Research summary
Output centres on neuropathology and biological frameworks for Alzheimer's disease and related neurodegenerative disorders. A linear and multivariate analysis of 15 Alzheimer-disease patients and 9 neuropathologically normal controls established that neocortical synapse density (measured by a then-new immunocytochemical/densitometric technique) correlates with three global neuropsychological tests far more strongly than plaque or tangle density, with midfrontal and inferior parietal synapse density emerging as primary predictors in stepwise regression [3]. TDP-43 was identified as the major disease protein in ubiquitin-positive tau-negative alpha-synuclein-negative inclusions characteristic of both frontotemporal lobar degeneration and amyotrophic lateral sclerosis; pathologic TDP-43 was hyperphosphorylated, ubiquitinated, and cleaved to C-terminal fragments and was recovered only from affected CNS regions [2]. A review of Alzheimer-disease neuropathology described the positive lesions (amyloid plaques, cerebral amyloid angiopathy, neurofibrillary tangles, glial responses) and negative lesions (neuronal and synaptic loss), the staging of amyloid and tangle pathology, and clinicopathological correlation underpinning current diagnostic criteria [5]. NIA-AA neuropathologic-assessment guidelines updated 1997 criteria to recognize the preclinical stage, integrate amyloid accumulation alongside neurofibrillary change and neuritic plaques, and add protocols for Lewy-body disease, vascular brain injury, hippocampal sclerosis, and TDP-43 inclusions [6]. A literature review on neuropathologic-cognitive correlations highlighted the biases of autopsy-confirmed studies and the contribution of co-existing non-AD lesions in advanced age [7]. The NIA-AA Research Framework redefined AD biologically through underlying pathologic processes documented in vivo, intended for observational and interventional research rather than routine clinical care [1]. Diagnostic and management criteria for dementia with Lewy bodies incorporated MIBG myocardial scintigraphy, refined pathologic categories, and recommended clinical management based largely on expert opinion [4]. Methodologically the corpus combines quantitative neuropathological measurement with consensus criteria development.
Recent publications
- NIA鈥怉A Research Framework: Toward a biological definition of Alzheimer's diseaseDOI
- Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral SclerosisDOI
- Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairmentDOI
- Diagnosis and management of dementia with Lewy bodiesDOI
- Neuropathological Alterations in Alzheimer DiseaseDOI
- National Institute on Aging鈥揂lzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's diseaseDOI
- National Institute on Aging鈥揂lzheimer鈥檚 Association guidelines for the neuropathologic assessment of Alzheimer鈥檚 disease: a practical approachDOI
- Alzheimer-type neuropathology in transgenic mice overexpressing V717F 尾-amyloid precursor proteinDOI
- 伪-Synuclein is phosphorylated in synucleinopathy lesionsDOI
- Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the LiteratureDOI
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Email Eliezer Masliah 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
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External profiles
- ORCID: https://orcid.org/0000-0002-2117-5569
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Kyoto University faculty directory). Last refreshed 2026-05. Report incorrect information.