<> Biology Essay Question <><>?

[jowee3000]

I have an essay to do based on this question but I really dont know where to start......please help!

Aging has a profound effect on cerebral function in human beings. From midlife on there is a continuing loss of neurons form the brain and parts of the spinal cord. Suggest factors that maybe involve in this aging process. (Remember that neurons normally do not divide after very early childhood).

Any information on this would be great!

[Upgrade]

Well, during DNA replication, there is the problem of shorter DNA emerging because DNA polymerase can only add nucleotides to 3' ends of DNA. So when the RNA primer is removed from the end of the daughter strand, only a 5' end is available and as a result, the daughter strand is shorter than the parent strand. To prevent shortening of DNA early in life, telomorase adds telomeres, repeating sequences of DNA, to the ends of the DNA strand so that the information lost during DNA replication is just nonesstial. I believe that the telomorase may not function after a certain age or maybe too many mutations in the DNA eventually cause apoptosis of the neuron.
Also from Wikipedia

Demyelination
Demyelination is the act of demyelinating, or the loss of the myelin sheath insulating the nerves. When myelin degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually withers. This leads to certain neurodegenerative disorders like multiple sclerosis, chronic inflammatory demyelinating polyneuropathy.


Axonal degeneration
Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute axonal degeneration (AAD), which is rapid separation of the proximal and distal ends within 30 minutes of injury. Degeneration follows with swelling of the axolemma, and eventually leads to bead like formation. Granular disintegration of the axonal cytoskeleton and inner organelles occurs after axolemma degradation. Early changes include accumulation of mitochondria in the paranodal regions at the site of injury. Endoplasmic reticulum degrades and mitochondria swell up and eventually disintegrate. The disintegration is dependent on Ubiquitin and Calpain proteases (caused by influx of calcium ion), suggesting that axonal degeneration is an active process. Thus the axon undergoes complete fragmentation. The process takes about roughly 24 hrs in the PNS, and longer in the CNS. The signaling pathways leading to axolemma degeneration are currently unknown.

Additional reasons for aging:
Reproductive-Cell Cycle Theory
The idea that aging is regulated by reproductive hormones that act in an antagonistic pleiotropic manner via cell cycle signaling, promoting growth and development early in life in order to achieve reproduction, but later in life, in a futile attempt to maintain reproduction, become dysregulated and drive senescence (dyosis).

Wear-and-Tear theory
The idea that changes associated with aging are the result of chance damage that accumulates over time.

Somatic Mutation Theory
The biological theory that aging results from damage to the genetic integrity of the body’s cells.

Error Accumulation Theory
The idea that aging results from chance events that gradually damage the genetic code.

Evolutionary Theories
See Theories of aging in Senescence. These have by far the most theoretical and empirical support.

Accumulative-Waste Theory
The biological theory of aging that points to a buildup of cells of waste products that presumably interferes with metabolism.

Autoimmune Theory
The idea that aging results from an increase in autoantibodies that attack the body's tissues. A number of diseases associated with aging, such as atrophic gastritis and Hashimoto's thyroiditis, are probably autoimmune in this way.

Aging-Clock Theory
The theory that aging results from a preprogrammed sequence, as in a clock, built into the operation of the nervous or endocrine system of the body. In rapidly dividing cells the shortening of the telomeres would provide just such a clock.

Cross-Linkage Theory
The idea that aging results from accumulation of cross-linked compounds that interfere with normal cell function.

Free-Radical Theory
The idea that free radicals (unstable and highly reactive organic molecules, also named reactive oxygen species or oxidative stress) create damage that gives rise to symptoms we recognize as aging.

Mitohormesis
It has been known since the 1930s that restricting calories while maintaining adequate amounts of other nutrients prevents aging across a broad range of organism. Recently, Michael Ristow has shown that this delay of aging is due to increased formation of free radicals within the mitochondria causing a secondary induction of increased antioxidant defence capacity.[29]


Hope this helps