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Thomas Wısnıewskı

Center for Neuro-Oncology

ORCID: 0000-0002-3379-8966

Publishes on Alzheimer's disease research and treatments, Prion Diseases and Protein Misfolding, Dementia and Cognitive Impairment Research. 713 papers and 36.9k citations.

713Publications
36.9kTotal Citations

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Top publicationsby citations

Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature
Peter T. Nelson, Irina Alafuzoff, Eileen H. Bigio et al.|Journal of Neuropathology & Experimental Neurology|2012
Cited by 2.1kOpen Access

Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research. Studies on human subjects with autopsy confirmation entail numerous potential biases that affect both their general applicability and the validity of the correlations. Many sources of data variability can weaken the apparent correlation between cognitive status and AD neuropathologic changes. Indeed, most persons in advanced old age have significant non-AD brain lesions that may alter cognition independently of AD. Worldwide research efforts have evaluated thousands of human subjects to assess the causes of cognitive impairment in the elderly, and these studies have been interpreted in different ways. We review the literature focusing on the correlation of AD neuropathologic changes (i.e. β-amyloid plaques and neurofibrillary tangles) with cognitive impairment. We discuss the various patterns of brain changes that have been observed in elderly individuals to provide a perspective for understanding AD clinicopathologic correlation and conclude that evidence from many independent research centers strongly supports the existence of a specific disease, as defined by the presence of Aβ plaques and neurofibrillary tangles. Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles.

Apolipoprotein E: A pathological chaperone protein in patients with cerebral and systemic amyloid
Thomas Wısnıewskı, Blas Frangione|Neuroscience Letters|1992
Cited by 800Open Access

Many biochemically diverse proteins can give rise to amyloid fibrils; however, they are all accompanied by P component and glucosaminoglycans. With antibodies specific to apolipoprotein E (apo E) we used immunohistochemical techniques to test for the presence of this protein in both cerebral and systemic amyloid. We found apo E immunoreactivity in all tested types of cerebral and systemic amyloid. In amyloid deposits apo E P, component and glucosaminoglycans may be acting as 'pathological molecular chaperones'. The latter we define as a group of unrelated proteins that induce beta-pleated conformation in amyloidogenic polypeptides.