Brain Reduction and Presence of Alzheimer’s Disease

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Table of Contents

Introduction
Article Summary
Conclusion
List of References

Introduction

The purpose of the study was to examine the correlation between brain reduction and the presence of Alzheimer’s disease (AD). The researchers used magnetic resonance imaging (MRI) to estimate 1-year atrophy in 132 healthy participants. The ‘selected group had not been diagnosed with AD or cognitive impairment within the last three years’ (Buckner & Carroll 2007, p. 52).

The approach was necessary towards understanding the issues associated with brain changes in elderly persons. The study was relevant because one-year changes are common in older adults. Such changes are ‘distinguished by unique frontotemporal patterns’ (Blennow & Zetterberg, 2006, p. 3661). The researchers wanted to examine the nature of such changes in elderly individuals at low risk for AD (Addis, Roberts & Schacter, 2011).

Article Summary

Several researchers have identified brain reductions in healthy adults. The outstanding challenge is that the presence of AD-related complications will hinder every effort aimed at examining different brain changes. The researchers identified ‘considerable volumetric reductions throughout the brain’ (Fjell et al. 2013, p. 8237).

Although the collected samples varied significantly, reductions were common in every subgroup. The researchers subdivided their participants into several low-risk groups. The researchers used cognitive, genetic, biomarker, or clinical criteria to define their subgroups. The observed volume reductions matched the previously examined frontotemporal changes in healthy individuals. The pattern was also associated with healthy aging.

According to Fjell et al. (2013, p. 8241), ‘normal aging will affect frontostriatal circuits. This development will result in reduced brain functions and secondary recollection problems. The findings also explain why patients with Alzheimer’s disease (AD) encounter frontotemporal vulnerabilities. Such changes are normal because they portray the process of aging. The authors also examined the possibility of different pathological changes.

A good example is a cerebrovascular disease (CVD). This disease is common among elderly members of society. The disease has profound effects on cognitive functions and brain structures. According to Fjell et al. (2013), the disease will affect different neural systems. The disease has also been associated with dementia.

This study explains why incipient AD is not the only cause of volumetric brain changes. Such volume changes are normal features of human growth and aging. It is also agreeable that brain changes can occur in individuals with incipient Alzheimer’s disease. The study explained how most of the brain reductions aligned with the DMN. This was something common in normal aging. The findings also explain why temporal changes are common in healthy individuals or older adults. The ‘outstanding challenge is that AD-related infection occurs in the brain several years before any detectable symptom’ (Jagust 2013, p. 230).

Statistics show that any person dying at the age of 80 years will have a 40 percent probability of portraying AD-associated brain changes. The same individual will have a 15 percent possibility of exhibiting dementia-related neuropathological changes in his or her brain (Strozyk et al. 2003). According to many professionals, such age-related atrophies are associated with inadequate screening for various neurodegenerative diseases. This situation explains why it has always been impossible to explain how preclinical AD might not facilitate any brain change.

Conclusion

The above understanding has encouraged scholars and researchers to investigate the potential causes of brain changes among the elderly. The findings also show that ‘one-year changes are detectable in a healthy elderly at very low risk of Alzheimer’s disease’ (Goedert & Spillantini 2006, p. 779). The authors also explain the change patterns tend to overlap with the DMN. Any hippocampal change will most likely result in new episodic functions of the brain. I will read more articles to understand this issue much better.

List of References

Addis, D, Roberts, P & Schacter, D 2011, ‘Age-related neural changes in autobiographical remembering and imagining’, Neuropsychologia, vol. 49, no. 1, pp. 3656-3669.

Blennow, K & Zetterberg, H 2006, ‘Alzheimer’s disease’, Lancet, vol. 368, no. 1, pp. 387-403.

Buckner, R & Carroll, D 2007, ‘Self-projection and the brain’, Trends Cognitive Science, vol. 11, no. 1, pp. 49-57.

Fjell, A, McEvoy, L, Holland, D, Dale, A & Walhovd, K 2013, ‘Brain Changes in Older Adults at Very Low Risk for Alzheimer’s Disease’, The Journal of Neuroscience, vol. 33, no. 19, pp. 8237-8242.

Goedert, M & Spillantini, G 2006, ‘A century of Alzheimer’s disease’, Science, vol. 314, no. 1, pp. 777-781.

Jagust, W 2013, ‘Vulnerable neural systems and the borderland of brain aging and neurodegeneration’, Neuron, vol. 77, no. 1, pp. 219-234.

Strozyk, D, Blennow, K, White, R & Launer, J 2003, ‘CSF Abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study’, Neurology, vol. 60, no. 1, pp. 652-656.

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Brain Reduction and Presence of Alzheimer’s Disease

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