Research Articles (PDF’s)


Reduction of inclusion body pathology in ApoE-deficient mice fed a combination of antioxidants. Veurink G, Liu D, Taddei K, Perry G, Smith MA, Robertson TA, Hone E, Groth DM, Atwood CS, Martins RN. Free Radic Biol Med. 2003 Apr 15;34(8):1070-7.PMID: 12684092 [PubMed – indexed for MEDLINE]


Genetics, lifestyle and the roles of amyloid beta and oxidative stress in Alzheimer’s disease.

Veurink G, Fuller SJ, Atwood CS, Martins RN.

Ann Hum Biol. 2003 Nov-Dec;30(6):639-67. Review.

PMID: 14675907 [PubMed – indexed for MEDLINE]

PhD Title:

The Role of Oxidative Stress and Cholesterol in Animal Models of Alzheimer’s Disease


Veurink, Gerald




Alzheimer’s disease (AD) is the most commonly diagnosed form of dementia in the aged, and is characterised by a progressive decline in memory, language and other cognitive functions, together with deterioration in behavioural, emotional and social skills. The earliest clinical symptoms include episodic memory loss and dysnomia. This is followed by other signs of cortical impairment including apraxia, agnosia, and visuospatial impairment. In advanced stages, victims become mute, cannot walk and are incontinent; they therefore become totally dependent on carers. AD is the third leading cause of death in the aging population after heart disease and cancer. The incidence of AD doubles every 5 years in subjects between the ages of 65 and 85 years, affecting one in three by the age of 80. AD is characterised by the existence of intracellular and extracellular amyloid deposits in the brain. Extracellular amyloid deposits consist of plaques, whereas the deposits within and around blood vessels are referred to as cerebral amyloid angiopathy (CAA). Neurofibrillary tangles (NFT) are characteristically found in AD; however, they are also found in some other neurodegenerative disorders such as tuberose sclerosis, amyotrophic lateral sclerosis, parkinson-dementia complex and dementia pugilistica.


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