Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer's disease

Abstract

These different regional CMRglc reductions substantiate the pathologic, neurochemical, and clinical differences between DLB and AD.

Differential Diagnosis of Dementia with Lewy Bodies and Alzheimer Disease Using Combined MR Imaging and Brain Perfusion Single-Photon Emission Tomography

“…This has been demonstrated by using SPECT and PET. [8][9][10] Recent studies have reported dopamine transporter loss in the striatal, caudate, and posterior putamen in patients with DLB. 11,12 Many studies investigating AD have found volume decreases in medial temporal structures and cerebral blood flow reductions in temporoparietal areas.…”

What can imaging tell us about cognitive impairment and dementia?

“…Amyloid PET imaging demonstrates similar uptake in AD and LBD (apart from occipital lobes which are spared in AD), making it difficult to differentiate between these two conditions. Similarly they are indistinguishable on rCBF SPECT and FDG PET, however involvement of the visual cortex would favour LBD [88][89][90] . A dopaminergic presynaptic ligand, iodine-123-bcarbo-methoxy-3-b-(4-iodophenyltropane) fluoropropyl (FP-CIT) or ioflupane, is used in SPECT studies.…”

“…C PIB, Florbetapir 3 uptake in amyloid plaques [42] Tau specific ligands -PET, MRI-BOLD, fMRI↓connectivity in DMN, MR perfusion [38] , MR spectroscopy, DTI -↓ medial temporal lobe and precuneus [34] , VBM LBD Intracellular Lewy bodiesaggregates of α-synuclein particles in pre-synaptic terminals Overlaps with Parkinson's disease Atrophy in inferior frontal lobe, visual cortex, insula, hypothalamus, midbrain, caudate, putamen and anterior hippocampi (CA1 subregion) [86] SPECT -↓in putamen and caudate, visual cortex [88,89] FDG PET -↓in visual cortices [88][89][90] FP-CIT-↓uptake in putamen and caudate [79] Cholinergic PET/ SPECT-↓in medial occipital lobe [95] 123 I MIBG-↓cardiac uptake [96] Diffusion weighted MR-DTI, ↓ in visual association cortex and posterior putamen MRS, fMRI ASL-MR…”

Microglia and Chitotriosidase in Multiple Sclerosis

“…Several lines of evidence exist that implicate impaired glucose metabolism in several CNS diseases. [25][26][27] It is known that brain hypoperfusion and several inflammatory conditions lead to increased glucose metabolism, which in turn strongly increases hexosamine pathway activity in endothelial cells, leading to synthesis of glucosamine polymers. 28,29 Glucosamine has various physiological properties: it inhibits pro-inflammatory cytokines from antigenpresenting cells (APCs), suppresses T-cell response by interfering with functions of APC and shows a direct inhibitory effect on CD3-driven T-cell proliferation.…”