Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synaptic plasticity at corticostraital synapses is proposed to fine tune movment and improve motor skills. We found paired-pulse plasticity at corticostriatal synapses reflected variably expressed short-term facilitation blended with a consistent background of longer-lasting depression. Presynaptic modulation via neuotransmitter receptor activation was ruled out as a mechanism for long-lasting paired-pulse depression by examining the effect of selective receptor antagonists. EPSC amplitude and paired-pulse plasticity, however, was influenced by block of D2 dopamine receptors. Block of glutamate transport with l-transdicarboxylic acid (PDC) reduced EPSCs, possibly through a mechanism of AMPA receptor desensitization. Removal of AMPA receptor desensitization with cyclothiazide reduced the paired-pulse depression at long-duration interstimulus intervals (ISIs), indicating that AMPA receptor desensitization participates in corticostriatal paired-pulse plasticity. The low-affinity glutamate receptor antagonist cis-2,3-piperidine dicarboxylic acid (PDA) increased paired-pulse depression, suggesting that a presynaptic component also exists for long-lasting paired-pulse depression. Low Ca(2+)-high Mg(2+) or BAPTA-AM dramatically reduced the amplitude of corticostriatal EPSCs and both manipulations increased the expression of facilitation and, to a lesser extent, they reduced long-lasting paired-pulse depression. EGTA-AM produced a smaller reduction in EPSC amplitude and it did not alter paired-pulse facilitation, but in contrast to low Ca(2+) and BAPTA-AM, EGTA-AM increased long-lasting paired-pulse depression. These experiments suggest that facilitation and depression are sensitive to vesicle depletion, which is dependent upon changes in peak Ca(2+) (i.e. low Ca(2+)-high Mg(2+) or BAPTA-AM). In addition, the action of EGTA-AM suggests that basal Ca(2+) regulates the recovery from long-lasting paired-pulse depression, possibly thourgh a Ca(2+)-sensitive process of vesicle delivery.
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PMID:Reliable long-lasting depression interacts with variable short-term facilitation to determine corticostriatal paired-pulse plasticity in young rats. 1723 3

The aim of this study is to investigate the changes of the pupil's light reflex (PLR) and mobility in Parkinson's disease (PD) patients with and without cognitive disorder. Twenty two (22) patients (ten males, twelve females, mean age: 72.7+/-7.3 years) with identified PD entered the study. The patients were examined with the Mini Mental State Examination (MMSE), the Wechsler II Memory Scale (WMS II) and the Hamilton Depression Scale (HAM-D17). Eleven (11) patients (five males, six females, mean age: 72.09+/-7.06 years) were free of any cognitive deficits and eleven (11) patients (five males, six females, mean age: 73.36+/-7.55 years) had cognitive disorder according to the aforementioned scales. None of the patients satisfied the DSM-IV-TR criteria for depression or anxiety disorder. The patients underwent a pupillometric study in both eyes with single flash stimuli of 24.6 candelas/m(2) intensity and 20 ms duration. The pupillometric parameters that were studied were: Latency for the onset of Constriction (T1), Baseline Pupil Radius (R1), Minimum Pupil Radius after the pupil reaction to light (R2), Amplitude (AMP, R1-R2), Time for maximum Miosis (T2), Maximum Constriction Velocity (VCmax) and Maximum Constriction Acceleration (ACmax). The pupillometric findings of each group were compared to those of an age and sex matched group of eleven healthy subjects. Furthermore, a comparison between the findings of the two groups was conducted. ACmax and VCmax were significantly lower in patients without (PD) and with coexisting cognitive impairment (PDC) compared to normal subjects (NC) (p<0.001). Patients with cognitive impairment (PDC) had significantly lower levels of ACmax, VCmax and AMP than patients without cognitive deficits (PD). Cognitive impairment in PD, which mainly reflects a central cholinergic deficit, may be a crucial pathogenetic factor for the decrease in the aforementioned pupillometric parameters. VCmax and ACmax can be considered as the most sensitive indicators of this central cholinergic deficiency.
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PMID:Pupillometric findings in patients with Parkinson's disease and cognitive disorder. 1904 1

Presented herein is evidence for criterion, content, and convergent/discriminant validity of the NIMH-Provisional Diagnostic Criteria for depression of Alzheimer's Disease (PDC-dAD) that were formulated to address depression in Alzheimer's disease (AD). Using meta-analytic and systematic review methods, we examined criterion validity evidence in epidemiological and clinical studies comparing the PDC-dAD to Diagnostic and Statistical Manual of Mental Disorders fourth edition (DSM-IV), and International Classification of Disease (ICD 9) depression diagnostic criteria. We estimated prevalence of depression by PDC, DSM, and ICD with an omnibus event rate effect-size. We also examined diagnostic agreement between PDC and DSM. To gauge content validity, we reviewed rates of symptom endorsement for each diagnostic approach. Finally, we examined the PDC's relationship with assessment scales (global cognition, neuropsychiatric, and depression definition) for convergent validity evidence. The aggregate evidence supports the validity of the PDC-dAD. Our findings suggest that depression in AD differs from other depressive disorders including Major Depressive Disorder (MDD) in that dAD is more prevalent, with generally a milder presentation and with unique features not captured by the DSM. Although the PDC are the current standard for diagnosis of depression in AD, we identified the need for their further optimization based on predictive validity evidence.
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PMID:The 2002 NIMH Provisional Diagnostic Criteria for Depression of Alzheimer's Disease (PDC-dAD): Gauging their Validity over a Decade Later. 2845 72

Background: Scarcity of prospective medication non-adherence cost measurements for the Australian population with no directly measured estimates makes determining the burden medication non-adherence places on the Australian health care system difficult. This study aims to indirectly estimate the national cost of medication non-adherence in Australia comparing the cost prior to and following a community pharmacy-led intervention. Methods: Retrospective observational study. A de-identified database of dispensing data from 20,335 patients (n=11,257 on rosuvastatin, n=6,797 on irbesartan and n=2,281 on desvenlafaxine) was analyzed and average adherence rate determined through calculation of PDC. Included patients received a pharmacist-led medication adherence intervention and had twelve months dispensing records; six months before and six months after the intervention. The national cost estimate of medication non-adherence in hypertension, dyslipidemia and depression pre- and post-intervention was determined through utilization of disease prevalence and comorbidity, non-adherence rates and per patient disease-specific adherence-related costs. Results: The total national cost of medication non-adherence across three prevalent conditions, hypertension, dyslipidemia and depression was $10.4 billion equating to $517 per adult. Following enrollment in the pharmacist-led intervention medication non-adherence costs per adult decreased $95 saving the Australian health care system and patients $1.9 billion annually. Conclusion: In the absence of a directly measured national cost of medication non-adherence, this estimate demonstrates that pharmacists are ideally placed to improve patient adherence and reduce financial burden placed on the health care system due to non-adherence. Funding of medication adherence programs should be considered by policy and decision makers to ease the current burden and improve patient health outcomes moving forward.
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PMID:Pharmacist-led medication non-adherence intervention: reducing the economic burden placed on the Australian health care system. 3121 79


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