How Does Excess Aβ Leave the Brain, How Does It Get In, And Can We Trap It Outside?

• 1 Comment

23 Jun 2003

1998;70:210-215. Abstract 18. Mackic JB, Bading J, Ghiso J, Walker L, Wisniewski T, Frangione B, Zlokovic BV.

New Frontier: Developing Outcome Measures for Pre-dementia Trials

• 3 Comments

09 Apr 2013

lengths for clinical trials of potential disease-modifying therapies in MCI would be one year, 18 months,

Alzheimer's: A Triple Whammy. Why are So Many Neurodegenerative Diseases Single, Double, or Triple Amyloidoses?

• 1 Comment

22 Oct 2003

tauists and baptists finally shake hands? Trends Neurosci. 2002 Jan ;25(1):22-6. Abstract 18. Soto C.

Cerebrometabolic Deficiency in Alzheimer's Disease

• 2 Comments

22 Apr 2002

J Neural Transm 1998;(105):415-422. Abstract. 18. Sorbi S, Bird ED, Blass JP. Decreased pyruvate

A "Mitochondrial Cascade Hypothesis" for Sporadic Alzheimer's Disease

24 Sep 2004

I'll read your paper Hemachandra We looked at time course (two months, 12 months, 18 months, and 24

Slow Aβ; Clearance Is ApoE4’s Modus Operandi in Late-Onset AD

26 Jul 2011

number one genetic risk factor for late-onset Alzheimer’s disease (see AlzGene Top Results), yet 18 years

The Pathogen Hypothesis

• 1 Comment

24 Nov 2008

J Pathol. 2008 Sep 18. Abstract   References [1] Balin BJ, Gerard HC, Arking EJ, Appelt DM, Branigan PJ,

Novel Substrates for BACE1 Beg the Question: What's the Biological Function of β-Secretase?

17 Dec 2003

limits amyloid beta-peptide production. J Biol Chem. 2002 Feb 15;277(7):5637-43. Abstract 18.

The Functional Roles of APP Cytoplasmic Domain—Conflicts and Consensus

21 Dec 2006

Atlanta (Tuesday, October 18, 8:30 a.m.). Some of the items up for discussion will include the following:

The Pathogen Hypothesis—Challenging the Primacy of Genetics in Late-Onset Alzheimer Disease.

• 5 Comments

22 Jan 2006

We invite you to participate in this "offline" Forum Discussion led by Brian Balin (Philadelphia College of Osteopathic Medicine). This discussion will extend our previously held live discussion on the Pathogen Hypothesis of Alzheimer Disease. T

Intracellular Aβ in Alzheimer's Disease

• 3 Comments

16 May 2000

Gunnar Gouras led this live discussion on 16 May 2000. Readers are invited to submit additional comments by using our Comments form at the bottom of the page. Transcript: Live discussion held 16 May 2000.   Participants: Bruce Yankner, Huaxi Xu, Austin Ya

Are Glia Active Participants in Neurodegenerative Disease?

• 1 Comment

05 Dec 2005

Ben Barres led the first in a series of Alzforum discussions about the role of glial cells in Alzheimer’s and other neurodegenerative diseases. It has become trendy to say that glia are more than just glue, but in reality, science has not yet advanced sig

Generation of an Apoptotic Intracellular Peptide by γ-secretase Cleavage of Alzheimer's β-amyloid Precursor Protein

20 Sep 2000

cleavage of poly [ADR-ribose] polymerase (PARP) by cell death protease known as caspases (18) also

RNAi in Neurodegenerative Diseases—What's the Therapeutic Potential?

18 Mar 2003

Medical School, Worcester, MA 01605 Zuoshang Xu led this live discussion on 18 March 2003. Readers are

From Epidemiology to Therapeutic Trials with Anti-inflammatory Drugs in Alzheimer's Disease: The Role of NSAIDs and Cyclooxygenase on Beta-amyloidosis and Clinical Dementia

• 4 Comments

20 Mar 2002

Giulio Maria Pasinetti led this live discussion on 20 February 2002. Readers are invited to submit additional comments by using our Comments form at the bottom of the page.   See Related News Story: NO-Releasing NSAID Reduces β-Amyloid, Activates Microgli