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Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis
It is shown that TDP-43 is the major disease protein in both frontotemporal lobar degeneration with ubiquitin-positive inclusions and amyotrophic lateral sclerosis. Expand
High-Level Neuronal Expression of Aβ1–42 in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation
- L. Mucke, E. Masliah, +7 authors L. McConlogue
- Medicine, Biology
- The Journal of Neuroscience
- 1 June 2000
It is concluded that Aβ is synaptotoxic even in the absence of plaques and that high levels of Aβ1–42 are insufficient to induce plaque formation in mice expressing wild-type hAPP, supporting the emerging view that plaque-independent Aβ toxicity plays an important role in the development of synaptic deficits in AD and related conditions. Expand
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Transgenic mice that express high levels of human mutant APP support a primary role for APP/Aβ in the genesis of AD and could provide a preclinical model for testing therapeutic drugs. Expand
Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment
Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays. Expand
Neuropathological alterations in Alzheimer disease.
- A. Serrano-Pozo, M. Frosch, E. Masliah, B. Hyman
- Cold Spring Harbor perspectives in medicine
- 1 September 2011
Postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and the development of diagnostic criteria that are now used worldwide, and these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloids PET and volumetric MRI. Expand
National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease
The new guidelines recognize the pre‐clinical stage of AD, enhance the assessment of AD to include amyloid accumulation as well as neurofibrillary change and neuritic plaques, and establish protocols for the neuropathologic assessment of Lewy body disease, vascular brain injury, hippocampal sclerosis, and TDP‐43 inclusions. Expand
alpha-Synuclein is phosphorylated in synucleinopathy lesions.
It is shown by mass spectrometry analysis and studies with an antibody that specifically recognizes phospho-Ser 129 of alpha-synuclein, that this residue is selectively and extensively phosphorylated in synucleinopathy lesions and promoted fibril formation in vitro. Expand
Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders.
Results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions. Expand
Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease.
- K. Uéda, H. Fukushima, +7 authors T. Saitoh
- Biology, Medicine
- Proceedings of the National Academy of Sciences…
- 1 December 1993
Primary structure predictions indicate that the NAC peptide sequence has a strong tendency to form beta-structures consistent with its association with amyloid, and the availability of the cDNA encoding full-length NACP should help to elucidate the mechanisms of amyloidsosis in AD. Expand
S-Nitrosylated protein-disulphide isomerase links protein misfolding to neurodegeneration
It is shown that PDI is S-nitrosylated, a reaction transferring a nitric oxide group to a critical cysteine thiol to affect protein function, which prevents neurotoxicity associated with ER stress and protein misfolding in neurodegenerative disorders. Expand