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Each dementia subtype damages a different brain network first, and imaging simply photographs where that network lives — memory circuits for Alzheimer's disease, visual and dopaminergicRelating to dopamine, a brain chemical involved in reward, motivation and movement.Read more → circuits for Lewy body dementia, and social-behavioural circuits for frontotemporal dementia.

• Alzheimer's disease, medial temporal (hippocampal/entorhinal) atrophy on structural MRI, with posterior cingulate and parietotemporal association-cortex hypoperfusion/hypometabolism on SPECT/PET, sparing primary sensorimotor and occipital cortex.
• Dementia with Lewy bodies, relatively preserved hippocampal volume on MRI (vs Alzheimer's disease) with occipital hypoperfusion on SPECT and reduced striatal dopamine transporter uptake on DAT-SPECT, reflecting nigrostriatal degeneration.
• Behavioural-variant frontotemporal dementia: frontal and anterior temporal lobeThe part of the brain by the ears, involved in hearing, language and memory.Read more → atrophy and hypoperfusion, sparing posterior parietal and occipital regions.
• Vascular dementia, patchy, asymmetric cortical/subcortical infarcts and confluent white-matter change on MRI, distributed along vascular territories rather than a single association-cortex pattern.

• Progressive memory loss, getting lost, with posterior cingulate/parietotemporal hypoperfusion sparing occipital cortex.
• Fluctuating cognition, visual hallucinationsSeeing, hearing, or otherwise sensing things that are not really there.Read more →, spontaneous parkinsonism, with reduced striatal DAT-SPECT uptake worse in putamen than caudate.
• Personality change, disinhibition, preserved memory and visuospatial skills, with frontal/anterior temporal atrophy.

• Hippocampal atrophy on MRI, prominent in Alzheimer's disease, relatively preserved in dementia with Lewy bodies — the single most useful structural discriminator between the two.
• Occipital function, hypoperfused in dementia with Lewy bodies, spared in Alzheimer's disease.
• Posterior cingulate, hypoperfused early in Alzheimer's disease, but relatively preserved in dementia with Lewy bodies (the "cingulate island sign" on FDG-PET).
• DAT-SPECT striatal uptake, reduced in dementia with Lewy bodies and Parkinson's disease dementia, normal in Alzheimer's disease and frontotemporal dementia.
• Distribution of atrophy, posterior (parietotemporal) in Alzheimer's disease versus anterior (frontotemporal) in behavioural-variant frontotemporal dementia.

• Assuming any generalised cerebral atrophy on a CT/MRI report confirms Alzheimer's disease — non-specific atrophy occurs with normal ageing and in every dementia subtype.
• Forgetting that DAT-SPECT distinguishes Lewy body dementia from Alzheimer's disease but does not distinguish Lewy body dementia from other Parkinsonian syndromes with nigrostriatal loss.
• Reading "posterior hypoperfusion" and assuming Alzheimer's disease without checking whether it specifically spares or involves the occipital cortex — occipital involvement points to Lewy body dementia, not Alzheimer's disease.
• Expecting frontotemporal dementia to show memory-predominant deficits or hippocampal atrophy on imaging — early-stage frontotemporal dementia classically spares these.

• Localise the clue to the relevant anatomical level, cell type, pathway or molecular process.
• Map that structure or process to its normal function.
• Predict the deficit or clinical sign produced when it is disrupted.
• Reject options that belong to a neighbouring structure, pathway or level of explanation.