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Omega-3 Fatty Acids in Early Prevention of Inflammatory Neurodegenerative Disease: A Focus on Alzheimer's Disease.

Thomas J, Thomas CJ, Radcliffe J, Itsiopoulos C - Biomed Res Int (2015)

Bottom Line: It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD.Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels.DHA supplementation can reduce markers of inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, VIC, Australia.

ABSTRACT
Alzheimer's disease (AD) is the leading cause of dementia and the most common neurodegenerative disease in the elderly. Furthermore, AD has provided the most positive indication to support the fact that inflammation contributes to neurodegenerative disease. The exact etiology of AD is unknown, but environmental and genetic factors are thought to contribute, such as advancing age, family history, presence of chronic diseases such as cardiovascular disease (CVD) and diabetes, and poor diet and lifestyle. It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD. Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels. DHA supplementation can reduce markers of inflammation. This review specifically focusses on the evidence in humans from epidemiological, dietary intervention, and supplementation studies, which supports the role of long chain omega-3 fatty acids in the prevention or delay of cognitive decline in AD in its early stages. Longer term trials with long chain omega-3 supplementation in early stage AD are warranted. We also highlight the importance of overall quality and composition of the diet to protect against AD and dementia.

No MeSH data available.


Related in: MedlinePlus

Schematic representation showing key pathological features of the degenerative process in Alzheimer's disease (AD). The common characteristics are (1) amyloid-β plaques and (2) neurofibrillary tangles. Neuroinflammatory changes (3) have been identified as the third important component of the disease. Microglia migrate to the plaques and enhance amyloid-β deposition with chronic activation. Brain and neuron images from Wikimedia Commons (http://upload.wikimedia.org/wikipedia/commons/c/cc/Alzheimers_brain.jpg. http://upload.wikimedia.org/wikipedia/commons/b/be/Derived_Neuron_schema_with_no_labels.svg).
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fig1: Schematic representation showing key pathological features of the degenerative process in Alzheimer's disease (AD). The common characteristics are (1) amyloid-β plaques and (2) neurofibrillary tangles. Neuroinflammatory changes (3) have been identified as the third important component of the disease. Microglia migrate to the plaques and enhance amyloid-β deposition with chronic activation. Brain and neuron images from Wikimedia Commons (http://upload.wikimedia.org/wikipedia/commons/c/cc/Alzheimers_brain.jpg. http://upload.wikimedia.org/wikipedia/commons/b/be/Derived_Neuron_schema_with_no_labels.svg).

Mentions: AD is characterized by cognitive alterations, memory loss, and behavioural changes which affect daily living. Table 1 records the well-characterised stages of slow but progressive AD development. The predominant theory for the degenerative process in AD (summarised in Figure 1) subscribes that the deposition in the brain of highly insoluble amyloid-β occurs early in AD and suppresses synaptic plasticity. Disruption of dendritic spine formation thereby interferes with memory consolidation. The formation of amyloid plaques also activates glial cells to augment inflammation in the brain. Subsequent signalling events trigger abnormal intraneural formation of hyperphosphorylated tau protein (pTau), resulting in neurofibrillary tangles years/decades later [36]. At autopsy, AD postmortem brains share a number of common features. These include significant cortical atrophy and secondary ventricular enlargement. Neuropathogenic assessment reveals the highly insoluble neuritic plaques (amyloid-β; extraneuronal) and neurofibrillary tangles (tau; intraneuronal). AD brains are also characterized by prominent reactive astrogliosis due to destruction of nearby neurons [37].


Omega-3 Fatty Acids in Early Prevention of Inflammatory Neurodegenerative Disease: A Focus on Alzheimer's Disease.

Thomas J, Thomas CJ, Radcliffe J, Itsiopoulos C - Biomed Res Int (2015)

Schematic representation showing key pathological features of the degenerative process in Alzheimer's disease (AD). The common characteristics are (1) amyloid-β plaques and (2) neurofibrillary tangles. Neuroinflammatory changes (3) have been identified as the third important component of the disease. Microglia migrate to the plaques and enhance amyloid-β deposition with chronic activation. Brain and neuron images from Wikimedia Commons (http://upload.wikimedia.org/wikipedia/commons/c/cc/Alzheimers_brain.jpg. http://upload.wikimedia.org/wikipedia/commons/b/be/Derived_Neuron_schema_with_no_labels.svg).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4537710&req=5

fig1: Schematic representation showing key pathological features of the degenerative process in Alzheimer's disease (AD). The common characteristics are (1) amyloid-β plaques and (2) neurofibrillary tangles. Neuroinflammatory changes (3) have been identified as the third important component of the disease. Microglia migrate to the plaques and enhance amyloid-β deposition with chronic activation. Brain and neuron images from Wikimedia Commons (http://upload.wikimedia.org/wikipedia/commons/c/cc/Alzheimers_brain.jpg. http://upload.wikimedia.org/wikipedia/commons/b/be/Derived_Neuron_schema_with_no_labels.svg).
Mentions: AD is characterized by cognitive alterations, memory loss, and behavioural changes which affect daily living. Table 1 records the well-characterised stages of slow but progressive AD development. The predominant theory for the degenerative process in AD (summarised in Figure 1) subscribes that the deposition in the brain of highly insoluble amyloid-β occurs early in AD and suppresses synaptic plasticity. Disruption of dendritic spine formation thereby interferes with memory consolidation. The formation of amyloid plaques also activates glial cells to augment inflammation in the brain. Subsequent signalling events trigger abnormal intraneural formation of hyperphosphorylated tau protein (pTau), resulting in neurofibrillary tangles years/decades later [36]. At autopsy, AD postmortem brains share a number of common features. These include significant cortical atrophy and secondary ventricular enlargement. Neuropathogenic assessment reveals the highly insoluble neuritic plaques (amyloid-β; extraneuronal) and neurofibrillary tangles (tau; intraneuronal). AD brains are also characterized by prominent reactive astrogliosis due to destruction of nearby neurons [37].

Bottom Line: It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD.Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels.DHA supplementation can reduce markers of inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora 3086, VIC, Australia.

ABSTRACT
Alzheimer's disease (AD) is the leading cause of dementia and the most common neurodegenerative disease in the elderly. Furthermore, AD has provided the most positive indication to support the fact that inflammation contributes to neurodegenerative disease. The exact etiology of AD is unknown, but environmental and genetic factors are thought to contribute, such as advancing age, family history, presence of chronic diseases such as cardiovascular disease (CVD) and diabetes, and poor diet and lifestyle. It is hypothesised that early prevention or management of inflammation could delay the onset or reduce the symptoms of AD. Normal physiological changes to the brain with ageing include depletion of long chain omega-3 fatty acids and brains of AD patients have lower docosahexaenoic acid (DHA) levels. DHA supplementation can reduce markers of inflammation. This review specifically focusses on the evidence in humans from epidemiological, dietary intervention, and supplementation studies, which supports the role of long chain omega-3 fatty acids in the prevention or delay of cognitive decline in AD in its early stages. Longer term trials with long chain omega-3 supplementation in early stage AD are warranted. We also highlight the importance of overall quality and composition of the diet to protect against AD and dementia.

No MeSH data available.


Related in: MedlinePlus