https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241555/pdf/ehp0111-001065.pdf

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Incidence of Parkinson’s disease in a large patient cohort with idiopathic smell and taste loss

Abstract

Introduction

Patients with idiopathic smell loss constitute an at-risk population for the development of Parkinson’s disease (PD). The study aimed to follow up a large number of patients with idiopathic smell and/or taste loss to define the incidence of PD in this population and, further, to assess characteristics of both olfactory and gustatory function and their possible association with PD development.

 

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1963 Sep;9:232-6.

PARKINSONISM BEFORE AND SINCE THE EPIDEMIC OF ENCEPHALITIS LETHARGICA.

https://www.ncbi.nlm.nih.gov/pubmed/14049396

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Abstract

BACKGROUND:

Influenza is the most frequent cause of acute upper respiratory tract infections during winter season. Although rare, neurological manifestations are known to occur during influenza infection and approximatively three-quarters of cases are in children. In this study, we aimed to characterize the burden and clinical spectrum of influenza-associated encephalopathy and encephalitis in children admitted at a tertiary pediatric hospital in Italy over two influenza seasons (2017-2019).

METHODS:

We retrospectively analyzed clinical, laboratory, instrumental data and outcome of patients discharged with ICD9-CM 487.0 code.

RESULTS:

Fifteen children (13.1% of those discharged with a diagnosis of influenza infection in the study period), had influenza-associated central nervous system (CNS) manifestations. Eight patients (53.3%) were diagnosed as influenza encephalitis, 7 (46.7%) as influenza encephalopathy. Median age was 27 months. In children under 2 years of age (40% of all cases) altered consciousness was the most frequent neurological manifestation while respiratory symptoms were present at admission in all cases. Younger children also required intensive care support more frequently. Five subjects (33.3%) presented comorbidity. None of the patients had received seasonal influenza vaccination. The median time from onset of respiratory signs to onset of neurological manifestations was 24 h. Cerebrospinal fluid (CSF) analysis was normal in most patients and polymerase chain reaction for influenza virus RNA on CSF, when performed, was negative in all samples. Neuroradiological investigations, performed in 5 children, reported cortical and subcortical white matter signal alterations. Oseltamivir was administered only in 2 cases. Fourteen patients recovered without sequelae, and only a 2-year-old girl had minimal impairment in fine motor skills at discharge.

CONCLUSIONS:

All children presenting acute neurological features during influenza season should be evaluated for influenza-associated CNS complications even if the respiratory involvement is mild. Absence of underlying diseases or other risk factors are not protective factors against CNS influenza-associated complications. The lack of CSF pleocytosis does not exclude CNS involvement. Children under 2 years of age are at higher risk of requiring intensive care support.

Mastrolia MV, Rubino C, Resti M, Trapani S, Galli L: Characteristics and outcome of influenza-associated encephalopathy/encephalitis among children in a tertiary pediatric hospital in Italy, 2017-2019. BMC Infect Dis. 19(1):1012 (2019).

https://www.ncbi.nlm.nih.gov/pubmed/31783806

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Abstract: “Parkinson’s disease is a synucleinopathy that is characterized by motor dysfunction, death of midbrain dopaminergic neurons and accumulation of α-synuclein (α-Syn) aggregates. Evidence suggests that α-Syn aggregation can originate in peripheral tissues and progress to the brain via autonomic fibers. We tested this by inoculating the duodenal wall of mice with α-Syn preformed fibrils. Following inoculation, we observed gastrointestinal deficits and physiological changes to the enteric nervous system. Using the AAV-PHP.S capsid to target the lysosomal enzyme glucocerebrosidase for peripheral gene transfer, we found that α-Syn pathology is reduced due to the increased expression of this protein. Lastly, inoculation of α-Syn fibrils in aged mice, but not younger mice, resulted in progression of α-Syn histopathology to the midbrain and subsequent motor defects. Our results characterize peripheral synucleinopathy in prodromal Parkinson’s disease and explore cellular mechanisms for the gut-to-brain progression of α-Syn pathology.”

Challis C, Horizon A, Sampson TR, Yoo BB, Challis RC, Hamilton AM, Mazmanian SK et al., Gut-seeded α-synuclein fibrils promote gut dysfunction and brain pathology specifically in aged mice. Nature Neuroscience 2020 Feb 17. doi: 10.1038/s41593-020-0589-7. [Epub ahead of print].

https://www.ncbi.nlm.nih.gov/pubmed/32066981

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Editor’s note: Air pollution may be outdoors (cars, traffic, industrial) or indoors (candles and other)……..

Lemprière S: Air pollution linked to multiple sclerosis and stroke. Nature Rev. Neurol. [Epub ahead of print, Feb 7, 2020; doi: 10.1038/s41582-020-0322-x]

https://www.ncbi.nlm.nih.gov/pubmed/32034296

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“Although AI companies market software for recognizing emotions in faces, psychologists debate whether expressions can be read so easily.”

Heaven D: Why faces don’t always tell the truth about feelings. Nature 578 (7796):502-504 (2020).

facial expression 2020 nature commentary

https://www.ncbi.nlm.nih.gov/pubmed/32103200

 

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https://www.ncbi.nlm.nih.gov/pubmed/30838645

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850653/

 

 

 

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Article excerpt:  “Nearly every scientist who has used mice or rats to study depression is familiar with the forced-swim test. The animal is dropped into a tank of water while researchers watch to see how long it tries to stay afloat. In theory, a depressed rodent will give up more quickly than a happy one — an assumption that has guided decades of research on antidepressants and genetic modifications intended to induce depression in lab mice.

But mental-health researchers have become increasingly sceptical in recent years about whether the forced-swim test is a good model for depression in people. It is not clear whether mice stop swimming because they are despondent or because they have learnt that a lab technician will scoop them out of the tank when they stop moving. Factors such as water temperature also seem to affect the results.

“We don’t know what depression looks like in a mouse,” says Eric Nestler, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York City.

Now, the animal-rights group People for the Ethical Treatment of Animals (PETA) is jumping into the fray. The group wants the US National Institute of Mental Health (NIMH) in Bethesda, Maryland, to stop supporting the use of the forced-swim test and similar behavioural assessments by its employees and grant recipients. The tests “create intense fear, anxiety, terror, and depression in small animals” without providing useful data, PETA said in a letter to the agency on 12 July.

The animal-rights group also singled out NIMH director Joshua Gordon for using the forced-swim test in the early 2000s, when he was a researcher at Columbia University in New York City.

“The National Institute of Mental Health has for some time been discouraging the use of certain behavioral assays, including the forced swim and tail suspension test, as models of depression,” Gordon said in a statement to Nature. “While no single animal test can capture the full complexity of a human disorder, these tests in particular are recognized by many scientists as lacking sufficient mechanistic specificity to be of general use in clarifying the neurobiological mechanisms underlying human depression.”

But Gordon said that the tests are still “crucial” for some specific scientific questions, and that the NIMH will continue to fund such studies.

Although scientists insist that behavioural tests that cause stress in animals are necessary for developing human treatments, the PETA campaign dovetails with scientists’ growing concern about the quality of data produced by forced-swim tests, says Hanno Würbel, a behavioural biologist at the University of Bern. “The point is that scientists shouldn’t use these tests anymore,” he says. “In my opinion it’s just bad science.”

Sink or swim

Scientists developed the forced-swim test in the 1970s. One of its earliest applications was studying the efficacy of drugs known as selective serotonin reuptake inhibitors (SSRIs) — a class of antidepressants that includes Prozac (fluoxetine). Mice and rats that received SSRIs swam for longer periods than animals that did not.

The test’s popularity grew in the early 2000s, when scientists began modifying mouse genomes to mimic mutations linked to depression in people. Many of these researchers adopted the forced-swim test as a “quick and dirty” way to assess their ability to induce depression, even though it was not designed for that purpose, says Trevor Robbins, a neuroscientist at the University of Cambridge, UK.

By 2015, mental-health researchers were publishing an average of one paper a day that used the procedure, according to an analysis by researchers at Leiden University in the Netherlands1. Yet the swim test’s track record is mixed. It has accurately predicted whether different SSRIs are effective treatments for depression, but yields inconsistent results when used with other types of antidepressant.

And some aspects of the SSRI results are puzzling. Mice given the drugs show measurable changes in behaviour during swim tests beginning one day after treatment, whereas in people SSRIs often take weeks or months to reduce symptoms of depression.

Due in part to concerns about the forced-swim test’s accuracy, major drug companies such as Roche, Janssen and AbbVie have abandoned the procedure in recent years. ….”

https://www.nature.com/articles/d41586-019-02133-2

https://media.nature.com/original/magazine-assets/d41586-019-02133-2/d41586-019-02133-2.pdf

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