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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 a variety of severe symptoms relating to brain function. Historically, AD has been linked to gray matter atrophy, but recently the theory of retrogenesis suggests that AD could be due to white matter atrophy, as well[1]. Human neuropathological 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[1]. Retrogenesis breaks down AD into specific mechanisms that characterize signs of cognitive and functional degeneration[2]. 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[3]. The retrogenesis hypothesis assumes that white matter atrophy takes place within the human nervous system with changes, such as myelin breakdown and axonal damage taking place[4] [5].
Research is ongoing and some studies have remarked that there is an odd parallel to personal growth in infants and children with individuals who have experienced the loss of life skills, memory related abilities, and general engagement with intellectual pursuits associated with Alzheimer's disease[5]. 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 for AD patients[5].
Historical background edit
The theory of retrogenesis is a new theory, with research being actively done to find more information. Barry Reisberg originally proposed the model of retrogenesis in the 1980s[2]. Reisberg developed the caregiving assessment tool known as "FAST" (Functional Assessment Staging Tool) in 1988 which he says allows those caring for AD patients to evaluate the stage of progress and symptoms throughout the disease[2].
Theory edit
The 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 embryonic development, growth 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[3]. Neurodegeneration supposedly occurs through the breakdown of primary white matter through myelin and axonal damage[4]. Small neurons are wrapped with less myelin compared to larger neurons, making them more susceptible to damage[4]. As an infant proceeds through normal development, basic acquired abilities are obtained as the developmental age increases, culminating in advanced abilities [2]. In AD patients, the developmental age decreases with advancement through the disease. In those experiencing AD, advanced abilities are lost, culminating in basic abilities as the developmental age decreases[2].
Degenerative Mechanisms edit
These degenerative mechanisms are subsets of the different areas of the body that the theory of retrogenesis addresses.
Functional Mechanism edit
The FAST (Functional Assessment Staging Tool) procedure is used by caregivers to observe and measure brain progression of patients. 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. 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)[5].
Cognitive Mechanism edit
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 Mechanism edit
Infant and children's developmental ages often exhibit similar emotional and behavioral changes as individuals with AD. During infancy, children progress through development by crying, smiling, and beginning to speak a few words. Retrogenesis explains how severe AD patients, who have lost most advanced functions, are still able to retain these infant emotions[5].
Neurologic and Neuropathologic Mechanism edit
Developmental reflexes from infancy have been found to occur during stages of AD. The development of reflexes has 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 by 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[5].
Biomolecular edit
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 to mental degradation[5].
Hypothesized Care Postulate of Alzheimer's Disease edit
Currently, there is no cure for Alzheimer's disease but there are hypothesized procedures to prolong the symptoms that occur at a molecular level. Non-nervous system tissues have a mitogenic response to toxins or [stressor]s that are similar to properties of those within the nervous system. This process is called a neoplastic response which allows the replacement of cells that have died from carcinogens. One way to delay AD is to introduce antineoplastic agents to decrease the amount of neurogenesis, neurofibrillary changes, and the possibility of apoptosis to occur [5].
See also edit
References edit
[[Category:Alzheimer's disease]] [[Category:Cognitive neuroscience]] [[Category:Medical terminology]] Emnett1031 (talk) 01:21, 28 April 2016 (UTC)
- ^ a b Fjell, AM (September 2014). "Diffusion tensor imaging of white matter degeneration in Alzheimer's disease and mild cognitive impairment". Neuroscience. 276: 206-215. doi:10.1016/j.neuroscience.2014.02.017. PMID 24583036.
- ^ a b c d e Kluger, A (1999). "Retrogenesis: clinical, physiologic, and pathologic mechanisms in brain aging, Alzheimer's and other dementing processes". European Archives Psychiatry and Clinical Neuroscience. 249 (3): 28–36. PMID 10654097. Retrieved February 2016.
{{cite journal}}: Check date values in:|accessdate=(help) - ^ a b Brenner Carson, Verna (2015). Caregiving for Alzheimer's Disease. New York: Springer New York Academy of Sciences. pp. 1–9. ISBN 978-1-4939-2406-6.
{{cite book}}:|access-date=requires|url=(help); Check date values in:|accessdate=(help) - ^ 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: 11. doi:10.1155/2015/291658. PMID 25685779.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b c d e f g h i Kenowsky, Sunnie (August 2002). "Evidence and mechanisms of retrogenesis in Alzheimer's and other dementias: management and treatment import". American Journal of Alzheimer's Disease and Other Dementias. 17 (4): 202–212. doi:10.1177/153331750201700411. PMID 12184509.