Notes from last night’s presentation organised by the Royal Society Te Apārangi on ‘Our mysterious brain: the making and breaking ofmemories’.
The session is presented by Emeritus Distinguished ProfessorCliff Abraham - who worked for many years at the University of Otago.
After a welcome from the Royal Society and ‘housekeeping’,
Professor Abraham is introduced through a background of his long research
career.
Began with an overview of the parts of the brain, its
structure and the function of various parts. Then the microscopic structure of
axons, nodes (90 million ++) and the speed at which it works. Defined learning
as the process by which experiences change the nervous system and hence
behaviour (referred to as memories).
Summarised memory hyper-functionality during early development.
Psychiatric disorders (psychosis, PTSD) and additions also bring about
hyper-functionality. Memory hypo-functionality occurs and exampled by amnesia
and dementia.
Mechanisms of memory storage through neural connections
include dendrites receiving inputs and axons sending outputs. The synapse forms
the connection between axon and the spines from the dendrite through
neurotransmitters (glutamate, dopamine, serotonin, adrenaline, histamine) and
electrical activity. Synapses are work-horses of memory, there are 1015 of them, they are
metabolically active and individually modifiable. Astrocytes are also in the
mix. All densely packed together.
Summarised the ‘making of memory’ through from the early 1900s.
Long term potential (LTP) or depression (LTD) allows for modifiability
(plasticity) of synaptic transmission. If the LTP is blocked, impairment of
spatial memory formation occurs.
Therefore, does altered plasticity contribute to memory
impairments in neurological disorders? Can knowledge drive new cognitive
enhances and disease therapies.
Introduced Alzheimer’s disease and its effect on the human
brain (lost of large amount of brain cells and inclusion of plaques and
tangles). Causes neuroinflammation, synapse dysfunction / loss and nerve cell
loss.
From a research and clinical perspective, understanding the
process helps inform prevention/delay, lead to earlier detection, and towards
more effective treatment.
Prevention involves ‘using it or losing it’. Good diet,
weight control, physical exercise, good quality sleep, and keeping up with mental and social activity. Early
detection of plaques with ‘PET’ scan. Blood tests being developed for early
stage Alzheimer. Shared work at University Otago on ‘microRNA’ that may be a
useful contribution.
Treatment – new drugs increase brain ‘tone’ – about ½ of the
people taking these drugs experience modest improvement in cognition. However,
effective treatment needs to be more effective, long-lasting, non-invasive,
have a brain-wide delivery, cross the blood-brain barrier, have few side effects and be
affordable. Some progress presently on antibodies that remove plaques from the
Alzheimer brain. Presently not widely available, very expensive and only deal
to the plaque, not the tangles.
Stressed the importance of building brain resilience and maintaining
cognitive reserve. Persons with brain resilience hold off dementia for longer. Shared
a new treatment strategy to amplify production of neuroprotective proteins. How
can these specific proteins in the brain be increased. Gene therapy approach
alters cell function at a genetic level to generate a therapeutic outcome. For
instance, to make more of its own neuroprotective proteins eg. sAPPa. Explained
how virus-mediated gene transfer can be used. The gene encoding protein (sAPPa)
is packaged into a virus shell (Trojan horse). This package is administered
(injection – intracranial, intravenous). The gene enters the nerve cell
nucleus, the virus shell dissolves and the protein enter the cell.
Trial of above through intracranial virus injection
increased sAPPa rescued spatial memory in mice with Alzheimer. Also reduced
plaque development in the hippocampus and the cerebral cortex. Future work on a
human-ready virus shell. The hope is to increase neuroprotective proteins in
the brain.
An interesting foray into neurobiology and neuroscience.
No comments:
Post a Comment