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1) There had previously been a long-standing dogma that the adult brain is incapable of

generating new neurons. This view has only recently shifted with findings suggesting
neurogenesis (the process of non-neuronal cells dividing to produce cells that will
differentiate into neurons) can/does occur throughout the lifespan and certainly into
adulthood. It remains difficult to get conclusive evidence of neurogenesis firstly because,
as with any shift in scientific opinion, many people are skeptical. In some cases, valid
findings are ignored. For example, when Joseph Altman used thymidine to uncover
continued neurogenesis in mammals, his findings were largely over-looked. In addition,
conclusive evidence of neurogenesis is hard to achieve with research techniques that are
limited in their demonstrative abilities. For example, there are great limitations to
findings that are based on techniques such as the injection of thymidine in adult animals
and not during embryonic stages. Researchers are restricted in what they can study within
the human species as most techniques are intrusive and require the retention of the brain
after the individual has died. Finally, adult neurogenesis produces a very small proportion
of neurons compared to neurogenesis during the embryonic stages and degradation post-
death can render analyses inconclusive/inaccurate. One method that advanced our
understanding of adult neurogenesis is the use of BrdU, a toxic and mutagenic substance
that has profound consequences on neurogenesis. Specifically, post-mortem examination
of the brains of cancer patients who had received BrdU intravenously, revealed neurons
in the dentate gyrus of the hippocampal which contained the toxic substance.
2) I believe adult neurogenesis is implicated in disease for a few reasons. Firstly, the
findings suggesting inhibition of neurogenesis interferes with memory functions that are
known to rely on the hippocampus, makes me think of its role in diseases of memory
such as Alzheimer’s disease. Alzheimer’s disease is marked by memory impairment and
cognitive decline as well as rapid loss of tissue in the hippocampus. This suggests that
functional adult neurogenesis is vital in the protection against such disease. In addition, it
seems likely to me that adult neurogenesis would be important in the fight against
Huntington’s disease; a disease that causes progressive degeneration of nerve cells in the
brain. Not only would neurogenesis help to protect against such disease, but it also seems
as though it would be important in the treatment to help reduce some of the associated
problems. For example, the cognitive decline typically seen throughout this disease, may
be mitigated by the increased learning capacity associated with continuing neurogenesis.
These ideas are based off my beliefs and prior knowledge, extensive research would need
to be done to understand the implications of neurogenesis in disease.
3) Since starting this course my understanding of neurogenesis has changed significantly. I
was previously under the belief that neurogenesis was the division of neurons to form
other neurons (which I now know is false). In addition, I was unaware of the research
demonstrating that adult neurogenesis occurs and plays a substantial role in continued
progression. This course has also provided me when extensive knowledge of the
distinction between neurogenesis and neuroplasticity, two seemingly linked concepts.

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