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In [update] , there were workers who commuted into the municipality and 1, workers who commuted away. Auch das Lernen einer Fremdsprache kann den Ausbruch einer Alzheimer-Demenz verzögern, zwei- und mehrsprachige Menschen erkranken im Schnitt mehrere Jahre später an Demenz als einsprachige.

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Diabetes und Fettleibigkeit, beide sind Risikofaktoren für Alzheimer: Wer im mittleren Erwachsenenalter stark übergewichtig ist, hat ein doppelt so hohes Risiko, im Alter zu erkranken. Wenn ein Patient eine TypDiabetes entwickelt, werden nicht nur die Körperzellen zunehmend unempfindlich gegen Insulin, auch die Gehirnzellen werden insulinresistent. In klinischen Studien konnte bereits gezeigt werden, dass durch die Gabe eines Medikaments, das die Zellen wieder sensibel für Insulin macht, die kognitive Leistung von einigen Patienten verbessert werden konnte.

Bei Mäusen wurden senile Plaques bereits mit Hilfe von Insulin verringert. Immuntherapien Eine klinische Studie mit dem Impfstoff AN musste abgebrochen werden, nachdem 18 von Probanden schwere Gehirnentzündungen entwickelten. Als die Gehirne verstorbener Studienteilnehmer Jahre später untersucht wurden, fand man, dass die Impfung tatsächlich die meisten senilen Plaques entfernt hatte — doch der Verlust von Nervenzellen und damit die fortschreitende Demenz waren nicht gestoppt worden.

Anscheinend reicht die Entfernung der Plaques alleine nicht aus, um die Krankheit zu bekämpfen. Eine Studie des Pharmakonzerns Pfizer mit Antikörpern scheiterte ebenfalls. Doch jetzt kommen gute Nachrichten aus der Schweiz: Durch solche Medikamente , die das Enzym Acetylcholinesterase hemmen, bleibt der Botenstoff Acetylcholin länger im Gehirn, was die Kommunikation zwischen Nervenzellen leicht verbessert.

Einer dieser Wirkstoffe wird häufig mit einem zweiten Wirkstoff kombiniert , der eine Übererregung des Gehirns durch den Botenstoff Glutamat verhindert, eine weitere Charakteristik der Alzheimerdemenz. Was hat Alzheimer mit Herpes zu tun?

Doch wenn man die gesamte Virusmenge im Gehirn analysiert, fällt auf, dass bei Gesunden nur 24 Prozent in Plaques vorkommen, bei Alzheimer-Patienten jedoch 72 Prozent. Es scheint, als würde es einen Zusammenhang zwischen Virenkonzentration in den Plaques und Alzheimer geben.

Die Behandlung von entsprechenden Zellkulturen mit antiviralen Mitteln war vielversprechend. Es könnte also sein, dass eines Tages solche Mittel als eine Strategie unter mehreren in der Alzheimer-Therapie eingesetzt werden. Nobelpreisträger Harald zur Hausen während einer Diskussion auf der In seiner neuesten Forschung geht er der Frage nach, welche Rolle Rinderviren bei neurodegenerativen Erkrankungen spielen.

Seine These lautet, dass neurodegenerative Erkrankungen durch eine Kombination von Rinderviren, mit denen wir uns alle in der frühen Kindheit durch Milch- und Fleischkonsum anstecken, mit Herpesviren entstehen. Diese starke Vermehrung ruft eine Immunreaktion hervor, die zu einer chronischen Entzündung führt. Sein Team befasst sich vor allem mit Multipler Sklerose, einer chronisch-entzündlichen Krankheit.

Doch er vermutet , dass ähnliche Prozesse auch bei Parkinson oder Alzheimer eine Rolle spielen könnten. Dafür spricht zum Beispiel, dass Rheumapatienten, die mit entzündungshemmenden Medikamenten behandelt werden, ein deutlich verringertes Alzheimer-Risiko haben. Es gibt gewisse Möglichkeiten, dem Ausbruch einer Alzheimer-Demenz vorzubeugen. Bei Alzheimer gibt es jedoch weitergehende Empfehlungen: Auch das Lernen einer Fremdsprache kann den Ausbruch einer Alzheimer-Demenz verzögern, zwei- und mehrsprachige Menschen erkranken im Schnitt mehrere Jahre später an Demenz als einsprachige.

All diese Aktivitäten scheinen die sogenannte kognitive Reserve zu mobilisieren, die in der Lage ist, die Auswirkungen einer frühen Demenz abzufangen. Und dass Prävention hilft, zeigen die Daten einer aktuellen Studie. Es gibt noch viele weitere, interessante Forschungsansätze: Zum Beispiel vermag ein Krebsmedikament , das den programmierten Zelltod stoppt, die senilen Plaques in Mäusehirnen zu verringern und gleichzeitig die kognitive Leistungsfähigkeit dieser Mäuse zu verbessern.

Oder eine Studie von fand überraschenderweise Pilzmaterial in den Gehirnen verstorbener Alzheimer-Patienten. Ist diese tückische Krankheit, die sich so hartnäckig einer einfachen Beschreibung entzieht, am Ende — unter anderem — eine Pilzinfektion? In diesem Artikel konnte also nur ein Bruchteil der aktuellen Forschungsansätze vorgestellt werden — aber wir sind sehr gespannt auf neue, überraschende Ergebnisse: Die Alzheimer-Forschung hat endlich Fahrt aufgenommen.

But numerous attempts to tranform this knowledge into effective therapies have failed: AD is a neurodegenerative disease, meaning that the functioning of the brain deteriotes until the patients cannot take care of themselves anymore, suffer severe memory loss, and finally even basic physical functions break down because the brain cannot send the relevant signals anymore. The brains of Alzheimer patients show typical atrophied areas see graph. In , an estimated number of 46 million people were suffering from dementia worldwide — and this number is expected to triple by due to increasing global life expectancy.

Advancing age is the largest risk factor: In , the costs in the US alone were estimated at over billion Dollars, including non-market costs of care at home. If dementia care were a country, it would be the 17th or 18th largest economy in the world. The plaques start to form when the amyloid precursor protein APP is degraded. Responsible for degradation are two proteins, gamma secretase and beta secretase, yet several drugs targeting gamma secretase were not very effective. Providing adequate care for a dementia patient is time-consuming — and expensive, especially in a nursing-home setting.

Two thirds of all nursing home residents have some sort of dementia. Human-to-human transmission A study from found that in some brains of Creutzfeld-Jakob patients who died young, many microscopic changes typical for AD were found. The researchers further suggest that there might be other human-to-human transmission routes for AD proteins.

Several genes have been identified to contribute to the development of AD, but only one variant of apolipoprotein, called APOE-e4 , has been discovered as a risk factor. So the hunt is on for more common AD risk genes. So for instance when a patient develops type II diabetes, not only the body cells but also the brain cells become increasingly insulin-resistant. In clinical trials, an insulin sensitizer was able to improve cognition in some AD patients. In a mouse model, insulin cleared soluble amyloid beta from the brain.

Ongoing research suggests that intranasal insulin — that increases insulin levels in the brain — might also be a therapeutic strategy against AD. But there are also simple, everyday diagnostic criteria everybody can check, as described in this graph. But a Phase II clinical trial had to be stopped in , because 18 of patients had developed serious brain inflammations.

An antibody treatment by drug giant Pfizer failed in But there is a new, promising antibody treatment developed at the University of Zurich, Switzerland: Involvement of Herpes infection? Studies from Manchester show a striking link between Herpes simplex type 1 viral DNA and plaques in the brain: The subsequent use of antivirals in cell cultures produced promising results.

So AD might one day be treated with antivirals, among other strategies. This picture was taken at the 65th Lindau Nobel Laureate Meeting in He assumes that neurodegenerative diseases develop as a combination of an early infection with bovine viruses through milk and meat consumption with a Herpes infection. In case of MS, he suggests vaccinating cattle against the most common viruses, thus eliminating the early infection of humans. And what about AD as a chronic inflammation? Already twenty years ago, it was found that patients with rheumatism who take strong anti-inflammatory drugs have a significantly lower AD risk.

Admittedly, many suggestions sound like something every GP says about times each day: And there are many other hypotheses, for instance a cancer drug that reduced amyloid plaques and improved cognitive performance in mice. Currently, about 90 drugs are being tested against AD in clinical trials in the US alone, and as of , there were open clinical trials under way.

Finally, things seem to be moving forward in AD research. From the same survey, housing and buildings made up 4. A total of Of the agricultural land, All the water in the municipality is flowing water. Lützelflüh lies in the lower Emmental , right on the Emme between Langnau and Burgdorf. The Emme divides the village into the older part on the right shore and the younger part on the left shore.

The exclaves Lauterbach and Oberried also belong to the municipality. It consists of the villages of Lützelflüh, Ramsei and Grünenmatt, parts of the villages of Trachselwald, Goldbach and Ranflüh and the hamlets of Waldhus and Flüele and the exclaves of Oberried and Lauterbach. On 31 December Amtsbezirk Trachselwald, the municipality's former district, was dissolved. On the following day, 1 January , it joined the newly created Verwaltungskreis Emmental.

The blazon of the municipal coat of arms is Gules a Bend wavy Argent and in a Chief of the first six Fir Trees Vert issuant from as many Mounts of the second. Lützelflüh has a population as of December [update] of 4, Between the last 2 years the population changed at a rate of Migration accounted for Most of the population as of [update] speaks German 3, or There are 14 people who speak French and 2 people who speak Romansh.

As of [update] , the population was The population was made up of 1, Swiss men There were 1, Swiss women There were 1, or As of [update] , children and teenagers 0—19 years old make up As of [update] , there were 1, people who were single and never married in the municipality.

There were 1, married individuals, widows or widowers and individuals who are divorced. As of [update] , there were households that consist of only one person and households with five or more people.

In , single family homes made up The historical population is given in the following chart: As of [update] , there were a total of 1, people employed in the municipality. Of these, there were people employed in the primary economic sector and about businesses involved in this sector.

The secondary sector employs people and there were 56 businesses in this sector. The tertiary sector employs people, with businesses in this sector. In [update] there were a total of 1, full-time equivalent jobs.

The number of jobs in the primary sector was , of which were in agriculture and 3 were in forestry or lumber production. The number of jobs in the secondary sector was of which or The number of jobs in the tertiary sector was In the tertiary sector; or In [update] , there were workers who commuted into the municipality and 1, workers who commuted away. The municipality is a net exporter of workers, with about 2. A total of workers In the average church, local and cantonal tax rate on a married resident, with two children, of Lützelflüh making , CHF was For comparison, the median rate for all municipalities in the entire canton was In there were a total of 1, tax payers in the municipality.

Of that total, made over 75, CHF per year. There were 10 people who made between 15, and 20, per year. In a total of 4. The former mill at Mühlegasse 29 now known as the Kulturmühle and used for concerts and events and the rectory at Rainbergliweg 2 are listed as Swiss heritage site of national significance.

In the federal election, a total of 1, votes were cast, and the voter turnout was From the census [update] , 3, or Of the rest of the population, there were 12 members of an Orthodox church or about 0. There were 42 or about 1. There were 4 individuals who were Buddhist , 50 individuals who were Hindu and 2 individuals who belonged to another church.

In Lützelflüh about The Canton of Bern school system provides one year of non-obligatory Kindergarten , followed by six years of Primary school. This is followed by three years of obligatory lower Secondary school where the students are separated according to ability and aptitude.