Would this help us in memory problems post-stroke? A damned simple question, but whom the FUCK will answer that? Your stroke association? Never. In this case it seems cholesterol is good for memory.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=157558&CultureCode=en
A new study, led by scientists at The Scripps Research Institute
(TSRI), the Veterans Affairs San Diego Healthcare System (VA) and
University of California (UC) San Diego School of Medicine shows that
increasing a crucial cholesterol-binding membrane protein in nerve cells
(neurons) within the brain can improve learning and memory in aged
mice.
“This is a novel strategy for treating neurodegenerative diseases,
and it underscores the importance of brain cholesterol,” said Chitra
Mandyam, associate professor at TSRI and co-first author of the study
with Jan M. Schilling of UC San Diego and the VA.
Senior author Brian Head, a research scientist with the VA and
associate professor at UC San Diego, added, “By bringing back this
protein, you’re actually bringing cholesterol back to the cell membrane,
which is very important for forming new synaptic contacts.”
The study, published recently online ahead of print in the journal Biological Psychiatry,
focuses on a specific membrane protein called caveolin-1 (Cav-1) and
expands scientists’ understanding of neuroplasticity, the ability of
neural pathways to grow in response to new stimuli.
Previous work by Head’s group at the VA and at UC San Diego had shown
that raising Cav-1 levels supported healthy “rafts” of cholesterol
involved in neuron growth and cell signaling; however, it wasn’t clear
if this new growth actually improved brain function or memory.
To find out, the researchers delivered Cav-1 directly into a region
of the brain known as the hippocampus in adult and “aged” mice. The
hippocampus is a structure thought to participate in formation of
contextual memories—for example, if one remembers a past picnic when
later visiting a park.
In addition to improved neuron growth, treated mice demonstrated
better retrieval of contextual memories—they froze in place, an
indication of fear, when placed in a location where they’d once received
small electric shocks.
Mandyam and Head believe that this type of gene therapy may be a path
toward treating age-related memory loss. The researchers are now
testing this gene therapy in mouse models of Alzheimer’s disease and
expanding it to possibly treat injuries such as spinal cord injury and
traumatic brain injury. Mandyam said this new understanding of Cav-1 and
neuroplasticity could also be relevant to memory loss due to alcohol
and drug use.
“We’re very interested in studying whether we can manipulate Cav-1 in other areas of the brain,” Mandyam said.
In addition to Mandyam, Schilling and Head, authors of the study,
“Neuron-targeted caveolin-1 improves molecular signaling, plasticity and
behavior dependent on the hippocampus in adult and aged mice,” were
Junji Egawa, Ingrid R. Niesman, Sarah E. Kellerhals, Anna R. Busija,
Edmund Posadas, Grace C. Grogman, Jamie W. Chang, Victoria B. Risbrough,
David M. Roth, Piyush M. Patel and Hemal H. Patel of UC San Diego and
the VA; Weihua Cui of UC San Diego, Capital Medical University and the
VA; and Miranda C. Staples of TSRI.
This study was supported by the Department of Veterans Affairs
(grants BX001225, BX000783 and BX001963) and the National Institutes of
Health (grants NS073653, HL091071, HL107200, GM085179 and DA034140.)
For more information on the paper, see:
http://www.biologicalpsychiatryjournal.com/article/S0006-3223(15)00817-3/abstract
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