A new clue to Alzheimer’s disease has been found by University of Haifa
They discovered a link between dementia, which is reaching
epidemic proportions due to aging of the world’s population, and the activity
level of a protein called eIF2alpha. The study, recently published in the
journal Neurobiology of Aging, brings hope for eventual new
Prof. Kobi Rosenblum, head of the university’s Sagol
Department of Neurobiology, said that altering the performance of this protein
through drug therapy could constitute a treatment for the incurable, progressive
Alzheimer’s research has mainly focused in recent years on
battling the disease once symptoms have appeared, even though researchers have
known for years that it is present in the brain for many years before symptoms
make their presence known.
In advanced stages of the disease, Rosenblum
explained, small lumps of amyloid protein called plaques are identified forming
in the brain. These plaques, he said, are typical of Alzheimer’s sufferers and
undermine brain functioning.
Much research has been directed at
understanding these plaques and trying to eliminate them or to restrict their
formation and growth.
Research has also involved mostly familial
(genetically transmitted) dementia, which is caused by known mutations. This new
research tried to understand the mechanisms in the development of Alzheimer’s
that are linked to molecular response to the metabolic distress that increases
The study, conducted by research student Yifat Segev in the
Haifa university’s Laboratory for Research of Molecular and Cellular Mechanisms
Underlying Learning and Memory that is headed by Rosenblum, in cooperation with
Prof. Danny Michaelson of Tel Aviv University, sought to identify factors that
could be linked to Alzheimer’s even before the plaques are formed and that are
connected to age, the disease’s primary risk factor.
According to Segev,
this is the first time that a link has been found between the activity of
eIF2alpha and the Apoe4 gene in relation to Alzheimer’s disease. She noted that
modification treatments for the eIF2alpha mechanism are being widely researched
and are developing quickly, and that the more that can be understood about the
connection between this mechanism and Alzheimer’s, the more researchers can find
ways to identify and slow the progress of the disease.
A previous study
coauthored by Canadian researchers and Rosenblum’s lab revealed that cognitive
abilities could be improved by altering the activity of the eIF2alpha protein,
which regulates the creation of proteins in all cells, including nerve cells.
That research gave Alzheimer’s researchers a glimmer of hope: Perhaps it would
be possible to improve cognitive abilities or even prevent cognitive damage in
Alzheimer’s patients at an early stage of the disease by intervening in the
mechanisms that regulate protein generation in nerve cells.
study compared mice that expressed the human Apoe4 gene – known as a central
risk factor for Alzheimer’s – with a group of mice with the parallel Apoe3 gene,
which does not constitute a risk factor for the disease.
Mice in the
former group showed a change in the regulating mechanism for protein generation
involving the eIF2alpha protein that damaged the cognitive abilities of those
mice at a young age. This sort of mechanism change is characteristic of aging,
and so also hints at the tendency of these mice toward premature aging.
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