Ageing and Disease: Alzheimer’s

Published by Blogger Emstar on

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Introduction to Alzheimer’s Research


I recently attended a lecture regarding an ANTI-AGEING PLAN that help retain youthfulness in middle-aged adults. As a big enthusiast of cutting-edge science, I found the lecture on ageing and processes highly interesting and very useful. The central nervous system (CNS) is generally overlooked as more superficial aspects of our body, such as skin, which are always apparent because we can see them in the mirror. So, I starting looking within myself to find out what’s important to me. I was already aware of the basic principles of how ageing occurs. However I found it helpful to learn from the lecture presentation, which explains that ageing occurs as a result of changes in cell function, cell turnover and cell death all of which contribute to deteriorating brain tissue, which was discussed in my article about Alzheimer’s – linking the condition to gum disease. I was unaware of the Disposable Soma Theory proposed by Kirkwood and Holliday in 1979, which suggests that the body must compromise the amount of energy which is available to it. It suggests that food energy is required for metabolism, reproduction and repair mechanisms. Therefore due to limited supply of food, a compromise in the energy distributed to repair mechanisms must take place which can cause to the body to deteriorate with age. We learn that according to the Darwinian Evolution theory, maximum fitness occurs at a lower energy expenditure, than is required for continual survival of the species.
The lecture also refers to Alzheimer’s disease which is a chronic neurodegenerative disease, which starts off slowly, with primary symptoms such as short-term memory problems and worsen over time with symptoms such as problems with language, mood swings, disorientation, etc. We learn that it has been discovered that amyloid plaques and neurofibrillary tangles occur much more at a much higher rate in Alzheimer patients compared to normal ageing population.
I was also fascinated to learn that there has been a link between herpes simplex virus-1 and Alzheimer’s people whom are carriers of the apolipoprotein E4 (ApoE4). During histological examination of samples from patients with Alzheimer’s disease, DNA from HSV-1 is attached to amyloid plaques. Overall this lecture helped me comprehend and further my knowledge of the processes of ageing and disease.

Question: How does ageing occur in the central nervous system?

Ageing results to changes in cognition, vasculature, in addition to brain size. It has been shown by MRI scans that the brain shrinks with increasing age. Changes from ageing are observed ranging from the molecular to the morphologic appearances. A greater incidence of dementia, stroke as well as white matter lesions are observed with an increasing age. Furthermore memory impairment, as well as changes in hormone and neurotransmitters occur with ageing. It has been implicated that a reduction in dopamine as well as serotonin is observed with increased ageing. Studies have revealed that dopamine levels decrease by approximately 10% per decade in adult brains and it has been implicated with a decline in motor performance and cognition. Declining levels of serotonin on the other hand has been implicated in the deregulation of synaptic plasticity as well as neurogenesis in an ageing brain. Protective factors which may help slow down the effects of ageing include regular exercise, a healthy diet as well as education and occupational attainment. However further research is essential to discover the complex mechanisms of ageing and help with age associated diseases, particularly dementia.

Articles
• Metabolic changes during ageing
Ageing declines the overall cellular function which affects the whole body homestasis. In addition to DNA damage and oxidative stress, metabolic dysfunction has been identified as a common hallmark for ageing. This article examines the metabolic changes that occur in two young and 2 year old mice. It integrates in its study the various methods of biochemical, gene expression, metabolism as well as in vivo phenotyping to determine a footprint a footprint for metabolism of ageing. It was found that in both muscle and liver pathways the glucose, fatty acid metabolism as well as the redox homeostasis were affected. A decline in long chain acyl-carnitines and various amino acids were found in the plasma of the aged mice [3]. In conclusion I believe this article has made a significant contribution to the field of ageing as it has identified with its mice model studies metabolites which are highly essential as biomarkers for ageing and lifespan.

• The role of Acetylcholine (Ach) in Alzheimer ’s disease
This scientific article examines the role of Ach in the development of AD. Ach plays an imperative role in the central and peripheral nervous system. It has been found that cholinergic neurons which are located in the basal of the forebrain, as well as neurons which make up the nucleus basalis of Meynert, as significantly lost in patients with AD. The loss of these cholinergic neurons results in memory and attention deficits. The article suggests that drugs which act on the cholinergic system, and therefore prevents the loss of theses neurons represents a promising treatment to AD [4].Overall I would suggest that this article does not make a highly significant difference to the field of ageing and AD, however the review does make a positive impact in where the direction of research and treatment ought to be heading towards.

• The role of the Amyloid-Beta (AB) in Alzheimer’s Disease
This article reviews the role of the amyloid-beta peptide deposition in the development of AD. Neuritic plaques and neurofibrillary tangles are a pathologic hallmark for AD, and have been found to correspond to the accumulation of AB peptide deposition in the brain of AD patients, in addition to cytoskeletal changes which arise as a result of hypophospholyration of Tau proteins in neurons. Characterisation of AB peptide by recent new technologies based on structural and functional imaging as well as biochemical analysis of cerebrial spinal fluid, present as an effective diagnostic tool for AD cases which can be identified at the earliest stages of the disease [5]. I believe this article presents a very effective and explanatory literature on the role of AB peptide deposition in AD and it effectively suggests diagnostic therapies targeting AB cascades which may halt the progression of AD, or may even be able to prevent the manifestation of the disease.

References

  1. KIRKWOOD. (1997). The origins of human ageing. Philosophical Transactions: Biological Sciences. 352, 1765-1772.
  2. LIU, J.-P. (2014). Molecular mechanisms of ageing and related diseases. Clinical and Experimental Pharmacology and Physiology. 41, 445-458.
  3. HOUTKOOPER, R. H., ARGMANN, C., HOUTEN, S. M., CANTÓ, C., JENINGA, E. H., ANDREUX, P. A., THOMAS, C., DOENLEN, R., SCHOONJANS, K., & AUWERX, J. (2011). The metabolic footprint of aging in mice. Scientific Reports. 1.
  4. FERREIRA-VIEIRA TH, GUIMARAES IM, SILVA FR, & RIBEIRO FM. (2016). Alzheimer’s disease: Targeting the Cholinergic System. Current Neuropharmacology. 14, 101-15.
  5. STOREY, & CAPPAI. (1999). The amyloid precursor protein of Alzheimer’s disease and the Aβ peptide. Neuropathology and Applied Neurobiology. 25, 81-97.