Microglia Activation—Venusberg Meeting Questions M1, M2 Designations

CONFERENCE COVERAGE 2013-03-14 Conference Coverage In England, the M1 and the M2 motorways take you in almost opposite directions. Does the same happen in the brain? In-vitro, microglia can be driven to adopt M1 and M2 phenotypes, with M1 believed primed to drive inflammation and M2 to ...

Tau, α-Synuclein Spread: Crazy Stuff—How Might It Work?

CONFERENCE COVERAGE 2013-03-18 Conference Coverage Read a PDF of the entire series. More and more researchers believe that a neurodegenerative condition’s slow, inexorable takeover of a person’s brain might be driven by pathogenic, misfolded proteins that spread through interconnected ...

Blessing or Curse? Peripheral Cytokines in the Brain

CONFERENCE COVERAGE 2013-03-22 Conference Coverage More friendly border than iron curtain, the blood-brain barrier lets all sorts of legitimate travelers pass. Could it also be letting some unsavory characters slip by? The subject of crosstalk between the peripheral circulation and the ...

ALS: Many Disparate Diseases, or Just Two?

RESEARCH NEWS 2011-08-12 Research News Amyotrophic lateral sclerosis is a many-headed beast: Several genes can cause it, or no genes at all, and several cell types are involved beyond the motor neurons that actually degenerate. Scientists hoping to slay the monster still need to ...

Going It Alone—APP, BACE1 Take Distinct Routes to Endosome

RESEARCH NEWS 2011-08-12 Research News Rather than tackle a criminal in your bedroom, why not prevent him from entering your home? That’s the therapeutic takeaway from a new study on intracellular trafficking of amyloid-β precursor protein (APP) and the protease that slashes it ...

Traffic Control—Curb Endocytosis to Curb AD Pathogenesis?

RESEARCH NEWS 2011-10-28 Research News One study views Aβ production as a normal part of synaptic plasticity, while another starts with the premise that Aβ buildup in neurons is a bad thing. Yet from these divergent starting points, both arrive at a similar conclusion—the ...

DC: Where Does TDP-43’s Toxic End Really Come From?

CONFERENCE COVERAGE 2011-11-25 Conference Coverage Clearly, the C-terminal of TDP-43 has something to do with amyotrophic lateral sclerosis (ALS). The toxic fragments appear as aggregating, 25- and 35-kiloDalton (kDa) species that supposedly result from cleavage by caspase 3 or another ...

TDP-43 Hangs Out With NF-κB, Puts Innate Immunity Into Hyperdrive

RESEARCH NEWS 2011-12-02 Research News TAR DNA binding protein 43, the RNA-binding protein linked to amyotrophic lateral sclerosis, is in the middle of an abnormal innate immune response that compromises the spinal cord of people with the disease, according to a paper published ...

DC: What’s That New Stuff in and Around Nuclei of AD Cells?

CONFERENCE COVERAGE 2011-12-09 Conference Coverage At this year’s annual meeting of the Society for Neuroscience, the number of mini- and nano-symposia dedicated to the molecular stalwarts of Alzheimer’s disease, Aβ and tau, was strikingly down. The trend may reflect both the field’s ...

SOS: Motor Neurons Send Angiogenin Cry for Help to Astroglia

RESEARCH NEWS 2012-04-16 Research News Floundering motor neurons rely on a support network for help, and they send out a distress call to astroglia in the form of angiogenin, report the authors of a paper in the April 11 Journal of Neuroscience. Angiogenin, a candidate gene for ...

Keystone: TBI—Learning From Markers, Models, and Diseases

CONFERENCE COVERAGE 2012-05-09 Conference Coverage Alzforum thanks Sam Gandy, Soong Ho Kim, and Effie Mitsis at Mount Sinai School of Medicine for preparing this meeting summary, edited by Tom Fagan. Injury to the brain, even what might be considered mild, can have devastating ...

Boost APP Ubiquitination, Wnt Signaling to Stave Off AD?

RESEARCH NEWS 2012-03-09 Research News The prevailing theory that Aβ peptides are a major culprit in Alzheimer’s disease offers no shortage of possible therapeutic approaches—two of which make the pages of this week’s Journal of Neuroscience. Patricia Salinas and colleagues at ...

San Diego: Tau Oligomer Antibodies Relieve Motor Deficits in Mice

CONFERENCE COVERAGE 2010-11-25 Conference Coverage Mirroring a trend in amyloid-β research, work on the tau protein seems to be moving from tangles toward that infamous “O” word—oligomers. At this year’s annual meeting of the Society for Neuroscience (SfN), held 13-17 November in San ...

San Diego: Pilin’ on the Pyro, Aβ Going Rogue

CONFERENCE COVERAGE 2010-11-29 Conference Coverage What causes Aβ to go rogue in Alzheimer’s disease? Some researchers believe that a modified, pyroglutamate form of Aβ is to blame. Pyroglutamate Aβ, first discovered almost 20 years ago, heated up as a research topic in recent years, ...

San Diego: Aβ Oligomers Seen, With ApoE, at Synapses of Human Brain

CONFERENCE COVERAGE 2010-12-06 Conference Coverage Apolipoprotein E is the strongest genetic risk factor for late-onset Alzheimer’s disease, accounting for more than 95 percent of cases. But despite decades of research, it is still not clear how it ties in with AD etiology. At the ...

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