Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The P-300 has been recently utilized as an objective electrophysiological index of cognitive function in some neurological disease. Hansch et al first described prolonged latency for the P-300 component in Parkinson disease patients and suggested these measures reflects a common, disrupted aspect of cognitive function in this disease. This cognitive disorder may be caused not only from the dysfunction of dopaminergic system but from non-dopaminergic lesions such as norepinephrine ones. On the other hand, L-threo-DOPS, a non-physiological precursor of norepinephrine, has been used for the treatment of some neurological illness such as the freezing phenomenon in Parkinsonism. In the present study we investigate the effect of L-threo-DOPS on cognitive function in Parkinsonism by measuring P-300 component succeedingly. Twenty-four patients, i.e. 19 cases of Parkinson disease (PD), 3 Juvenile Parkinsonism (JP) and 2 cerebrovascular Parkinsonism, are studied. The latencies of P-300 are significantly shortened after treatment of DOPS compared with those of the previous treatment and placebo administration respectively (p less than 0.05, p less than 0.01). The main factors which have influence upon these shortened latencies are analyzed multivariate analysis. The factor analysis and principal component analysis suggest three main factors such as DOPS, age (onset of age), and duration of illness. The patients' groups are divided into three by cluster analysis. The most effective group mainly consists of JP. The least effective one mainly consists of older, long-duration Parkinson disease patients. And there is another group which consists of younger, short-duration PD cases with moderate effect of DOPS. This tendency seems to suggest the different pathological findings between JP and PD. It is postulated that L-threo-DOPS would raise the level of attention and arousal mediated by norepinephrine neuronal system which may improve the cognitive disorder in Parkinsonism.
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PMID:[The effect of L-threo-DOPS on P-300 in parkinsonism]. 211 67

We investigated the influence of age on the occurrence of cognitive disturbances in Parkinson's disease (PD), by evaluating neuropsychological performances in early- and late-onset groups of patients (less than 45 and greater than 65 years, respectively), individually paired for all the variables of parkinsonism and compared with age-matched controls. Cognitive disorders were limited in the early-onset PD group compared with their age-matched controls. Conversely, we found global cognitive changes, including marked frontal lobe dysfunction, in the late-onset group. This specific cognitive impairment in older patients related to a significant interaction between the aging and disease processes. Late onset seemed to compound the subtle cognitive changes associated with the disease for which the early-onset group compensated. This compounding effect of aging may explain, at least partially, the high frequency of dementia in older PD patients.
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PMID:Age-induced cognitive disturbances in Parkinson's disease. 229 80

We report the impaired performance by a group of 27 patients with Parkinson's disease (vs matched controls) on semantic and letter-initial verbal fluency tasks, carried out in both single and alternating category conditions. Individual differences in fluency were significantly correlated with confrontation picture naming scores in the patient group, but not in control subjects. However, the PD patients showed no significant correlation between verbal fluency scores, and rate of reciting days of the week as rapidly as possible. Both controls and patients produced more items when retrieving words from a single category than when alternately retrieving words from two categories. The magnitude of the decrement was nonetheless no greater in the patient than in the control population. This finding shows that "task switching" per se is not impaired in PD. We suggest that the verbal fluency deficit, while it may in part be attributed to motor-speech factors, primarily reflects an underlying cognitive disorder.
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PMID:Retrieval from semantic and letter-initial categories in patients with Parkinson's disease. 273 97

In Parkinson's disease, mental disturbances frequently accompany the typical motor disorder. Subcortical dementia develops in 10 to 20% of patients. Contrary to the dementia of Alzheimer's type, the apraxia-aphasia-amnesia syndrome is uncommon. Depression and specific impairment of speech, visuospatial functions, and memory are present in an important proportion of patients. As a principal feature of cognitive disorder, deficit of executive functions can be characterised by decreased mental flexibility and inability to cope with changing external conditions. Further, psychiatric complications of pharmacological treatment of Parkinson's disease are briefly described. Finally, presumed pathophysiological mechanisms of cognitive dysfunction are characterized involving dopaminergic and non-dopaminergic changes and complex interactions on the subcortico-cortical level.
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PMID:[Mental dysfunction in Parkinson's disease]. 868 66

There has been gradual increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (IPD) and Alzheimer-type dementia. It is an intriguing observation that a premonitory sign of a disorder hitherto regarded as one of movement or cognition may be that of disturbed sense of smell. In this review of aging, IPD, parkinsonian syndromes, tremor, Alzheimer's disease (AD), motor neuron disease (MND), Huntington's chorea (HC) and inherited ataxia, the following observations are made: (1) olfactory senescence starts at about the age of 36 years in both sexes and accelerates with advancing years, involving pleasant odours preferentially; (2) olfactory dysfunction is near-universal, early and often severe in IPD and AD developing before any movement or cognitive disorder; (3) normal smell identification in IPD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease; (4) anosmia in suspected progressive supranuclear palsy and corticobasal degeneration is atypical and should likewise provoke diagnostic review; (5) subjects with hyposmia and one ApoE4 allele have an approximate 5-fold increased risk of later AD; (6) impaired sense of smell may be seen in some patients at 50% risk of parkinsonism, and possibly in patients with unexplained hyposmia; (7) smell testing in HC and MND where abnormality may be found is not likely to be of clinical value, and (8) biopsy of olfactory nasal neurons reveals non-specific changes in IPD and AD and at present will not aid diagnosis.
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PMID:Olfaction in neurodegenerative disorder. 1673 38

Cognitive and affective dysfunctions are frequent but often neglected symptoms in Parkinson's disease (PD). We developed the screening tool Parkinson neuropsychometric dementia assessment (PANDA) with five cognitive tasks and a short depression questionnaire. Healthy subjects and patients without cognitive impairment (PD), mild cognitive disorder (PD-MCD), or dementia (PDD) were examined. The cognition part had a specificity of 91% and a sensitivity of 90% for PDD and 77% for PDD plus PD-MCD patients. The mood questionnaire also had high sensitivity and specificity. We conclude that the PANDA is an economical, easy-to-use and sensitive tool to detect neuropsychological dysfunctions in PD patients in clinical practice.
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PMID:Screening for cognitive deficits in Parkinson's disease with the Parkinson neuropsychometric dementia assessment (PANDA) instrument. 1770 78

In Parkinson disease patients who receive long-term antiparkinsonian medication, their original symptoms of rigidity, tremor and related motor disturbances markedly improve or disappear. However, the condition is still far from satisfactory in terms of maintaining independence in daily life activities even in these patients in whom the drug treatment is for improving motor disturbances. The reason is that they show abnormal behavior characterized by "spending the entire day in an idle state, which is perceived as laziness."This behavior is very annoying for the patient and the family. Despite the excellent effectiveness of drug treatment, this propensity toward idleness in mental and motor functions is not improved. Despite the denial of the depressive state and the absence of obvious cognitive disorder, such patients lack ambition and spend their time idly. However, although their motor function remains subliminal, such patients can carry out motor activities when the situation requires, but usually they do not have the drive to move. If we use the current nosological descriptions, the former is called "bradyphrenia" or psychic akinesia or slowness of thinking and the latter is called "akinesia". Akinesia is composed of two cardinal elements "bradykinesia" and "hypokinesia". Bradykinesia is the evaluation of quality of appeared motor behavior, and hypokinesia is the poverty of movement behavior. These two symptoms differ essentially. Hypokinesia is much more essential and is a cardinal element of akinesia. It indicates that the current drug treatment is ineffective for the improvement of hypokinesia and bradyphrenia. That is, these symptoms are a result of a dysfunction different from that causing residual motor symptoms or a result of other additional dysfunctions developing during the pathophysiological course of the disease. The dopamine (DA) system of the dorsal striatal pathway projecting from the substantia nigra pars compacta (A9) to the dorsal part of the striatum (motor striatum) functions in the control of speed and dexterity of movement. On the other hand, the DA system through the medial forebrain bundle projecting from the ventral tegmental area (VTA-A10) to the nucleus accumbens, ventral striatum (limbic striatum) and the cortex is associated with hypokinesia and bradyphrenia. This association can be confirmed by a long-term follow-up of Parkinson disease patients and experimental animal models lesioned in the ventral DA pathway (mesolimbic and mesocortical pathways).
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PMID:[Mesolimbic and mesocortical pathways in Parkinson disease]. 1788 76

Parkinson's disease (PD) is a neurodegenerative disorder, predominantly characterized by the presence of motor symptoms. However, the non motor manifestations (NMM) are a frequent complaint in the PD patients. There is a lack of information about the risk factors associated with the NMM in these patients. The aim of this study is to evaluate the prevalence of the more common NMM in a population of PD patients and to determine the features associated with its development. We studied 124 ambulatory PD patients. NMM were defined by the presence of neuropsychiatric manifestations, cognitive disorder, autonomic dysfunction or sleep related problems. In a multivariate analysis we found that the years of evolution of the PD and the presence of cognitive dysfunction are the risk factors for the neuropsychiatric and autonomic manifestations, whereas axial impairment is a risk factor for cognitive disorders and dyskinesias is for sleep related problems. In conclusion, this study shows that the features related to the PD progression appear as the main risk factors associated with NMM.
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PMID:Features associated with the development of non-motor manifestations in Parkinson's disease. 1839 8

Allon Therapeutics Inc is developing AL-108, an intranasally administered, eight-amino-acid peptide fragment (known as NAP) of activity-dependent neuroprotective protein, and AL-208, an intravenous formulation of NAP. AL-108 is undergoing phase II trials for cognitive impairment in Alzheimer's disease and schizophrenia. AL-108 is also being investigated as a neuroprotective agent, including for the treatment of Parkinson's disease and ocular disease. AL-208 is undergoing phase II clinical trials for the treatment of cognitive disorder and phase I clinical trials for ocular disease and cognitive deficits associated with coronary artery bypass graft or ischemia.
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PMID:AL-108 and AL-208, formulations of the neuroprotective NAP fragment of activity-dependent neuroprotective protein, for cognitive disorders. 1860 May 85

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


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