The Neuroplasticity Theory of Alzheimer's Disease
neurofibrillary tangles. The neurofilaments appear to clog dendrite segments (Ashford et al., 1998), which leads
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Vascular Disease, Parkinson's, and Now Alzheimer's—Is Homocysteine the New All-Around Bad Guy?
levels and neuropathologically pure AD (Clarke et al., 1998). That is, the homocysteine-AD link seems to
How the Other Half Lives—Or the What, How, and Where of the AβPP Intracellular Domain
One paper showed Ab to bind to APP. Does this seem reasonable? (See Lorenzo, et al., Nature Neurosci
Intraneuronal Aβ Accumulation—More Evidence, Less Controversy?
out there! (See Jaworska-Wilczynska et al., 2002.) Jorge Busciglio Gunnar, you see particularly
Axonal Transport Hypothesis Moves On to Implicate Presenilin
(Cai et al., 2002; Naruse et al., 1998; ARF related news story). One way in which PS1 might modulate
How Does Excess Aβ Leave the Brain, How Does It Get In, And Can We Trap It Outside?
hypothesis of Ab and related Ab-lowering strategies in more breadth and detail. Synposis of Deane et al
Is Alzheimer's an Autoimmune Disease?
neurons that light up. Dara Dickstein We have recently published in Microcirculation (Ujiie et al., 2003)
Androgens, ApoE, and Alzheimer's Disease
This discussion was produced in collaboration with SAGE KE. Jacob Raber led this live discussion on 7 May 2004. Readers are invited to submit additional comments by using our Comments form at the bottom of the page. Transcript unavailable. Background Text
Alzheimer's Disease: A Re-examination of the Amyloid Hypothesis
apoptosis even when Aβ 42 was not produced from them. Peter Nelson: And yet, La Ferla et al. showed that
Is Alzheimer's a Type 3 Diabetes?
Einstein College of Medicine in 1997 (see Heitner et al., 1997) and found nothing, but it was spotty
Are Glia Active Participants in Neurodegenerative Disease?
injury (see Bush et al., 1999). Gabrielle Strobel And I believe Tony Wyss-Coray has data on active
Probing PPARγ? Agonists: Could Diabetes Drugs Treat Alzheimer's Disease?
Jiang et al., 1998), together with the commercial availability of PPARγ agonists, has raised interest in
The Pathogen Hypothesis
associated mental impairment in mice (see Aleksandrova et al., 2004). Thus the need for many more controls to
Are Neurons Just Too Laissez-Faire about Repair?
do not efficiently repair the bulk of their genome (see, for example, Gobbel et al., 1998). Neurons
Clearing the Fog Around Aβ Oligomers
concentrations (see ARF related news story and Lambert et al., 1998). Soon, numerous other labs fingered Aβ
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