To report two cases of eyelash loss in Frontal Fibrosing Alopecia, providing microscopic description of the eyelashes and possible association with Demodex folliculorum. We present two cases of postmenopausal women diagnosed with frontal fibrosing alopecia who consulted the ophthalmology department for eyelid itching and eyelash loss. On examination, there were no signs of blepharitis, but loss of lashes was observed, and the remaining eyelashes detached easily from the eyelid. The eyelashes were examined microscopically. The bulbs were small and narrow, and the caliber of the lashes was irregular, with thinner and thicker areas. The pigment distribution was irregular; there were portions with greater or lesser accumulation. In the second case, clusters of Demodex folliculorum were observed near the eyelash root. This is the first microscopic description of eyelash loss in frontal fibrosing alopecia in the published literature. We describe small, narrow bulbs, irregular caliber of the eyelashes and irregular pigment distribution. In the second case, in which we found Demodex folliculorum infestation, there was eyelash loss even though the disease was not very advanced. We suggest that there might be an association whereby Demodex infestation might accelerate autoimmune inflammation, leading to premature eyelash loss. This is the first microscopic description of eyelash loss in frontal fibrosing alopecia in the published literature. We describe small, narrow bulbs, irregular caliber of the eyelashes and irregular pigment distribution. In the second case, in which we found Demodex folliculorum infestation, there was eyelash loss even though the disease was not very advanced. We suggest that there might be an association whereby Demodex infestation might accelerate autoimmune inflammation, leading to premature eyelash loss. Population ageing poses a challenge for countries in preventing and detecting neurodegenerative disorders. The Montreal Cognitive Assessment (MoCA), a short, simple, valid, and reliable screening test, assesses general cognitive status, and is useful in public health contexts. This study aims to normalise and standardise the MoCA test for the Chilean population. We performed a descriptive, correlational validation study of the MoCA test, using a sample including 526 healthy individuals of both sexes, aged between 18 and 90 years, from the north, centre, and south of Chile. We analysed the effects of age, education level, and sex on MoCA performance. Age and education level had a significant impact on general cognitive performance, as determined by MoCA score. Age, education, and sex account for 1-7% of variance. The mean (standard deviation) score for the total sample was 24.04 (3.22), whereas the normal range originally defined for the instrument is 26-30 points. Older adults with less formal education presented poorer results and lower cognitive performance. We propose a protocol for evaluating results by percentiles and scores for different age ranges, and an individual normalised scalar score. We present normative data for the MoCA test in the Chilean population, and propose cut-off points for different age ranges to discriminate normal cognitive performance from neurocognitive disorders; results are adjusted for education level. This proposal would assist in the use of the test and reduce the rate of false positives. We present normative data for the MoCA test in the Chilean population, and propose cut-off points for different age ranges to discriminate normal cognitive performance from neurocognitive disorders; results are adjusted for education level. This proposal would assist in the use of the test and reduce the rate of false positives.Parkinson's disease is a neurodegenerative disorder that affects more than 7 million people worldwide. Its aetiology is unknown, although the hypothesis of a genetic susceptibility to environmental agents is accepted. These environmental agents include fungi, bacteria, and viruses. Three microorganisms are directly associated with a significantly increased risk of developing Parkinson's disease the fungal genus Malassezia, the bacterium Helicobacter pylori, and the hepatitis C virus. https://www.selleckchem.com/products/AG-490.html If the host is vulnerable due to genetic susceptibility or immune weakness, these microorganisms can access and infect the nervous system, causing chronic neuroinflammation with neurodegeneration. Other microorganisms show an epidemiological association with the disease, including the influenza type A, Japanese encephalitis type B, St Louis, and West Nile viruses. These viruses can affect the nervous system, causing encephalitis, which can result in parkinsonism. This article reviews the role of all these microorganisms in Parkinson's disease. We present an update of the Spanish Society of Neurology's recommendations for prevention of both primary and secondary stroke in patients with dyslipidaemia. We performed a systematic review to evaluate the main aspects of the management of dyslipidaemias in primary and secondary stroke prevention and establish a series of recommendations. In primary prevention, the patient's vascular risk should be determined in order to define target values for low-density lipoprotein cholesterol. In secondary prevention after an atherothrombotic stroke, a target value <55mg/dL is recommended; in non-atherothombotic ischaemic strokes, given the unclear relationship with dyslipidaemia, target value should be established according to the vascular risk group of each patient. In both primary and secondary prevention, statins are the drugs of first choice, and ezetimibe and/or PCSK9 inhibitors may be added in patients not achieving the target value. In primary prevention, the patient's vascular risk should be determined in order to define target values for low-density lipoprotein cholesterol. In secondary prevention after an atherothrombotic stroke, a target value less then 55mg/dL is recommended; in non-atherothombotic ischaemic strokes, given the unclear relationship with dyslipidaemia, target value should be established according to the vascular risk group of each patient. In both primary and secondary prevention, statins are the drugs of first choice, and ezetimibe and/or PCSK9 inhibitors may be added in patients not achieving the target value.