Neurological Processes

New Zealand Dementia Foundation > Research Radar > Neurological Processes
Changes in Plasma cGP/IGF-1 Molar Ratio With Age Are Associated With Cognitive Status of Parkinson’s Disease.


Fan, D., Pitcher, T., Dalrymple‐Alford, J., MacAskill, M., Anderson, T., & Guan, J. (2020). 
Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, 12(1), e12025.

This study examined the association between plasma cGP/IGF-1 molar ratio and cognitive scores or age in patients with Parkinson’s disease (intact, MCI, or dementia) and healthy controls.  Increased cGP/IGF-1 molar ratio with age may contribute to cognitive retention.

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Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson’s Disease.


Melzer, T. R., Stark, M. R., Keenan, R. J., Myall, D. J., MacAskill, M. R., Pitcher, T. L., Livingston, L., Grenfell, S., Horne, K., Young, B., Pascoe, M., Almuqbel, M. A., Wang, J., Marsh, S., Miller, D. H., Dalrymple-Alford, J. C., Anderson, T. J. (2019). 
Frontiers in Neurology, 10, 391

Amyloid deposition in the brain was compared for 115 participants with Parkinson’s disease who were classified as having normal cognition, mild cognitive impairment, or dementia. The study did not find an association between amyloid deposition and cognitive impairment.

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Acute Tryptophan Depletion and Lewy Body Dementias.


Mace, J. L., Porter, R. J., Dalrymple-Alford, J. C., Collins, C., & Anderson, T. J. (2016).
International Psychogeriatrics, 28(9), 1487–1491.

This study used acute tryptophan depletion (ATD) to examine the effects of a rapid reduction in serotonin function in people with Alzheimer’s disease (AD) and Parkinson’s disease (PD). D in a double-blind, placebo-controlled, randomised, counterbalanced, crossover design. While the study intended to enrol 20 patients, the protocol was poorly tolerated and was terminated after 6 patients had attempted it. The reduction in global cognitive function and the poor tolerability found may fit with the hypothesis that people with dementia with Lewy bodies have sensitivity to the effects of reduced serotonin function.

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Evidence for Widespread, Severe Brain Copper Deficiency in Alzheimer’s Dementia.


Xu, J., Church, S. J., Patassini, S., Begley, P., Waldvogel, H. J., Curtis, M. A., … & Cooper, G. J. (2017)
Metallomics, 9(8), 1106-1119.

This study measures post-mortem levels of 8 essential metals and selenium in the brains of 9 New Zealand cases with Alzheimer’s disease, compared to 13 controls. Copper levels were substantially decreased in all Alzheimer’s Disease-brain regions compared to the control brains.

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Metabolite Ratios in the Posterior Cingulate Cortex Do Not Track Cognitive Decline in Parkinson’s Disease in a Clinical Setting.


Almuqbel, M., Melzer, T. R., Myall, D. J., MacAskill, M. R., Pitcher, T. L., Livingston, L., … & Anderson, T. J. (2016).
Parkinsonism & Related Disorders, 22, 54–61.

The study assesses the posterior cingulate cortex (PCC) and cognitive impairment. There was no association with disease or cognitive ability at baseline or over time. MR spectroscopy of PCC does not appear to be a useful clinical marker for cognitive impairment in Parkinson’s disease.

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Elevation of Brain Glucose and Polyol-Pathway Intermediates With Accompanying Brain-Copper Deficiency in Patients With Alzheimer’s Disease: Metabolic Basis for Dementia.


Xu, J., Begley, P., Church, S. J., Patassini, S., McHarg, S., Kureishy, N., … & Lin, W. (2016).
Scientific Reports, 6, 27524.

This study employed mass spectrometry (MS) to measure metabolites and metals in seven post-mortem brain regions from nine New Zealand AD patients and nine controls, and plasma glucose and plasma copper levels in an ante-mortem case-control study. There were pervasive defects in the regulation of glucose and copper in the AD brain, but no evidence for corresponding systemic abnormalities in plasma.

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Effects of Rapid Tryptophan Depletion on Salivary and Plasma Cortisol in Alzheimer’s Disease and the Healthy Elderly.


Porter, R. J., Marshall, E. F., & O’Brien, J. T. (2002).
Journal of Psychopharmacology, 16(1), 73–78.

Effects of lowering brain serotonin on salivary and plasma cortisol were assessed in patients with Alzheimer’s disease and in control subjects. The authors conclude that acute tryptophan depletion had no effect on cortisol secretion.

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Global Changes in DNA Methylation and Hydroxymethylation in Alzheimer’s Disease Human Brain.


Coppieters, N., Dieriks, B. V., Lill, C., Faull, R. L. M., Curtis, M. A., & Dragunow, M. (2014).
Neurobiology of Aging, 35(6), 1334–1344.

This study investigated epigenetic markers altered in the brains of people with Alzheimer’s disease. The study clearly demonstrates the involvement of 5mC and 5hmC in Alzheimer’s disease.

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TBP, a Polyglutamine Tract Containing Protein, Accumulates in Alzheimer’s Disease.


Reid, S. J., Van Roon-Mom, W. M. C., Wood, P. C., Rees, M. I., Owen, M. J., Faull, R. L. M., et al. (2004).
Molecular Brain Research, 125(1–2), 120–128.

This paper provides evidence that TBP (TATA binding protein) accumulates in the brains of people with Alzheimer’s disease, localising to neurofibrillary tangle structures.

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A Splice Variant of the TATA-Box Binding Protein Encoding the Polyglutamine-Containing N-Terminal Domain That Accumulates in Alzheimer’s Disease.


Reid, S. J., Whittaker, D. J., Greenwood, D., & Snell, R. G. (2009).
Brain Research, 1268, 190–199.

Previously, this research group reported the accumulation of an N-terminal fragment of the TATA-box binding protein (TBP) in Alzheimer’s disease brain tissue, and here they identify a naturally occurring TBP splice variant as a likely mechanism for its production.

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