Retrogenesis (also known as retro-genesis) is a medical term used to describe a scientific hypothesis about the development and progress of Alzheimer's disease(AD), an affliction that features variety of severe symptoms relating to brain function. Human neuro-pathological studies have determined that AD impairs tens of millions of people worldwide, with cognitive abilities suffering in victims as the structure of minute tissues within their brain becomes altered. Giving the patients the best, most effective care has been seen as a difficult issue given the radically negative changes that AD can cause in people's life skills. The retrogenesis hypothesis assumes that white matter atrophy takes place within the human nervous system, changes such as myelin breakdown and axonal damage taking place[1][2].
While research is ongoing and findings are under dispute, multiple studies have remarked that individuals find that the loss of life skills, memory related abilities, and general engagement with intellectual pursuits associated with Alzheimer's disease feature an odd parallel to the personal growth that in infants and children. The atrophy on the one side and development on the other side, as the retrogenesis hypothesis goes, seems to follow the same steps yet in opposite order[1][2].
Historical background
editThe model of Retrogenesis was originally proposed by Braak and Braak in 1991 and then they modified it again in 1997. Since then, others have either added data or criticism to the theory such as Reisberg in 1999 and Bartokis in 2007 and again in 2011[3].
Theory
editThe theory of retrogenesis characterizes the multiple stages of cognitive and functional ability a patient experiencing Alzheimer’s Disease (AD) goes through. As the brain develops during early childhood development, begins with neurulation and ends with myelination. According to retrogenesis, the last neurons to be myelinated during neural development are the first neurons to be affected in AD[4]. Neuronal degradation supposedly occurs through the breakdown of primary white matter through myelin and axonal damage. Small neurons are wrapped with myelin less than larger neurons, making them more susceptible to damage[1].
Mechanisms
editFunctional: The FAST (Functional Assessment Staging) procedure is used by caregivers to observe and measure brain progression of patients[4]. The developmental age (DA) is used as a tool in the FAST procedure to compare Alzheimer’s Disease with normal brain development. The procedure shows a correlation between brain progression and hippocampal volume loss, cell loss, and neurofibrillary changes of deceased Alzheimer’s patients[5]. The mechanism of functional retrogenesis describes the digression of normal human development. This digression happens in the mental processes in a patient with Alzheimer’s Disease (AD).
Cognitive: In patients with AD, cognitive capacity is reversed and follows a similar path as that of functional retrogenesis. The developmental age in AD is about the same for loss of both cognitive and functional capacity[5].
Emotional: Infant and children’s developmental ages often exhibit similar emotional and behavioral changes as individuals with AD[5].
Neurologic and Neuropathologic: Developmental reflexes from infancy have been found to occur during stages of AD. The development of reflexes have been found to be indicators of AD stages. Parts of the brain that are last to develop during childhood are the first to be affected during AD. Axons which were developed last are less myelinated than those that were developed previously. Axons with less myelination are more susceptible to degradation due to AD.
Biomolecular: Neurons responding to degradation seek to generate anew through the activation of molecules important in the development of mitosis. Brain regions that undergo the most activity are most susceptible in mental degradation.
Treatment
editCurrently, there is no cure to Alzheimer’s disease but there are hypothesized procedures to treat it. This is due to similar properties of non-nervous system tissues with the nervous system when it comes to mitogenic properties. Non-nervous system tissues have a neoplastic response to toxinsor stressors. This neoplastic response is also known as a mitogenic response that replenish cells that have died from carcinogens. One way to prevent retrogenesis is to introduce antineoplastic agents to decrease the amount of neurogenesis, neurofibrillary changes, and the possibility of apoptosis to occur[2].
References
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- ^ a b c Laks, J (2015). "Integrating Retrogenesis Theory to Alzheimer's Disease Pathology: Insight from DTI-TBSS Investigation of the White Matter Microstructural Integrity". BioMed Research International. 2015: 1–11. doi:10.1155/2015/291658. PMC 4320890. PMID 25685779.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b c Kenowsky, Sunnie (July 2002). "Evidence and mechanisms of retrogenesis in Alzheimer's and other dementias: Management and treatment import". Sage Journals. 17 (4): 202–12. doi:10.1177/153331750201700411. PMID 12184509.
- ^ Fjell, A.M. (Sep 2014). "Diffusion tensor imaging of white matter degeneration in Alzheimer's disease and mild cognitive impairment". Neuroscience. 276: 206–15. doi:10.1016/j.neuroscience.2014.02.017. PMID 24583036.
- ^ a b Carson, Brenner (2015). Care Giving for Alzheimer's Disease. New York Academy of Sciences.
- ^ a b c Kluger, A. (1999). "Retrogenesis: Clinical, physiologic, and pathologic mechanisms in brain aging, Alzheimer's and other dementing processes". European Archives of Psychiatry and Clinical Neuroscience. 249 Suppl 3: 28–36. PMID 10654097.