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Neuroinflammation plays an important role in the pathological cascade of Alzheimer's disease (AD) along with aggregation of extracellular amyloid-β (Aβ) plaques and intracellular aggregates of tau protein. In animal models of amyloidosis, local immune activation is centered around Aβ plaques, which are usually of uniform morphology, dependent on the transgenic model used. In postmortem human brains a diversity of Aβ plaque morphologies is seen including diffuse plaques (non-neuritic plaques, non-NP), dense-core plaques, cotton-wool plaques, and NP.

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The objective of the study was to demonstrate whether athletes, players, boxers and military personnel can really be victims of Chronic traumatic encephalopathy (CTE), and to elucidate this pathology. In 53 articles, 14 were selected for qualitative synthesis in the results table that addresses CTE in football, soccer and rugby players, boxers and the military. Neuropathologically, CTE shows cerebral atrophy, a pelvic septum cavity with fenestrations, dense diffuse immunoreactive inclusions and a TDP-43 proteinopathy.

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Background: Amyloid-β proteins, a hallmark of Alzheimer's disease, are believed to play an adaptive role in the cerebral immune response.

Objective: Amyloid is believed to play a role in cerebral immune response and could play a similar role in response to air pollution exposures. In the present study, we examined whether WTC exposure duration was associated with cerebral amyloidosis in WTC responders.

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Post-mortem neuropathology of idiopathic rapid eye movement sleep behaviour disorder: a case series.

Lancet Neurol

December 2024

Neurological Tissue Bank of the Biobank, FRCB-IDIBAPS, Hospital Clínic de Barcelona, Universitat de Barcelona, Barcelona, Spain; Department of Pathology, Biomedical Diagnostic Center (CDB), Hospital Clínic de Barcelona, Universitat de Barcelona, Barcelona, Spain.

Article Synopsis
  • The study examines post-mortem brain tissues from individuals diagnosed with idiopathic REM sleep behavior disorder (IRBD) to investigate its potential link to neurodegenerative diseases, specifically focusing on signs of neuronal loss and the presence of key protein deposits.
  • Researchers analyzed samples from 20 participants, most of whom were diagnosed with Lewy body disease, while a small number had Parkinson's disease-related conditions, revealing significant findings of neuronal damage associated with α-synuclein proteins, particularly in brain regions controlling REM sleep.
  • While the sample size limited the statistical analysis, the outcomes suggest a strong correlation between IRBD and neurodegenerative diseases, emphasizing the importance of these pathological features for understanding the progression
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Protein tau phosphorylation in the proline rich region and its implication in the progression of Alzheimer's disease.

Exp Neurol

January 2025

Laboratorio Cajal de Circuitos Corticales, Centro de Tecnología Biomédica, Universidad Politécnica de Madrid, Campus Montegancedo S/N, Pozuelo de Alarcón, 28223 Madrid, Spain; Departamento de Química y Bioquímica, Facultad de Farmacia, Universidad San Pablo-CEU, CEU Universities, Urbanización Montepríncipe, 28660, Boadilla del Monte, Madrid, Spain. Electronic address:

Tau has a wide variety of essential functions in the brain, but this protein also plays a determining role in the development of Alzheimer's disease (AD) and other neurodegenerative diseases called tauopathies. This is due to its abnormal aggregation and the subsequent formation of neurofibrillary tangles. Tau hyperphosphorylation appears to be a critical step in its transformation into an aggregated protein.

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