Cognitive impairment therapy

Sacktor N, Nakasujja N, Skolasky R, Robertson K, Wong M, Musisi S, Ronald A, Katabira E (2006) Antiretroviral therapy improves cognitive impairment in HlV-l- individuals in sub-Saharan Africa. Neurology 67(2) 311-314... 

The WHI study found that postmenopausal women 65 years or older taking estrogen plus progestogen therapy had twice the rate of dementia, including Alzheimer s disease. Combined therapy also did not prevent mild cognitive impairment. 

The most commonly used therapies for anxiety and depression are selective serotonin reuptake inhibitors (SSRIs) and the more recently developed serotonin noradrenaline reuptake inhibitors (SNRIs). SSRIs, which constitute 60% of the worldwide antidepressant and antianxiety market, are frequently associated with sexual dysfunction, appetite disturbances and sleep disorders. Because SSRIs and SNRIs increase 5-HT levels in the brain, they can indirectly stimulate all 14 serotonergic receptor subtypes [2,3], some of which are believed to lead to adverse side effects associated with these drugs. Common drugs for short-term relief of GAD are benzodiazepines. These sedating agents are controlled substances with addictive properties and can be lethal when used in combination with alcohol. The use of benzodiazepines is associated with addiction, dependency and cognitive impairment. 

Electroconvulsive therapy is generally given two or three times a week. In adult patients, there is no difference in outcome between the two schedules. Rate of response may be more rapid with thrice-weekly ECT, but this regimen may also be associated with greater cognitive impairment (Shapira et ah, 1998). 

This disease develops when an abnormal prion protein present in the cadaveric material induces a cascade of conformational changes in host protein. Creutzfeldt-Jakob disease in recipients of somatropin differs from the sporadic form, in that it usually presents with cerebellar signs rather than cognitive impairment, and also in the prominence of prion protein amyloid plaques in nervous tissue (18). In a review, 139 cases of Creutzfeldt-Jakob disease were identified worldwide in people treated with cadaveric somatropin before recombinant human growth hormone became available in the mid-1980s (19). The prevalence of this fatal neurodegenerative condition in recipients of somatropin ranges from 0.3% in the USA to 4.4% in France. Creutzfeldt-Jakob disease has been reported to start at 4-30 years after therapy with cadaveric somatropin (18), so that further cases are anticipated and continue to be reported (20). 

Emerging data associate statins with a reduced risk of Alzheimer s disease however, two women had significant cognitive impairment temporally related to statin therapy (18). One took atorvastatin, and the other first took atorvastatin then simvastatin. Cognitive impairment and dementia as potential adverse effects associated with statins has been reviewed (17). 

The cognitive effects of topiramate and valproate as adjunctive therapy to carbamazepine have been compared in 53 patients (637). Topiramate was given in an initial dose of 25 mg and increased weekly by 25 mg/day increments to a minimum of 200 mg/day. Cognition was significantly worsened by topiramate and improved by valproate. Gradual introduction of topiramate reduced the extent of cognitive impairment. 

Cognitive impairment, labeled as moderate to marked dementia was first reported in a large number of patients to occur tenfold more commonly than in controls (Lieberman et al., 1979). Demented PD patients in this study responded less well to levodopa therapy and it was suggested that PD with dementia may represent a different disorder from PD without dementia. We distinguish select cognitive impairments from dementia in PD and discuss neurochemical and molecular mechanisms of cognition in PD. 

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