“The environmental risk factors of Parkinson’s are relatively understudied, particularly in cities, where the vast majority of patients with Parkinson’s, said by e-mail Dr. Brad A. Racette, School of Medicine at Washington University in St. Louis, Missouri.

Racette’s team analyzed data from 5 million Medicare beneficiaries had not moved from county between 1995 and 2003. They then compared the number of cases of Parkinson industrial emissions of copper, lead and manganese obtained from the Environmental Protection Agency.

By 2003, less than 1 percent of city dwellers had Parkinson’s. In counties with low or no emission of metals, 274, 100,000 residents had the disease, compared with 489 residents in counties with high levels of manganese. The risk remained high after accounting for age, sex and ethnicity, published in the American Journal of Epidemiology. In areas with high levels of copper releases also reported more cases of Parkinson’s, but this increase was so slight that it could be attributed to chance.

The team known whether manganese actually made ​​more people develop Parkinson’s. It is possible that in counties with high emissions of manganese influenced other risk factors.

Parkinsonism is a clinical syndrome that encompasses four aspects cardinal bradicinecia (slowness and lack of movement), muscle rigidity, tremor at rest (usually killed during voluntary movements) and postural balance disorders generated gait disorders and falls to soil.

The most common cause of parkinsonism is idiopathic Parkinson’s disease, first described by James Parkinson in 1816 under the name of “paralysis” agitans or shaking palsy “, who takes its current name.

The pathological hallmark of Parkinson’s disease is loss of pigmented dopaminergic neurons of the pars compacta of the substantia nigra, with the appearance of intracellular inclusions called Lewy bodies. The progressive loss of dopaminergic neurons is a normal aspect of aging, but most people do not lose the ratio of 70 or 80% of dopaminergic neurons is required to produce symptomatic Parkinson’s disease.

Untreated Parkinson’s disease evolves within 5 to 10 years to a rigid akinetic state in which patients do not avail themselves. Death usually occurs from complications of immobility, including aspiration broncho-pneumonia or pulmonary embolism.

We conclude that with the availability of effective pharmacological treatment has radically changed the prognosis.

It is well known that neuroleptics (phenothiazines, butyrophenones) may trigger events and parkinsonian tremor by blocking postsynaptic dopamine receptors in the striatum. The same happens with the depleting dopamine (reserpine, tetrabenazine).

Selective blockers of calcium channels (cinnarizine, flunarizine), masked in various commercial preparations of routine administration can produce similar manifestations full or partial recovery in all patients after discontinuation of medication and within a variable.

Some authors argue that drug-induced parkinsonism may be a latent or subclinical parkinsonism revealed by antidopaminergic medication. It is noteworthy that late buccolingual dyskinesia caused by prolonged use of neuroleptics may be associated with parkinsonian manifestations but hardly reason for misdiagnosis is the presence of stereotyped slow and continuous movements that occur in the lower face (lips , jaw and tongue).

The distal parts of the body and trunk tend to show small movements of flexion and extension, while the proximal muscles are not compromised. When the patient is standing may have repetitive movements of the lower extremities (go hard). The patient often develops secondary akathisia. It is assumed that tardive dyskinesia was given to a hypersensitivity of postsynaptic receptors for dopamine and its increased secretion secondary to blockade of these receptors.

In particular, nerve tracts and neural systems involved in the pathophysiology of the disease: the efferent fibers of the substantia nigra to the anterior horn cells of spinal cord, the substantia nigra receives numerous stimuli of various cortical regions and striatum inhibitory stimuli ; the efferent fibers pass from the front of the substantia nigra to the medial region of the globus pallidus, where stimuli are converted into impulses that are transmitted to the premotor cortex.

These circuits may explain the different symptoms of the disease. The akinesia may be explained by the lack of stimuli that regulate involuntary automatic movements, since the passage through the substantia nigra to the bone is altered. The stiffness is the result of hyperactivity, producing clumsy movements.

“The treatment of Parkinson’s disease is symptomatic. Levodopa combined with peripheral decarboxylase inhibitor is the most effective medicine. These are enzyme inhibitors carbidopa and benzeracida. By not crossing the blood brain barrier preventing thus, the metabolism of levodopa to dopamine outside the central nervous system, allowing a higher concentration of levodopa in the latter, favoring its conversion to dopamine in the striatum (JCFustinoni).

Although the diagnosis of Parkinson’s disease is largely clinical, can take account of hyposmia (may precede up to 20 years to your appearance), positron emission tomography showing decrease of dopamine in the striatum, markers recently biological and electromyography to show subclinical tremor.

An important chapter of this issue is that of drug-induced parkinsonism, which generally refers to the interruption but not always. Drugs that can induce are neuroleptics (phenothiazines, butyrophenones), depleting dopamine (reserpine, tetrabenazine) and calcium channel blockers (cinnarizine, flunarizine).

The clinician, before diagnosing Parkinson’s disease, should take into account the possibility cited in the preceding paragraph as well as a number of neurological disorders that are targets of specialized study.

Fustinoni (in Semiology Nervous System [1997]) says the following signs and symptoms exclude the diagnosis of Parkinson’s disease:

Signs and Symptoms that exclude Parkinson

l buccolingual dyskinesia (parkinsonism drug)

l hyperreflexia not justified by previous stroke (Vascular parkinsonism)

l pseudobulbar syndrome (vascular parkinsonism)

l or intentional tremor predominant attitude (Essential tremor)

l Paralysis of vertical gaze downward or lateral (Progressive supranuclear palsy)

l Early by gait disorders (Hakim-Adams syndrome)

l Early urinary incontinence (Hakim-Adams syndrome)

l marked orthostatic hypotension (Shy-Drager syndrome)

l Cognitive discordant severity or prominence in connection with rigidity, bradykinesia or tremor (DAT)

l oculogyric crisis (parkinsonism drug, posencefalítico)

Inhibition and excitation – dopamine and acetylcholine

In a normal brain, the levels of dopamine and acetylcholine, are in equilibrium and equal in their inhibitory and excitatory roles. When lower levels of dopamine, this balance is broken, because the acetylcholine begins to have an excess of excitatory activity, which causes Parkinson’s disease. Dopamine is found in the pars compacta of the substantia nigra and ignored the reasons why their neurons die and cease to keep the system balanced on the striatum.

Since the caudate nucleus and putamen, there is a path to the black substance secreted by the inhibitory neurotransmitter GABA (gamma aminobutyric acid). In turn, a series of fibers originating in the substantia nigra send axons to the caudate and putamen, secreting an inhibitory neurotransmitter from their terminals, dopamine. This pathway maintains a degree of mutual inhibition of the two areas and the injury causes a series of neurological syndromes, among which is Parkinson’s disease.

The fibers from the cerebral cortex secrete acetylcholine, an excitatory neurotransmitter, in the neostriatum. The causes of abnormal motor activities that make up Parkinson’s disease are related to the loss of the secretion of dopamine by nerve endings in the substantia nigra on the neostriatum (nigrostriatal tract) to the left of suppression.

Thus, neurons that secrete predominantly acetylcholine, excitatory signals broadcast to all basal ganglia, responsible in whole, motor planning and some cognitive functions. It requires a loss of approximately 80% of striatal dopamine to the symptoms.

Histologically, the disease is characterized by the presence of Lewy bodies in the substantia nigra and locus coeruleus, but can also appear in other locations of the extrapyramidal system. These intracytoplasmic inclusions composed of protein, free fatty acids, sphingomyelin, and polysaccharides.

The incidence of Parkinson’s disease, assessment difficult, is variable ranging from 4.5 to 21 cases per 100,000 population per year. It is the most accurate estimate of the disease and the extent of new cases in a period of time. Prevalence is the total number of cases in a population and at the same time.

It can be set in four ways:

1. For the reference of medical centers, as does the Italian National Health System, statistics are borne by general practitioners (found a prevalence of 1.48 to 1.90 patients per 1,000 people)

2. Done in similar fashion but with doctors specializing in neurology (in closed groups of neurological patients the prevalence is, obviously, greater)

3. For the individual test door to door in a given population (the average is higher because they include parkinsonism of various etiologies), and

4. It is based on the amount of anti-parkinsonian drugs consumed by a particular community. The geographic distribution is variable: a range of prevalence of 18 cases per 100,000 people in China to 234 in Montevideo, Uruguay. It is a fact difficult to assess because the low prevalence rate may reflect worsening economic conditions and, consequently given the incidence of Parkinson’s disease in the elderly, short life expectancy.

In Europe, seems to increase towards the north of the continent, along with the United States, report the highest mortality rate (increases above 75 years). In the countries studied deaths from this disease increased between 1920 and 1950. This has been reduced after the introduction of levodopa.

The extrapyramidal motor system is the set of motor pathways that exert a major influence on spinal motor circuits, brain stem, cerebellum and cortex. Has fibers from the motor cortex that connect with the basal ganglia, particularly the caudate and putamen, as well as bulbar nuclei (red nucleus, substantia nigra and reticular formation) or midbrain and terminate in the anterior horn of the spinal cord.

Several hypotheses attribute the disease to genetic factors (genes have been identified as responsible mutants), metabolic (oxidative stress) or environmental (pesticides, aluminum). 10% of patients exhibit genetic predisposition. One out of every thousand people with the disease is less common in blacks and Japanese.

The onset of the disease is insidious and, retrospectively, patients may report having suffered from hyposmia, pain erratic confused as arthritic origin, dysesthesias burning sensations, depression, mental or seborrheic dermatitis, which can not always be taken into account as a prodrome.

The fall in the content of dopamine in the striatum will generate later, the symptoms suffered three out of four patients: resting tremor that typically is unilateral in its infancy (hands have made the movement of currencies .) In almost all cases the upper limbs are involved.

When will this disease progresses to muscle rigidity and bradykinesia (delay in the initiation of an involuntary movement or sudden inhibition during the same), the amimia and bradilalia. When walking there is a lack of arm swing.

Neurovegetative symptoms are also characteristic: seborrhea, excessive salivation, sweating, feeling hot, flushing.

Researchers at Boston University, U.S., in collaboration with scientists from the Rotterdam Study, coordinated by Monique Breteler, the Cardiovascular Health Study, led by Oscar Lopez, AGES-Reykjavik study, coordinated by Lenore Launer, the study in May AD , directed by Steve Younkin, the European Consortium of Alzheimer’s Disease, who leads Philippe Amouyel, the ACE Foundation in Barcelona, coordinated by Merce Boada, and the Consortium for Genetic and Environmental Risk of Alzheimer’s Disease, directed by Julie Williams, have identified two genes that may be risk factors for developing Alzheimer’s disease late onset.

The work, published today in The Journal of the American Medical Association, was carried out by analysis of genome wide association. The researchers have identified two new genes in specific locations in DNA. These genes appear to be independent of those already established by its association with the disease of Alzheimer’s, such as apolipoprotein E (APOE).

The first is located near a gene called BIN1 on chromosome 2, while the second gene is located near several genes as EXOC3L2, BLOC1S3 and mark4 on chromosome 19. “The identification of these new genes points to new biological pathways involved in the development of Alzheimer’s disease. Despite the benefits will probably be within a decade, to examine these pathways could lead to new ways to postpone, and perhaps avoid treat neurodegenerative diseases, “said Sudha Seshadri, a researcher at the Framingham Heart Study.

For its part, Breteler, of University Medical Center Rotterdam, the Netherlands, has warned that “these findings were replicated in an independent population, noting that the locations found not improve the quantification of risk of AD. The value of these is that associations could provide findings on the pathophysiological mechanisms of Alzheimer’s disease. ”

Family history
In an accompanying editorial, Nancy L. Pedersen of the Karolinska Institute in Stockholm (Sweden), says that this multicenter study points out that family history is of great importance, including Alzheimer’s disease late onset. “Today the world population faces an increased prevalence Alzheimer’s disease because life expectancy has risen past 75 years.

Findings like this reinforce the limited utility of individual genetic profiles for Alzheimer’s and lead us to collect information on age, sex, and family history and APOE status. “

To these conclusions did a study at the University of Iowa (USA). “A simple visit or phone call by a relative may have a very positive influence on the happiness of patients, even if quickly forgotten the event. By contrast, negligence in the treatment given in an institution where they are interned could generate sadness, frustration and loneliness but can not remember why, “said Justin Feinstein, the lead author of the research.

Bad Brain

Alzheimer’s disease is a neurodegenerative disorder that is generated by the progressive deterioration and death of brain cells. This evil is strongly associated with age. The first symptoms often include memory loss and confusion, but it gets worse causing personality change, loss of cognitive skills and difficulty recognizing other people.

By 2050 an estimated 100 million people suffer from this disease. Currently there is not a cure, but treatments that aim to relieve symptoms and slow its progression.

Enduring Emotions

The researchers worked with people suffering a deterioration in the hippocampus, a brain region that is essential to transform short-term memory long-term memories. Damage to these neurons produce the type of amnesia that affects people with Alzheimer’s.

Each of the participants looked for 20 minutes, sad or happy scenes of movies, with the aim to generate an emotion in them. Next, the authors tested whether the volunteers could recall what they had seen. According to expectations, none managed to retain many details of the images.

However, all maintained the sensations generated by the movies. “They could retain the emotion. Tended to take more sadness than happiness, but both feelings lasted much longer than the memory of the movie,” said Feinstein.

The specialist noted that in healthy people these feelings eventually dissolve, but it lasted even longer in research volunteers. “We found clear evidence that treating Alzheimer’s patients with respect and dignity is much more than a matter of simple morality,” he said Feinstein.

A new study has been first discovered a molecular link between Parkinson’s disease and defects in nerve cell communication. The work, published in Molecular Cell, provides new insights into the mechanisms underlying Parkinson’s disease, which could lead to new therapeutic strategies.

Mutations in parkin gene are responsible for an inherited form of Parkinson’s disease. Although the function of Parkin protein is not well defined, seems to be involved in the degradation of other proteins.

To understand how the mutated Parkin protein cause Parkinson’s, Dr. Fon and his colleagues sought which are mutations in the gene and, specifically, what is the role of the region that is mutated normally.

The protein binds to a protein called endofilina-A, instrumental in the synapses, specifically in the trafficking of synaptic vesicles. These findings show the molecular link between Parkinson-causing recessive genes and defects in synaptic transmission.