MUTATIONS MAPT 44071294 GRCh37/hg19 rs62063845 T C Exon 8 Point, Silent Coding Unknown. Not applicable. T504T Frontotemporal Dementia: BenignNone This variant resides in exon 8, which is excluded from the majority of tau isoforms. Exon 8 is included in transcripts

PAPER Swainston Harrison T, Perry CM

Aripiprazole: a review of its use in schizophrenia and schizoaffective disorder.

Drugs. 2004;64(15):1715-36. PubMed: 15257633

PAPER Costentin J

[A new approach to antischizophrenic therapeutics: D2 dopamine receptor partial agonists].

Ann Pharm Fr. 2009 Sep;67(5):310-9. Epub 2009 Jul 18 PubMed: 19695367

Virgil Muresan on Loss of c-Jun N-terminal kinase-interacting protein-1 does not affect axonal transport of the amyloid precursor protein or Aβ production.

COMMENT In this paper, Vagnoni et al. reassess the role of c-Jun N-terminal kinase (JNK)-interacting protein-1 (JIP-1) in the transport, phosphorylation, and amyloidogenic processing of Aβ precursor protein (APP). Specifically, they ask whether the axonal transpo

Sara Sanz-Blasco on Picomolar Amyloid-β Peptides Enhance Spontaneous Astrocyte Calcium Transients.

COMMENT This manuscript complements, in a very good way, work we recently published (Talantova et al., 2013),describing for first time the important role of astrocytic α7-nAChRs in Aβ amyloid calcium dysregulation and toxicity. 0 sarasanzb Aβ induces astrocytic g

PAPER Tagliavini F, Rossi G, Padovani A, Magoni M, Andora G, Sgarzi M, Bizzi A, Savoiardo M, Carella F, Morbin M, Giaccone G, Bugiani O

A new βPP mutation related to hereditary cerebral haemorrhage

Alzheimer's Rep, 1999;2(Suppl 1):S28.

Simi Howard on Antibodies Stop Toxic Tau in Its Extracellular Tracks

COMMENT This is a very interesting paper. Regarding phosphorylated tau that has been shown to be secreted via various mechanisms from dendrites (e.g., via exosomes in association with proteins such as fyn), does anyone know whether the focal tau deposits immobili

Sanjay Pimplikar on More Evidence for AD Starting Without Brain Amyloid

COMMENT The significance of these findings, which now validate the phenomenon of SNAP, cannot be overstated. In 2009, based on the data then available, I suggested that amyloid is not the cause of AD, but a cause of AD (Pimplikar, 2009), and that amyloid-independ

PDGF-APPSw,Ind (line J9)

RESEARCH MODELS Summary Like the J20 mice, these mice over-express human APP with the Swedish and Indiana mutations. Transgene expression level is relatively low in J9 mice, approximately half the expression seen in J20 mice. Compared with J20 mice, J9 mice develop amylo

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Pathway Analysis of ChIP-Seq-Based NRF1 Target Genes Suggests a Logical Hypothesis of their Involvement in the Pathogenesis of Neurodegenerative Diseases.

Comparison of Neuroprotective Effects of Melissa officinalis Total Extract and Its Acidic and Non-Acidic Fractions against A β-Induced Toxicity.

Fragment-based Binding Efficiency Indices in Bioactive Molecular Design: A Computational Approach to BACE-1 Inhibitors.

Alzheimer's disease risk assessment using large-scale machine learning methods.

[Autonomy or compassion? Values to be taken into account in the treatment of patients suffering Alzheimer's disease].

Family composition and expressions of family-focused care needs at an academic memory disorders clinic.

MAPT T504T