Mary Reid on Statins Boost α-Secretase, but Not Through Cholesterol

COMMENT BRG1 and BRM are subunits of the SWI/SNF chromatin remodeling complex which have been implicated in the regulation of gene expression, cell cycle control, and oncogenesis. The Liu group [1] reports that the BAF (BRG1 associated factor) complex results in

Parhatsathid Nabadalung on Relation between aluminum concentrations in drinking water and Alzheimer's disease: an 8-year follow-up study.

COMMENT This paper fails to mention that trace amounts of other types of soluble silicates also help with excretion of aluminum, namely sodium metasilicate, sodium silicate. There is an issue of chlorine/fluoride/aluminum in water or food that may be involved in

Alexei Koudinov on Statins Boost α-Secretase, but Not Through Cholesterol

COMMENT Please see our commentary on this important study at PLoS Medicine eLetters page postmaster 0

Steven Greenberg on Exacerbation of cerebral amyloid angiopathy-associated microhemorrhage in amyloid precursor protein transgenic mice by immunotherapy is dependent on antibody recognition of deposited forms of amyloid beta.

COMMENT This very nice study confirms the finding of Matthias Jucker and colleagues [1] that anti-Aβ antibody treatment can provoke CAA-related hemorrhage, in particular, antibodies that bind to deposited rather than soluble Aβ. The mechanism remains unclear; a l

Joseph Hendrick on San Diego: γ-Secretase Takes Scientists on a Wild Ride

COMMENT In this report, Todd Golde is quoted: “'This is the most convincing demonstration yet that you can distinguish between APP and Notch cleavage." The authors continue, "This does not mean that a drug is at hand." Results presented by Bar

Elizabeth Petersen on Window to the Brain Shows Dystrophic Neurites Shrinking

COMMENT Thank you for offering such a variety of papers by people who are spending their lives looking for answers. PS: Footnotes for lay persons would help. ladybetty_8 0

Jacob Mack on Increased T cell reactivity to amyloid beta protein in older humans and patients with Alzheimer disease.

COMMENT Although it is true that immune response, and the resulting higher levels of selective immunoglobulins, are present in AD, this can only (and at best) imply immune system components. We cannot jump the gun on proposing an autoimmune response. It may be wi

William Grant on Caloric Restriction: Eat Less, Live Longer!

COMMENT As noted in Deibel et al. [1996], Grant [1997, 1999a, 1999b] and Grant et al. [2002], one of the hallmarks of Alzheimer disease (AD) is the elevation of transition metal ions (Ag, Fe, Mn, Zn, etc.), aluminum and a decrease of base cations (Ca, Mg, etc.).

J. Lucy Boyd on Spigot Closed on Industry Consulting for NIH Scientists

COMMENT I definitely have mixed emotions about this issue. If it harms the NIH's ability to recruit the best minds in our country, we have definitely lost. Surely these professionals can be trusted to conduct themselves with dignity without these new rules.

John Trojanowski on Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice.

COMMENT This paper by Brendza et al. elegantly confirms and extends previous studies by this group and others. It uses living PDAPP:Thy-1:YFP transgenic mice and multiphoton microscopy to show that passive immunization with anti-Aβ antibodies not only is able to

Frank Bernier on Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice.

COMMENT This paper by the Holtzman group supports the original work of the Bacskai/Hyman group that also showed that reduction of Aβ in the brain can induce a rapid structural recovery of existing amyloid-associated neuritic dystrophy. The originality of this new

Thomas Bayer on Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice.

COMMENT The authors used multiphoton microscopy, an elegant technique, to monitor the dynamics of neuritic plaques in living mice. They used the PDAPP;Thy-1:YFP transgenic mouse model, which develops plaque pathology and expresses yellow fluorescent protein in a

Sam Gandy on Window to the Brain Shows Dystrophic Neurites Shrinking

COMMENT "Until the Last Dog(ma) Dies": Some Neuritic Dystrophy Is Reversible by Passive Immunization of PDAPP Mice A multidisciplinary group has demonstrated that at least some neuritic dystrophy in PDAPP mice is reversible. Holtzman from Wash U, Paul f

Eugenia (Jania) Trushina on Altered cholesterol metabolism in Niemann-Pick type C1 mouse brains affects mitochondrial function.

COMMENT It is always fascinating to think why, in neurodegenerative disorders characterized by the loss of neurons in completely different regions, the signs of neuronal dysfunction are similar. Why do neurons display similar symptoms of degeneration despite very

Nikolaos K. Robakis on Neuronal dysfunction in a polyglutamine disease model occurs in the absence of ubiquitin-proteasome system impairment and inversely correlates with the degree of nuclear inclusion formation.

COMMENT This paper reports additional evidence that nuclear inclusions of polyglutamine-containing proteins may actually be protective because they may segregate and inactivate the free mutant proteins (for example, huntingtin), which may be more toxic to the cel