Drug Treatment of Alzheimer's Disease

Cooper, James

doi:10.1001/archinte.1991.00400020021006

Cited by 24 publications

(3 citation statements)

References 59 publications

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“…44,45 Studies suggest that strategies to revaluate drug treatment and reduce PIM use during hospitalization of patients should be undertaken by physicians and pharmacists in a collaborative manner. 46,47…”

Section: Discussionmentioning

confidence: 99%

Potentially Inappropriate Prescribing in Older Patients Discharged From Acute Care Hospitals to Residential Aged Care Facilities

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Potentially Inappropriate Prescribing in Older Patients Discharged From Acute Care Hospitals to Residential Aged Care Facilities

et al. 2014

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“…Because of the multifactorial cerebral disturbances associated with this disease, authors such as Cooper (1991) and Davis (1991) have suggested that a combination therapy should be used. The progress of SDAT is associated with the degeneration of neuronal systems.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of the Peptidergic Nootropic Drug Cerebrolysin in Patients with Senile Dementia of the Alzheimer Type (SDAT)

Rüther

Ritter²,

Apecechea³

et al. 1994

Pharmacopsychiatry

104

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Cerebrolysin is a peptidergic nootropic drug with a multimodal mechanism of action. It is expected to have a positive influence on neurodegenerative diseases such as senile dementia of the Alzheimer type (SDAT). Experimental studies have shown Cerebrolysin to have a regulatory effect on energy metabolism, a positive influence on behavior through neuromodulation due to its peptide fraction, and most important, a neurotrophic stimulation. In SDAT and related disorders the neurotrophic effect of the drug could play a major role and influence the progress of the illness. A placebo-controlled double-blind trial was designed to examine the efficacy of the drug in SDAT. Confirmatory statistics were used for analysis. 120 subjects with mild to moderate dementia according to the Global Deterioration Scale (GDS) were included in the trial. Their performance on the Mini Mental State Examination (MMSE) was between 15 and 25. The diagnosis was substantiated by the Hachinski Ischemic Score and cranial computed tomography. The inclusion and exclusion criteria were formulated so as to prevent a distortion between the two arms by secondary dementia or other disease. The two arms received either placebo or the drug once a day (30 ml Cerebrolysin in 100 ml physiological saline i.v.) from Monday to Friday for four weeks. Physiological saline (130 ml) was used as placebo. Primary variables used for the statistical analysis were the Clinical Global Impression (CGI), which measures the improvement in symptoms, the SCAG score, and the performance in the trial-making test (ZVT-G). The self-assessment in the Bf-S and the activities of daily living in the NAI were used as secondary variables.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…And it has several other characteristics, which are independent of its action on MAO-B, include antioxidant action, induction of scavenger enzyme activity, and this may partially explain the described neuroprotection of L-deprenyl [19] [20] [21] [22]. L-Deprenyl is known to reduce the neurodegeneration in nigrostriatal dopamine system after chronic administration and recover the neurological symptoms of Alzheimer's disease [23] [24]. In addition, L-deprenyl showed anticonvulsive effect against various seizure models in mice [25].…”

Section: Introductionmentioning

confidence: 99%

Effect of L-Deprenyl on the Putrescine Level and Neuronal Damage after Transient Global Cerebral Ischemia in Gerbils

Lee¹,

Chu²,

Shon³

et al. 2017

IJOC

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L-Deprenyl is selective and irreversible monoamine oxidase B inhibitor, known to have neuroprotective properties. Putrescine, one of polyamine, is thought to be important in the neuronal cell damage associated with various type of excitatory neurotoxicity. We examined the effects of L-deprenyl on the changes in putrescine level and neuronal damage after transient global ischemia in gerbils. Male Mongolian gerbils weighing 65-75 g were used in the experiment. Global ischemia was induced by occlusion of common carotid arteries for 3 min to observe neuronal injury in hippocampal pyramidal cells. L-Deprenyl group was given 10 mg/kg of L-deprenyl intraperitoneally immediately after, 3 h and 6 h after global ischemia. Treated animals were processed in parallel with ischemic animals receiving saline as a vehicle and with shamoperated controls. Hippocampal putrescine level was increased by global ischemia and inhibited by L-deprenyl treatment. In histological findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 3 days after ischemic insult. The number of viable neurons in the pyramidal cell layer of CA1 area was significantly increased in animals treated with L-deprenyl compared to vehicle-treated ischemic animals (p < 0.05). In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was also a significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and L-deprenyl-treated animals (p < 0.05). These data show L-deprenyl is effective as a prophylactic treatment for neuronal injury

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Drug Treatment of Alzheimer's Disease

Cited by 24 publications

References 59 publications

Potentially Inappropriate Prescribing in Older Patients Discharged From Acute Care Hospitals to Residential Aged Care Facilities

Potentially Inappropriate Prescribing in Older Patients Discharged From Acute Care Hospitals to Residential Aged Care Facilities

Efficacy of the Peptidergic Nootropic Drug Cerebrolysin in Patients with Senile Dementia of the Alzheimer Type (SDAT)

Effect of L-Deprenyl on the Putrescine Level and Neuronal Damage after Transient Global Cerebral Ischemia in Gerbils

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