Abstract
Pantothenic acid (vitamin B5) is an essential trace nutrient required for the synthesis of coenzyme A (CoA). It has previously been shown that pantothenic acid is significantly decreased in multiple brain regions in both Alzheimer’s disease (ADD) and Huntington’s disease (HD). The current investigation aimed to determine whether similar changes are also present in cases of Parkinson’s disease dementia (PDD), another age-related neurodegenerative condition, and whether such perturbations might occur in similar regions in these apparently different diseases. Brain tissue was obtained from nine confirmed cases of PDD and nine controls with a post-mortem delay of 26 h or less. Tissues were acquired from nine regions that show high, moderate, or low levels of neurodegeneration in PDD: the cerebellum, motor cortex, primary visual cortex, hippocampus, substantia nigra, middle temporal gyrus, medulla oblongata, cingulate gyrus, and pons. A targeted ultra–high performance liquid chromatography—tandem mass spectrometry (UHPLC-MS/MS) approach was used to quantify pantothenic acid in these tissues. Pantothenic acid was significantly decreased in the cerebellum (p = 0.008), substantia nigra (p = 0.02), and medulla (p = 0.008) of PDD cases. These findings mirror the significant decreases in the cerebellum of both ADD and HD cases, as well as the substantia nigra, putamen, middle frontal gyrus, and entorhinal cortex of HD cases, and motor cortex, primary visual cortex, hippocampus, middle temporal gyrus, cingulate gyrus, and entorhinal cortex of ADD cases. Taken together, these observations indicate a common but regionally selective disruption of pantothenic acid levels across PDD, ADD, and HD.
Highlights
This article is an open access articleParkinson’s disease (PD) is a common neurodegenerative disorder, primarily characterised clinically by bradykinesia, resting tremor, and rigidity, and neuropathologically by extensive dopaminergic neuronal loss and accumulation of α-synuclein deposits known as Lewy bodies
Cases and controls were matched for age, sex, post-mortem delay (PMD), and brain weight, with no significant differences in any of these variables
Huntington’s disease (HD) studies, and cannot investigating case–controlincomparisons of pantothenic acid in so Parkinson’s disease dementia (PDD), we be compared to showed significantly decreased pantothenic acid compared the current results with those we obtained in previous analyses of other in the entorhinal cortex (ENT), thishas region was notperformed investigated in theofcurrent
Summary
Parkinson’s disease (PD) is a common neurodegenerative disorder, primarily characterised clinically by bradykinesia, resting tremor, and rigidity, and neuropathologically by extensive dopaminergic neuronal loss and accumulation of α-synuclein deposits known as Lewy bodies. Age is a primary risk factor for the development of symptoms ( HD is always caused by a dominant autosomal mutation in the huntingtin gene; the development of symptomology generally occurs with older age), cerebral protein deposition is present in each condition (α-synuclein in PD, tau and amyloid-β in ADD, and huntingtin in HD), and the clinical presentation can show significant overlap, with increased risk of psychological complaints [7], issues with sleep [8], and difficulty walking [9], as well as the progressive development of cognitive impairment [10,11] These findings have raised the question as to whether there may be common pathogenic insults present across multiple neurodegenerative diseases contributing to these similarities in presentation. This investigation is, to our knowledge, the first to report dysregulation of cerebral pantothenic acid in PDD, similar to that previously observed in ADD and HD
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