Glitch in “Garbage Removal” Ups Dementia Risk

An international team of researchers identified a pathogenic mechanism that is common to several neurodegenerative diseases. The findings suggest that it may be possible to slow the progression of dementia even after the onset of symptoms.

A release from Ludwig Maximillians Universitat München in Germany notes that relentless increase in the incidence of dementia in aging societies poses an enormous challenge to health-care systems. The team of researchers led by Professor Christian Haass and Gernot Kleinberger at the LMU‘s Adolf-Butenandt-Institute and the German Center for Neurodegenerative Diseases (DZNE) has now elucidated the mode of action of a genetic defect that contributes to the development of several different dementia syndromes. The study was published in July 2014 in Science Translational Medicine.

Neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases or frontotemporal dementia display a number of common features. They are all characterized by the appearance in the brains of affected patients of abnormally high levels of insoluble protein deposits, which are associated with massive loss of nerve cells. In order to minimize further damage to nerve cells in the vicinity of such deposits, dead cells and the proteinaceous aggregates released from them must be efficiently degraded and disposed of. This task is performed by specialized phagocytic cells – the so-called microglia – which act as “sanitary inspectors” in the brain to ensure the prompt removal of debris that presents a danger to the health of nearby cells. Microglia are found only in the central nervous system, but functionally they represent a division of the body’s innate immune system.

As Haass and his colleagues now report in the latest issue of the journal Science Translational Medicine, specific mutations in the gene for a protein called TREM2, which regulates the uptake of waste products by microglia, lead to its absence from the cell surface. TREM2 is normally inserted into the plasma membrane of microglial cells such that part of it extends through the membrane as an extracellular domain. This exposed portion of TREM2 is responsible for the recognition of waste products left behind by dead cells. “We believe that the genetic defect disrupts the folding of the protein chain soon during its synthesis in the cell, so that it is degraded before it can reach the surface of the microglia,” says Kleinberger. As a result, the amount of debris that the microglia can cope with is significantly reduced. Consequently, the toxic protein deposits, as well as whole dead cells, cannot be efficiently removed and continue to accumulate in the brain. This is expected to trigger inflammatory reactions that may promote further nerve-cell loss.
The new study thus pinpoints a mechanism that influences the course of several different brain diseases.

“In addition, our findings may perhaps point to ways of slowing the rate of progression of these illnesses even after the manifestation of overt signs of dementia, which has not been possible so far,” says Haass. “That this may indeed be feasible is suggested by the initial results of an experiment in which we were able to stimulate the phagocytic activity of microglia by pharmacological means.”

you may also like

Recipes We

Khela88

Fancywin

Jita Ace

Betjili

https://betvisa1.org/

jeetbuzz লগইন

jeetwin app

baji999

winbuzz

betvisa login

winbuzz

six6s

babu88

marvelbet

krikya

mostplay

4rabet

leonbet

pin up

mostbet

all rummy app

Fastwin

Jitawin

R777

Bhaggo

PBC88

Winbdt

Crickex

Betjee

Glory Casino

Jita Bet

Melbet

Jwin7

Jita Ace

Krikya

Six6s

Betjili

Mostplay

Jeetbuzz

Jeetwin

Mostbet

Baji999

Marvelbet

Betvisa

Mcw

Nagad88

Babu88

Jaya9

babu88 babu88 jeetwin abbabet nagad88 marvelbet melbet mostbet six6s crickex mcw casino baji999 betvisa krikya mostplay crazy time jeetbuzz 79king1 good88 11bet xoso66 nohu78 xin88 nohu90 v9bet fastwin betvisa
jeetbuzz
babu88
babu888
jeetwin
nagad88
jaya9
khela88
mostplay
baji999
abbabet
1xbet 12bet marvel bet 91 club betvisa login baji999 sky247 gugobet lotus365 yolo247 bsport loto188 bsport site 8day xoso66 v9bet rummy deity yono rummy new88 typhu88 jeetbuzz dafabet lotus365 bet88 v9bet đăng nhập thienhabet 188bet link dafabet login betvisa king567 yolo247 login 1xbet login 24betting 91club crickex kubet new88 hi88 jun88 w88 shbet mksports 33win f8bet 123b fb88 vn88 mu88 five88 bk8 w388 gnbet mcw casino thienhabet sodo casino cmd368 bsport eubet sbobet mibet cmd368 Faridabad Satta Satta King 786 Dafabet betvisa yono rummy rummy apk

alo789

https://metalwave.com.mx/app/

https://meisetio.com/wp-includes/js/jquery/ai/index.php?tunnel=alo-789

https://purneauniversity.ac.in/assets/js/mk/?tunnel=baji999

fastwin

fastwin

winzo

winzo

futemax

Kèo nhà cái

bongdadzo

Tỷ số bóng đá

KQBD

Kết quả bóng đá

rummy nabob

hi88

8day

97win

n88

red88

king88

j88

i9bet

good88

nohu78

99ok

bet168

satta king

satta matta matka

Canais Play

ALO789

yono rummy
rummy deity
rummy nabob
rummy wealth
daman games
jeetbuzz
yolo247
baji999
rummy gold
188bet
v9bet
789bet
crickex
1xbet
thienhabet
c54
sky88
33win
79king
kubet
shbet
good88
3king
nohu
lucky88
97win
xoso66
xin88
daga88
yolo247
jeetbuzz
betvisa
jeetwin
baji999
nagad88
babu88
mostplay
babu888
jaya9
khela88
jaya9
khela88
jeetbuzz
betvisa
abbabet
babu88
babu888
jeetwin
nagad88
jaya9
joya 9
khela88
mostplay
marvelbet
baji999

Sponsored From Malaysia

말레이시아에서 후원