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Hi. My name is Suzie Bash.

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I'm a neuroradiologist at RadNet.

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And thank you so much for joining us today

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for this dementia mastery series.

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These are a few disclosures.

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So, there are a lot of different causes

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of significant memory loss

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that can result in a clinical picture of dementia.

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Now, some of these include Alzheimer's disease,

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vascular dementia, dementia with Lewy bodies,

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frontotemporal dementia,

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logopenic progressive aphasia,

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traumatic brain injury,

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cerebral amyloid angiopathy,

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CAA-related inflammation,

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and normal pressure hydrocephalus.

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And then we'll talk about these,

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and we'll also focus on the multimodal imaging appearance

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and approach to the workup of these different diagnoses.

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And then we'll spend some time discussing

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what causes dementia,

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as well as potential disease-modifying therapy

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and the imaging impact for patients that are on therapy.

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So, when a patient presents with memory loss,

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they'll often see a neurologist,

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and then they will do cognitive testing,

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such as a mini mental status exam, etc.

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And the neurologist will often order an MRI of the brain,

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and that's also typically to rule out any other

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pathology that may be causing memory loss.

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And it's at this point in time that we encourage the

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neurologist to order a quantitative

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volumetric imaging study.

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I've been using these in my clinical practice for the

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past 16 years.

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Our referring neurologists love it,

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and so we'll talk in more detail about that.

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And then if there remains clinical ambiguity,

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sometimes a PET is ordered.

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So there are three different PETs that we use for dementia.

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FDG PET, amyloid PET, and Tau PET.

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Right now, FDG is the only one that's covered by CMS,

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so we get that ordered much more frequently.

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Back during the ideas trial, I read over 200 amyloid PETs,

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but it's almost cost prohibitive for patients out of

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pocket these days.

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And then tau also is very useful,

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but again, not covered by insurance.

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So this is what a PET CT looks like.

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Here's a PET MR fusion.

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Here's the PET CT fusion.

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You see cortical hypometabolism

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in the bilateral temporal lobes.

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And so, this is a patient with Alzheimer's disease.

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Had we gone up higher,

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we'd also see hypometabolism in the parietal

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lobes and the posterior cingulate gyri.

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And this is what a positive amyloid PET looks like.

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You have diffuse binding of the tracer to the cortex.

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This is grayscale. This is color.

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And just for your reference,

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this is what an amyloid PET would look like where we have

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this sort of tree and branch pattern,

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where the white matter looks dark but the cortex looks light.