Michael Schlossmacher on Alpha-synuclein locus duplication as a cause of familial Parkinson's disease.
COMMENT in this comment fits in logical succession with the body of work on gene dosage. It revisits the
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George Martin on The MAP2/Tau family of microtubule-associated proteins.
COMMENT Trainees wanting a succinct overview of the MAP2/Tau family of microtubular-associated proteins should start here. They should be aware, however, to expect larger numbers of interacting partners than the list in Table 2. Pathophysiology is not within the
Michael Wolfe on Identification of a new presenilin-dependent zeta-cleavage site within the transmembrane domain of amyloid precursor protein.
COMMENT The findings in the paper by Zhao and colleagues are intriguing: The presence of a 46-residue form of Aβ inside the cell, but not secreted, raises the question of whether this longer, presumably more amyloidogenic Aβ might serve as a nidus for intracellul
Andrew Singleton on Dopaminergic dysfunction in unrelated, asymptomatic carriers of a single parkin mutation.
COMMENT I think this will be a well-cited paper; the authors have performed a large amount of work, 18F-dopa PET scanning of 13 apparently asymptomatic carriers of single heterozygous parkin mutations. This is not the first paper to tackle this subject but it is
Suzana Petanceska on Statins Boost α-Secretase, but Not Through Cholesterol
COMMENT Gary Landreth's paper in the current issue of The Journal of Neuroscience on statins reducing Aβ-induced microglial inflammatory responses is very elegant work (Cordle and Landreth, 2005). This study shows that statin treatment of microglia and monoc
Mary Michaelis on Microtubule-binding drugs offset tau sequestration by stabilizing microtubules and reversing fast axonal transport deficits in a tauopathy model.
COMMENT This paper describing the effects of Taxol on axonal transport deficits in a tauopathy mouse model represents a milestone in drug discovery efforts for a number of reasons, not the least of which is the targeting of tau rather than amyloid neurofibrillary
Luigi Puglielli on Statins Boost α-Secretase, but Not Through Cholesterol
COMMENT Since the appearance of the first epidemiological and animal studies claiming a connection between cholesterol and Alzheimer disease, at least four different aspects of cholesterol metabolism have been directly linked to AD neuropathology: (i) clustering
Kate Webber on GSK-3—A Peripheral Marker for AD?
COMMENT Peripheral Diagnosis of Signaling Intermediates in Alzheimer Disease The need for accurate diagnostics in Alzheimer disease is one of the most pressing issues in the field today, and this is especially true for diagnostic tools, which employ easily attain
Benjamin Wolozin on Statins Boost α-Secretase, but Not Through Cholesterol
COMMENT Statins are known to increase secretion of APP, but the mechanism by which this occurs is poorly understood [1]. The current manuscript by Pedrini et al. focuses on the effect of statins on Rho and Rho-associated coiled-coil containing kinase 1 (ROCK). Th
Lon S. Schneider on Glucose metabolism in patients with schizophrenia treated with atypical antipsychotic agents: a frequently sampled intravenous glucose tolerance test and minimal model analysis.
COMMENT Antipsychotic medications include haloperidol, thiothixine, trifluoperazine, perphenazine, thioridazine, and then the newer antipsychotics, clozapine, risperidone, olanzapine, quetiapine, ziprasidone, and aripiprazole. The latter are called “atypical” or
Andrew Singleton on Failure to find alpha-synuclein gene dosage changes in 190 patients with familial Parkinson disease.
COMMENT Further evidence that α-synuclein gene dosage mutations are rare In this simple paper, the authors screened for SNCA gene dosage mutations in a cohort of 190 unrelated PD patients who presented with a positive family history. No mutations were identified,
William Glimm on Alzheimer's disease: the two-hit hypothesis.
COMMENT This article is original, well thought out, persuasive in its logic. 0 bill.glimm
Raphael Kopan on Notch-1 activation and dendritic atrophy in prion disease.
COMMENT This paper describes a correlation between prion infection and increase in NICD. To establish a causative role for Notch in the pathology, the authors reproduce the observations establishing that Notch can control neurite outgrowth in cell lines. These tw
Michael Wolfe on Notch-1 activation and dendritic atrophy in prion disease.
COMMENT This article shows that the Notch intracellular domain (NICD), the proteolytic fragment that mediates signaling from the Notch receptor, is increased in prion-infected CD1 mice, and this increase correlates with dendritic atrophy. Moreover, cultured neuro
Carlos Saura on Notch-1 activation and dendritic atrophy in prion disease.
COMMENT Notch signaling is a highly conserved pathway that plays essential roles in cell proliferation and differentiation. It is unclear, however, whether Notch-1 signaling does participate in cellular events leading to neurodegeneration. In this, S. J. DeArmond