326), a selective MAO-B inhibitor, which regulates APP translation and processing (114); iv) the selective MAO inhibitors selegiline and rasagiline have been proven to possess neuroprotective activities in cell cultures and animal models of neurodegenerative diseases through the activation of certain signaling pathways, including p42/44 MAPK and PKC (61); v) inhibition of ChE activity by the MAO inhibitor rasagiline (62)(63)(64), with MAO inhibitors also affecting other chemicals throughout the body and acting by correcting chemical imbalances in the brain.…”

Section: Evidence For the Neuroprotective Effect Of Mao Inhibitors In Admentioning

confidence: 99%

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Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

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Abstract. Activated monoamine oxidase (MAO) has a critical role in the pathogenesis of Alzheimer's disease (AD), including the formation of amyloid plaques from amyloid β peptide (Aβ) production and accumulation, formation of neurofibrillary tangles, and cognitive impairment via the destruction of cholinergic neurons and disorder of the cholinergic system. Several studies have indicated that MAO inhibitors improve cognitive deficits and reverse Aβ pathology by modulating proteolytic cleavage of amyloid precursor protein and decreasing Aβ protein fragments. Thus, MAO inhibitors may be considered as promising therapeutic agents for AD.

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Section: Involvement Of Mao In Neurodegenerationmentioning

confidence: 99%

Section: Evidence For the Neuroprotective Effect Of Mao Inhibitors In Admentioning

confidence: 99%

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Cai

2014

Molecular Medicine Reports

180

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“…For example, MAO inhibitors enhance memory and attenuate age, neuropathologically, and experimentally induced amnesia (Roberts et al 1970;Botwinick and Quartermain 1974;Knoll et al 1977;Timar et al 1979;Finali et al 1991;Stoll et al 1994;Yavich et al 1996). Typically, activation of the dopaminergic, noradrenergic, or serotoninergic systems enhances memory, whereas inhibition of these systems produces memory deficits (Decker and McGaugh 1991;McNamara and Skelton 1993;Izquierdo and Medina 1995;Harvey 1996;Buhot 1997;White 1997).…”

Section: Introductionmentioning

confidence: 99%

Task-dependent effects of the antidepressant/antipanic drug phenelzine on memory

1999

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Phenelzine (PLZ) is a non-selective monoamine oxidase (MAO) inhibitor commonly used to treat depression and panic disorder. In addition to increasing levels of biogenic amines in the brain, PLZ elevates brain levels of the amino acid gamma-aminobutyric acid (GABA; Baker et al. 1991; present study). Given the extensive evidence implicating biogenic amines and GABA in mnemonic processes, PLZ may affect learning and memory. To investigate this possibility, male Sprague-Dawley rats were given PLZ sulfate (15 or 30 mg/kg, based on free base weight) 2 h prior to training in a continuous multiple trial inhibitory avoidance (CMIA) and spatial water maze task. Retention was assessed 48 h later. The results indicated that PLZ enhanced CMIA and impaired water maze retention performance. Compared to control rats, rats given PLZ took significantly longer to re-enter the shock compartment and swam longer distances before reaching the escape platform on the retention tests. These effects of PLZ did not appear to be the result of PLZ-induced changes in acquisition or retrieval processes, activity levels, or footshock sensitivity. Combined, these findings indicate that PLZ influences memory in a task-dependent manner. These differential effects of PLZ may be the result of contrasting influences of GABA and biogenic amines on memory.

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“…Regarding the possible effect of drug treatment on cog nitive functions [30], we took into consideration the type and the dosage of the drugs administered to the patients at the second neuropsychological evaluation. The patients were examined in a period when no modifications in the therapy had been made, and any treatment with other psychoactive drugs was discontinued whenever possible.…”

Section: Resultsmentioning

confidence: 99%

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

Piccirilli

D’Alessandro²,

Finali³

et al. 1994

Dement Geriatr Cogn Disord

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In order to evaluate possible progression in the severity of their cognitive impairment, 34 parkinsonians with intellectual impairment were followed longitudinally for 7 years. Each patient was matched for age, sex, severity and duration of illness, and pharmacological treatment, with a parkinsonian patient without cognitive impairment. Results suggest that cognitive deficits are not static but rather there is a progression in the severity. Furthermore, patients suffering from severe dementia are more likely to die during the follow-up period. The prognosis of Parkinson''s disease seems to be changed substantially by the occurrence of dementia. The natural history of parkinsonian dementia does not seem to differ from the history of other forms of dementia with a progressively disabling course leading to a complete loss of autonomy.

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L-Deprenyl Therapy Improves Verbal Memory in Amnesic Alzheimer Patients

Cited by 47 publications

References 0 publications

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

Task-dependent effects of the antidepressant/antipanic drug phenelzine on memory

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

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