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Greetings: RIKEN BSI Proteolytic Neuroscience Laboratory BSI Central Building, April 17, 2014.

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Page 1: Takaomi Saido

Greetings: RIKEN BSI Proteolytic Neuroscience Laboratory

BSI Central Building, April 17, 2014.

Page 2: Takaomi Saido

Takaomi C. SaidoLaboratory for Proteolytic NeuroscienceRIKEN Brain Science InstituteJAPAN

Alzforum WebinerApril 22, 2014

2nd generation mouse models of Alzheimer’s disease:12 years of work and future perspectives

Page 3: Takaomi Saido

Crossing Tg mice overexpressing mutant APP with other Tg mice is a risky paradigm.

Example: APP-Tg X Calpastatin-Tg/KO.

Page 4: Takaomi Saido

0

20

40

60

80

100

0 10 20 30 40 50 60

Age (weeks)

Pro

po

rtio

n s

urv

ivin

g (

%) WT

CS-KO

APP/CS-Tg

APP-TgAPP-TgCS-KO (+/-)

APP-TgCS-KO (-/-)

Effect of calpastatin (CS) overexpression & deficiency on life span of APP-Tg mice

Higuchi et al. FASEB J. (2012)

Page 5: Takaomi Saido

2nd generation KI mouse model of A amyloidosis: β APPNL-F

β-cleavage site γ-cleavage site

67

1

Aβ42Aβ40

R Y Hhumanization

Aβ:3-fold

NL

SEVKM DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV IA TVIVITLVMLK

67

0

Overproduction of Aβ1-42 Aβ42/Aβ40 ratio: 30-fold

F Beyreuther/Iberianmutation

Saito et al. (Nat Neurosci, 2014)

Overproduction of APPsβ

NL-F

Relevant negative control?

Page 6: Takaomi Saido

A negative control for the 2nd generation KI mouse model: APPNL

β-cleavage site γ-cleavage site

67

1

Aβ42Aβ40

R Y Hhumanization

Aβ:3-fold

NL

SEVKM DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV IA TVIVITLVMLK

67

0

Overproduction of Aβ1-40/42

Saito et al. (Nat Neurosci, 2014)

Age of onset: 50-60 years

Overproduction of APPsβ

NL

Relevant negative control!

Page 7: Takaomi Saido

500 µm

Am

yloi

d bu

rden

(%) HippocampusCortex

4G8 15 mo 18 mo12 mo9 mo

21 mo 24 mo

Age-dependent Aβ deposition in NL-F/NL-F

Aβ deposition could be detected from 6 mo of NL-F/NL-F brains.

Page 8: Takaomi Saido

APP KICS-KO

CS-KO; APP KI

Modulation of calpain activity in APP-KI mouse brain by crossbreeding with Calpastatin (CS)-KO mice

New!

Page 9: Takaomi Saido

Survival of APPNL/F-KI x Calpastatin (CS)-KO mice

CS deficiency did not affect the survival of APPNL-F KI mice at least up to 20 months.

Page 10: Takaomi Saido

1. Role of inflammation2. Role of various proteases3. Effect of Aβ vaccination4. Effect of ApoE45. Effect of the environmental

enrichment6. Effect of various diets and

supplements7. Others (Tau, Dynamin, Arc, etc.)

Major issues to be re-addressed

Page 11: Takaomi Saido

3 rd generation KI mouse model of A amyloidosis: APPβ NL-G-F

β-cleavage site γ-cleavage site

67

1

Aβ42Aβ40

R Y Hhumanization

NL

SEVKM DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV IA TVIVITLVMLK

67

0

F Beyreuther/Iberianmutation

Saito et al. (Nat Neurosci, 2014)

SEVNL DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV IA TVFVITLVMLK

G (Arctic mutation)

Oligomerization-prone

NL-G-F

Page 12: Takaomi Saido

500 µm

2 months 4 months 7 months

Aβ42 pathology of NL-G-F KI mice

Page 13: Takaomi Saido

Neuroinflammation in APPNL-G-F/NL-G-F KI

Greater neuroinflammation was found around the plaques in APPNL-G-F/NL-G-F mice than aged APPNL-F/NL-F KI mice.

APPNL-F/NL-F (24 mo) APPNL-G-F/NL-G-F (9 mo)

Aβ(82E1) microglia astrocyte merge

Page 14: Takaomi Saido

Differential utility of NL-F and NL-G-F mice

1. NL-F: Mechanism of Aβ deposition (up-stream targets).

2. NL-G-F: Mechanism of inflammation, tauopathy and neurodegeneration (down-stream targets).

Page 15: Takaomi Saido
Page 16: Takaomi Saido

Finally, we should compare our mice with APPNL/NL mice crossbred with mutant presenilin 1 (PS1) knockin mice24, which also overproduce Aβ 42 without overexpressing APP. These APP/PS1 double knockin mice are comparable to the APPNL-F/NL-F mice in this respect. There are, however, two major difficulties that limit the utility of the double knockin mice. The first is that they are doubly homozygous: crossing them with other mutant mice is practically impossible. To our knowledge, no researchers have done so as yet. The second is that presenilin mutations affect biological processes other than γ-cleavage of APP25; no perfect negative controls exist. It should also be noted that the function(s) of PS1 may, at least in part, differ between humans and mice26.

Page 17: Takaomi Saido

RIKEN BSI  Lab. for Proteolytic Neuroscience

Takashi SaitoNobuhisa Iwata (Nagasaki U)

Makoto Higuchi (NIR)Jiro TakanoSatoshi TsubukiPer NilssonNaomasa KakiyaKaori TsukakoshiHayato IsshikiKo SatoShoko Hashimoto

Contributors and Collaborators

RIKEN BSI Lab. for Behavioral Genetics  Shigeyoshi ItoharaNational Institute for Geriatrics and Gerontology

Akihiko TakashimaUniversity of Minnesota Karen Hsiao-AsheNovartis Institute of Medical Research

Matthias StaufenbielJichi Medical University

Shin-ichi MuramatsuHarvard Medical School

Cynthia Lemere