The X11 proteins, A beta production and Alzheimer's disease

C C J Miller; D M McLoughlin; K F Lau; M E Tennant; B Rogelj

doi:10.1016/j.tins.2006.03.001

The X11 proteins, A beta production and Alzheimer's disease

C C J Miller, D M McLoughlin, K F Lau, M E Tennant, B Rogelj

Basic and Clinical Neuroscience

Research output: Contribution to journal › Literature review › peer-review

86 Citations (Scopus)

Abstract

Cerebral deposition of amyloid-beta peptide (A beta) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting A beta deposition or removing A beta deposits once they are formed represent therapeutic targets for Alzheimer's disease. A beta is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11 alpha and X11 beta (the two neuronal X11s) inhibit APP processing and A beta production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms

Original language	English
Pages (from-to)	280 - 285
Number of pages	6
Journal	Trends in Neurosciences
Volume	29
Issue number	5
DOIs	https://doi.org/10.1016/j.tins.2006.03.001
Publication status	Published - May 2006

Access to Document

10.1016/j.tins.2006.03.001

Cite this

@article{1b51e3807b82417ba3f6124e42a0faae,

title = "The X11 proteins, A beta production and Alzheimer's disease",

abstract = "Cerebral deposition of amyloid-beta peptide (A beta) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting A beta deposition or removing A beta deposits once they are formed represent therapeutic targets for Alzheimer's disease. A beta is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11 alpha and X11 beta (the two neuronal X11s) inhibit APP processing and A beta production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms",

author = "Miller, {C C J} and McLoughlin, {D M} and Lau, {K F} and Tennant, {M E} and B Rogelj",

year = "2006",

month = may,

doi = "10.1016/j.tins.2006.03.001",

language = "English",

volume = "29",

pages = "280 -- 285",

journal = "Trends in Neurosciences",

publisher = "Elsevier Limited",

number = "5",

}

TY - JOUR

T1 - The X11 proteins, A beta production and Alzheimer's disease

AU - Miller, C C J

AU - McLoughlin, D M

AU - Lau, K F

AU - Tennant, M E

AU - Rogelj, B

PY - 2006/5

Y1 - 2006/5

N2 - Cerebral deposition of amyloid-beta peptide (A beta) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting A beta deposition or removing A beta deposits once they are formed represent therapeutic targets for Alzheimer's disease. A beta is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11 alpha and X11 beta (the two neuronal X11s) inhibit APP processing and A beta production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms

AB - Cerebral deposition of amyloid-beta peptide (A beta) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting A beta deposition or removing A beta deposits once they are formed represent therapeutic targets for Alzheimer's disease. A beta is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11 alpha and X11 beta (the two neuronal X11s) inhibit APP processing and A beta production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms

U2 - 10.1016/j.tins.2006.03.001

DO - 10.1016/j.tins.2006.03.001

M3 - Literature review

VL - 29

SP - 280

EP - 285

JO - Trends in Neurosciences

JF - Trends in Neurosciences

IS - 5

ER -

The X11 proteins, A beta production and Alzheimer's disease

Abstract

Access to Document

Fingerprint

Cite this