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| Parameter | Normal aging | Vascular dementia | Alzheimer’s disease | Other neurodegenerative disorders |
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| CBF | Diminished with lower velocity, but with preserved dynamic adaptability [84] | Diminished in parietal and frontal lobes, some authors reported also a decrement in superior temporal gyri, thalami, anterior cingulate gyri [85] | Diminished only in parietal cortices and later in advanced disease in frontal lobes [86] | Diminished in preoccipital and occipital regions in PD [87] and LBD [88] |
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| VEGF -A | Low basal levels produced by astrocytes [89] | Upregulation of VEGF and VEGF R2 in astrocytes [90] | Low serum levels and decreased secretion by peripheral immune cells [91] | FTLD—associated with VEGF gene promoter polymorphism in selected populations [92] |
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| Inflammatory cytokines | | | | |
| IL-6 | Increased mRNA compared to young subjects [93] | High blood levels, associated with high CRP may be associated with high risk [94] | Positive immunoreactivity in amyloid plaques and increased concentration in AD brain, compared to age-matched subjects [95] | Increased in cerebral and cerebellar cortex of Huntington patients [96] |
| TNFα | Increased basal levels in aged laboratory animals with week induction injury response [97] | Modulates neuronal cell loss in cerebral ischemia [98] | Increased expression in AD brain, along with TNF-R1 [99] | Increased in plasma [100], CSF of PD patients and in PD brains, especially in areas with greatest loss of dopaminergic neurons [101] |
| TGFβ1 | Detected at low levels in CSF and produced in CNS at low levels by neuronal cells [102] | Increased in CNS and CSF after stroke [103] | Increased in areas with amyloid burden [104] | CAA—directly related to amyloid vascular deposition [105] |
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| Adhesion molecules | sVCAM increased [106] | sVCAM increased in atherosclerotic disease [107]; sE-selectin increased in severe cerebrovascular disease [108] | sVCAM elevated in late onset AD [50] | sVCAM increased in Down Syndrome [100] |
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| ROS | Increased accumulation with aging [109] | Increased in ischemia animal models and stroke patients [110] | Increased: Aβ-related ROS generation and MAOS [111] | Increased in PD in vitro models [112] and animal models [113] |
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| Lipid metabolism | Accumulation of ceramides and free cholesterol in cerebral cortex [114] | Hypercholesterolemia is a known risk factor for VaD | Increased levels of cholesterol, and activation of cholesterol biosynthesis pathway [115] | PD dementia does not correlate with apoE polymorphism or lipid profile [116] |
| GLUT 1 | Altered structure and function of GLUT-1 [117] | Downregulated in prolonged hypoxia [118] | Low expression in AD hippocampus and double transgenic APP/PS1 animal model Learning increases expression in mouse brain [119] | Insufficiently investigated in neurodegeneration, but involved in “Glut-1 deficiency syndrome”— a treatment-resistant form of epilepsy [120] |
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| BDNF | Decreased mRNA in human plasma and hippocampus [121] | Increased expression following hypoxic stress in cell cultures [122, 123] and lab animals [123] | Decreased expression in hippocampus temporal and frontal cortex [124] | Reduced BDNF expression in the caudate and putamen in HD patients [96] Reduced mRNA BDNF expression [125] and protein [126] in striatal neurons in PD patients |
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| Calcium | Reduced homeostatic reserve [33] | Involved in ischemia-induced excitotoxicity [127] | Aβ disrupts Ca homeostasis in cortical neuronal cell cultures [117] | Excitotoxicity and excessive Ca2+-mediated nitric oxide production are believed to contribute to the death of dopaminergic neurons in PD [118]; Huntingtin transgenic mice express mitochondrial Ca overload upon glutamate stimulation [119] |
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