0:00

Dr. Laser,

0:01

this is a patient who's currently going to be 91.

0:04

It's a relative of mine,

0:05

and so I know the case well.

0:07

On the far right is a study from five years ago,

0:11

and the patient at that time

0:13

had Mild Cognitive Impairment Syndrome.

0:15

You could hardly tell,

0:16

but on careful questioning, you could tell.

0:18

But on general activities of everyday living,

0:21

totally fine.

0:22

And now, full-blown Alzheimer's disease.

0:25

And you can compare the two,

0:26

especially,

0:27

you know,

0:28

we didn't have coronal imaging on follow-up.

0:30

The original study had a coronal,

0:31

which you should always get in any dementia,

0:33

but they didn't get it.

0:35

And here's the new study that

0:37

shows the temporal horns.

0:39

Compare the old temporal horns from five

0:41

years ago with the temporal horns now,

0:43

especially on the left.

0:44

Look at the difference.

0:44

Oh, markedly widened.

0:45

Substantially different.

0:46

And look at the volume of the parahippocampal tissue.

0:49

Much thicker before, much thinner now.

0:52

There's no question that this patient has

0:55

a primary neurodegenerative disease.

0:57

Look at the horizontal fissure right here.

0:59

Severely atrophic.

1:00

And that atrophy has progressed.

1:02

Little hard to tell on the axial projection.

1:04

She's got just a little bit of atrophy in the

1:07

olfactory region, but for the most part,

1:09

the frontal region less involved than the parietal

1:12

region in the back.

1:13

Also goes along with ALZ.

1:15

Her clinical history of difficulty with word finding,

1:19

her short-term memory loss,

1:20

her lack of disinhibition,

1:22

the fact that she doesn't have tremors

1:24

or any movement disorder,

1:25

all completely supportive of the diagnosis

1:28

of a Tauopathy, namely ALZ,

1:32

progressed from MCI,

1:33

Mild Cognitive Impairment Syndrome to ALZ.

1:36

So you can see the actual progression.

1:37

So, what are Tauopathies?

1:39

Some examples would be TDP-43, proteinopathies,

1:43

neurofilamentopathies, and Alzheimer's disease.

1:46

Now,

1:46

you can evaluate someone like this for amyloid

1:51

in the brain by using F-18 amyloid PET.

1:54

There are three or four agents that are available.

1:56

We won't delve into those.

1:58

But I will say that if you don't have any

2:00

enhancement at all,

2:01

it's a good rule out for ALZ.

2:04

She did not have one, but if she did,

2:05

it would be positive.

2:06

But the number one biomarker,

2:08

as we've discussed,

2:09

is hippocampal volume loss.

2:11

And she totally has it.

2:13

She had it when she had MCI,

2:14

but she has it even more profoundly now,

2:17

five years later.

2:18

You can see the AP dimension of the

2:19

hippocampus is decreased.

2:21

Now, cerebral amyloid occurs in normal individuals.

2:26

It increases in the brain with age.

2:28

It's different than inflammatory or noninflammatory

2:31

primary amyloid angiopathy,

2:33

in which they get multiple low bar hemorrhages.

2:35

That's not the case with standard ALZ.

2:39

And then most patients,

2:41

the beta amyloid precedes the deposition

2:44

of Tau proteins in Alzheimer's disease.

2:48

Do you have any other comments about this case?

2:50

No. Laser and Pomeranz out.