Table 2.
Dementia | Pathological feature | Structural imaging CT/MRI | Molecular imaging (non-specific) | Molecular imaging (specific) | Research |
Alzheimer’s disease | Primary neurodegenerative, extracellular amyloid plaques (Aβ42), intracellular tau aggregates[13], Autosomal dominant early onset inherited form - presenelins are also implicated[22] | Hippocampal-medial temporal lobe (CA2 and CA3 hippocampal subregions are more affected), posterior cingulate gyrus and postero-medial parietal lobe atrophy on MRI and CT | SPECT1- ↓perfusion FDG PET2- ↓glucose uptake in medial temporal lobe and hippocampi[39-41] | 11C PIB, Florbetapir3 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 bodies-aggregates 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[88-90] | FP-CIT-↓uptake in putamen and caudate[79] Cholinergic PET/SPECT- ↓in medial occipital lobe[95] 123I MIBG-↓cardiac uptake[96] | Diffusion weighted MR-DTI, ↓ in visual association cortex and posterior putamen MRS, fMRI ASL-MR |
FTD | Various proteins including tauopathies, TDP43, FUS- clinically can overlap with PSP, MSA, MND[100,101] | Variable-predominantly anterior frontal, temporal and insular atrophy[102,103] | FDG PET and SPECT-↓anterior, frontal and temporal uptake[107] | - | fMRI, DTI-↓ in WM of affected regions[104] fMRI-↓"salient" network’ but ↑DMN connectivity on resting fMRI- unlike AD[105,106] |
Vascular dementia | Small and large vessel disease - vascular risk factors like HT, smoking and DM implicated[61] CADASIL- hereditary form | CT-cortical infarct, macrohaemorrhage, frontal subcortical and periventricular WMH, lacunes[62-67] MRI-CT features as above and PVS, CMB | FDG PET and rCBF SPECT-↓ frontal and periventricular regions | - | - |
CJD sCJD vCJD | Prion protein - sources include food, tissues, genetic variation | MRI-↑signal on T2W and DWI in the caudate and cortex ("cortical ribboning") MRI-↑ on T2W and DWI in the pulvinar of thalami | |||
Autoimmune encephalitis related dementia | Previously limbic encephalitis -neuron specific CSF autoantibodies Paraneoplastic syndrome | MRI-↑ signal on T2W and FLAIR in the mesial temporal lobe | FDG PET -↑ uptake in the medial temporal lobe Whole body PET to identify underlying primary malignancy[110] |
SPECT-radiotracer is 99mTc hexamethylpropylene amine oxime;
FDG PET-radiotracer is 18F-FDG;
Recently approved by FDA for clinical use in specific cases, primarily to exclude Alzheimer’s disease.↑: Increased; ↓: Decreased; Aβ42: Beta amyloid protein with 42 amino acids; CA1, CA2, CA3: Subfields of hippocampus; ASL- MR: Arterial spin labelling MR; BOLD: Blood oxygenation level dependent; CADASIL: Congenital autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; CMB: Cerebral microbleeds; CSF: Cerebrospinal fluid; DM: Diabetes mellitus; DTI: Diffusion tensor imaging; FDG: Fludeoxyglucose; FLAIR: Fluid-attenuated inversion–recovery; fMRI: Functional MRI; DMN: Default mode network; FP-CIT: Dopaminergic presynaptic ligand iodine-123-b-carbo-methoxy-3 b-(4-iodophenyltropane) fluoropropyl; FUS: Fused in sarcoma protein; HT: Hypertension; LBD: Lewy body dementia; MSA: Multisystem atrophy; MND: Motor neuron disease; MRS: MR spectroscopy; PET: Positron emission tomography; PIB: Pittsburgh compound B; PSP: Progressive supranuclear palsy; PVS: Perivascular spaces; rCBF SPECT: Regional cerebral blood flow SPECT; sCJD: Sporadic form of Creutzfeldt–Jacob disease; vCJD: Variant form of Creutzfeldt–Jacob disease; SPECT: Single photon emission computed tomography; T2W: T2 weighted; TDP43: Transactive DNA-binding protein; VBM: Voxel-based morphometry; WMH: White matter hyperintensities.