PAPER Sato N, Okochi M, Shinohara M, Thinakaran G, Takeda S, Fukumori A, Shinohara-Noma M, Mori-Ueda M, Hamada H, Takeda M, Rakugi H, Morishita R

Differential regulation of amyloid precursor protein/presenilin 1 interaction during Ab40/42 production detected using fusion constructs.

PLoS One. 2012;7(11):e48551. PubMed: 23152781

Guoping Feng

MIT
Cambridge, United States

Ivan Maksimovich on New Strategies for Early Diagnosis of AD

COMMENT Long before AD symptoms, perhaps even in childhood (congenital causes cannot be excluded), people with a high likelihood of acquiring AD show degeneration of the brain capillary bed (1,2). This is manifested in reduction of the capillaries in the temporal

Elizabeth Mormino on Region-specific hierarchy between atrophy, hypometabolism, and β-amyloid (Aβ) load in Alzheimer's disease dementia.

COMMENT In this paper, La Joie et al. provide convincing evidence for distinct patterns of brain changes (atrophy, hypometabolism, and amyloid deposition) across different brain regions in Alzheimer’s disease. Although the presence of regional discrepancies requi

PAPER La Joie R, Perrotin A, Barré L, Hommet C, Mézenge F, Ibazizene M, Camus V, Abbas A, Landeau B, Guilloteau D, De la Sayette V, Eustache F, Desgranges B, Chételat G

Region-specific hierarchy between atrophy, hypometabolism, and β-amyloid (Aβ) load in Alzheimer's disease dementia.

J Neurosci. 2012 Nov 14;32(46):16265-73. PubMed: 23152610

Kristel Sleegers on Enter the New Alzheimer’s Gene: TREM2 Variant Triples Risk

COMMENT These studies provide further evidence that the genetic architecture of Alzheimer's disease does indeed include rare variants of intermediate penetrance, analogous to our work on rare variants in the GRN (Brouwers et al., 2008) and CLU genes (Bettens

Sylvain Lesne on Accuracy of a panel of 5 cerebrospinal fluid biomarkers in the differential diagnosis of patients with dementia and/or parkinsonian disorders.

COMMENT This new report from Kaj Blennow and Oskar Hansson's group appears to support our own findings that soluble α-synuclein levels are increased in brains of subjects with AD (Larson et al., 2012). Whether this elevation corresponds to a "leakage of

David Sulzer on Development and characterization of a new Parkinson's disease model resulting from impaired autophagy.

COMMENT The line of mice introduced in this study indicates what happens when macroautophagy is specifically blocked in dopamine (DA) neurons by deletion of Atg7, a key component of the autophagy machinery. There have been, to my knowledge, three such floxed Atg7

Kristel Sleegers

University of Antwerp
Antwerpen, Belgium

PAPER Sulzer D, Mosharov E, Talloczy Z, Zucca FA, Simon JD, Zecca L

Neuronal pigmented autophagic vacuoles: lipofuscin, neuromelanin, and ceroid as macroautophagic responses during aging and disease.

J Neurochem. 2008 Jul;106(1):24-36. PubMed: 18384642

PAPER Lazarou M, Jin SM, Kane LA, Youle RJ

Role of PINK1 binding to the TOM complex and alternate intracellular membranes in recruitment and activation of the E3 ligase Parkin.

Dev Cell. 2012 Feb 14;22(2):320-33. PubMed: 22280891

PAPER Ahmed I, Liang Y, Schools S, Dawson VL, Dawson TM, Savitt JM

Development and characterization of a new Parkinson's disease model resulting from impaired autophagy.

J Neurosci. 2012 Nov 14;32(46):16503-9. PubMed: 23152632

Gunjan Joshi

United States

Toxic Synuclein Corrupts Native in Wild-Type Mice

RESEARCH NEWS 2012-11-16 Research News The spread of toxic α-synuclein through the brain is not just for transgenic mice anymore. A new study from Virginia Lee and colleagues at the University of Pennsylvania School of Medicine, Philadelphia, suggests that toxic α-synuclein creep

PAPER Oyebode JR, Bradley P, Allen JL

Relatives' experiences of frontal-variant frontotemporal dementia.

Qual Health Res. 2013 Feb;23(2):156-66. PubMed: 23150527