This brings up the interesting question; Does this inflammation cause a stroke and then those various percentages of post-stroke survivors getting dementia is just a follow on result of the initial inflammation? We'll never know because we have
NO fucking stroke leadership or strategy.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=160334&CultureCode=en
Roughly twenty years before the first symptoms of Alzheimer’s disease
appear, inflammatory changes in the brain can be seen, according to a
new study from Sweden´s Karolinska Institutet published in the medical
scientific journal
Brain. The findings of the researchers, who
monitored several pathological changes in the brain, suggest that
activation of astrocytes at an early stage can greatly influence the
development of the disease.
Alzheimer’s disease is characterised by the atrophy of brain neurons,
especially those involved in memory, and is our most common dementia
disease. Exactly what causes the cells to die is not known, but many
years before the first symptoms present themselves, pathological changes
occur, such as the deposition of the protein amyloid in the form of
amyloid plaques, the accumulation of tau proteins and inflammatory
changes that eventually degrade the points of contact between neurons.
Exactly when the changes take place along this chain of events remains,
however, an unanswered question.
By studying families of people with known Alzheimer’s mutations and
who therefore run a much higher risk of developing the disease, the
researchers were able to examine changes that appear at a very early
stage of the disease. The study included members of families with four
different known Alzheimer’s mutations and a group of patients with
non-inherited, ‘sporadic’ Alzheimer’s disease. All participants
underwent memory tests and scans using PET (positron emission
tomography), whereby radioactive tracer molecules with a short half-life
are introduced into the brain via injection into the blood. For this
study, the team used the tracer molecules PIB, Deprenyl and FDG to study
the amount of amyloid plaques, inflammatory changes in the form of
astrocyte activation, astrocytes being the most common type of glial
(supporting) cell in the brain. They also studied neuronal function in
the brain by measuring glucose metabolism (FDG). In order to monitor the
changes over time, the PET scans were repeated after three years for
half of the just over fifty participants.
The mutation carriers were found to have amyloid plaque and
inflammatory changes almost twenty years before the estimated debut of
memory problems. The number of astrocytes reached a peak when the
amyloid plaque started to accumulate in the brain, and neuronal
function, as gauged by glucose metabolism, began to decline roughly
seven years before the expected disease symptoms. The individuals from
families with inherited Alzheimer’s who did not carry any mutation
showed no abnormal changes in their brain.
“Inflammatory changes in the form of higher levels of brain
astrocytes are thought to be a very early indicator of disease onset,”
explains principal investigator Professor Agneta Nordberg at the
Department of Neurobiology, Care Sciences and Society, Center for
Alzheimer Research at Karolinska Institutet. “Astrocyte activation peaks
roughly twenty years before the expected symptoms and then goes into
decline, in contrast to the accumulation of amyloid plaques, which
increases constantly over time until clinical symptoms show. The
accumulation of amyloid plaque and the increase in number of astrocytes
therefore display opposing patterns along the timeline.”
These studies demonstrate that the pathological processes that lead
ultimately to Alzheimer’s disease commence many years before symptoms
start to show, and that it should be possible to provide early
prophylactic or disease modifying treatment. According to the
researchers behind the study, the findings indicate that astrocytes can
be a possible target for new drugs.
First author of the study is Elena Rodriguez-Vieitez, PhD, senior
scientist at Karolinska Institutet’s Department of Neurobiology, Care
Sciences and Society. The study was financed by grants from, among
others, the Swedish Research Council, the Swedish Foundation for
Strategic Research (SFF), the Knut and Alice Wallenberg Foundation, the
Stockholm County Council/KI ALF fund, Swedish Brain Power, the Swedish
Brain Fund, and a GE Healthcare unrestricted research grant.
Karolinska Institutet − a medical university: ki.se/english
http://news.cision.com/karolinska-institutet/r/inflammatory-changes-in-the-brain-twenty-years-before-alzheimer-onset,c9903037
