Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664.

Behavioural brain research - 22 Aug 2008

Galvan Veronica, Zhang Junli, Gorostiza Olivia F, Banwait Surita, Huang Wei, Ataie Marina, Tang Huidong, Bredesen Dale E

Abstract excerpt

The deficits of Alzheimer's disease (AD) are believed to result, at least in part, from neurotoxicity of beta-amyloid (Abeta), a set of 38-43 amino acid fragments derived from the beta-amyloid precursor protein (APP). In addition, APP generates the APP-C31 and Jcasp toxic fragments intracellularly by cleavage at Asp664. We reported that mutation of Asp664 to Ala in a FAD-human APP transgene prevented AD-like...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alanine
Share to Amyloid beta-Protein Precursor

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Aspartic Acid

Share to Glial Fibrillary Acidic Protein

Share to Maze Learning

Share to Mental Disorders

Share to Reaction Time

Share to Swimming

Source

Open in PubMed Open full text

Identifiers

PMID: 18485495
DOI: 10.1016/j.bbr.2008.03.035
PMCID: PMC2757410

Genes

APP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 11 closest

Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664.PMID 18485495Read ↗

Reversal of Alzheimer's-like pathology and behavior in human APP transgenic mice by mutation of Asp664Semantic proximity Read ↗

Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein.Semantic proximity Read ↗

Treatment with an Amyloid-β Antibody Ameliorates Plaque Load, Learning Deficits, and Hippocampal Long-Term Potentiation in a Mouse Model of Alzheimer's DiseaseSemantic proximity Read ↗

Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouseSemantic proximity Read ↗

Effect of the Icelandic Mutation APPA673T in the Murine APP Gene on Phenotype of Line 66 Tau Mice.Semantic proximity Read ↗

The effect of the Icelandic mutation APP <sup>A673T</sup> in the line 66 model of tauopathySemantic proximity Read ↗

Active beta-amyloid immunization restores spatial learning in PDAPP mice displaying very low levels of beta-amyloid.Semantic proximity Read ↗

Behavioral characterization of the Tg2576 transgenic model of Alzheimer's disease through 19 months.Semantic proximity Read ↗

Decreased behavioral impairments in an Alzheimer mice model by interfering with TNF-alpha metabolism.Semantic proximity Read ↗

Dendritic spine loss in the hippocampus of young PDAPP and Tg2576 mice and its prevention by the ApoE2 genotype.Semantic proximity Read ↗

Behavioral Assessment of Alzheimer's Transgenic Mice Following Long-Term A β Vaccination: Task Specificity and Correlations between A β Deposition and Spatial MemorySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.