The histopathological hallmarks of Alzheimer disease are the extracellular amyloid plaques, composed principally of the amyloid beta peptide, and the intracellular neurofibrillary tangles, composed of paired helical filaments of the microtubule-associated protein, tau. Other histopathological structures involving actin and the actin-binding protein, cofilin, have more recently been recognized. ...

The report by Oddo and colleagues in this issue of Neuron demonstrates for the first time that clearance of amyloid also results in the removal of early-stage tau pathology in mice that develop both amyloid plaques and neurofibrillary tangles (NFT), the two hallmark lesions of Alzheimer's disease (AD). This result supports a primary role for Abeta in AD etiology.

Brains from a prospective study of demented patients were investigated post mortem. Of the 27 patients with clinical diagnosis of vascular dementia, 23 showed multiple cerebral infarcts but senile plaques and neurofibrillary tangles were absent or in insignificant numbers. This gives an accuracy of 85%, a figure higher than previously documented.

Immunohistochemical studies, using a monoclonal antibody, SMP, raised in a mouse against aged human peripheral blood white cells, are described. This antibody reacts with dendritic reticulum cells in lymph node and tonsil, and, in Alzheimer brain, with argyrophilic plaques, neurofibrillary tangles, and cerebral vascular amyloid.

We examined the topography and degree of cell loss within basal ganglia structures commonly involved in progressive supranuclear palsy in order to identify any relationship between degeneration in these nuclei and gaze palsy. Serial section analyses and unbiased quantitative techniques were applied to brain tissue from six cases with progressive supranuclear palsy (four with gaze palsy and two ...

Oligomeric and fibrillar beta-amyloid (Abeta) may be toxic in Alzheimer disease (AD), especially after post-translation modification cumulative over time. Racemization of Ser and Asp residues of Abeta in senile plaques (SPs) occurs as an age-dependent process in AD. We previously reported that Abeta1-40 racemized at Ser26 is soluble and susceptible to proteolysis yielding toxic [D-Ser26]Abeta25...

Alzheimer’s disease (AD) is a neurodegenerative disease with proteopathy characterized by abnormalities in amyloid beta (Aβ) and tau proteins. Defective amyloid and tau propagate and aggregate, leading to eventual amyloid plaques and neurofibrillary tangles. New data show that a third proteopathy, an altered conformation of the scaffolding protein filamin A (FLNA), is critically linked to the a...

Over a century ago Alois Alzheimer described the importance of neurofibrillary tangles in a woman who died with dementia at the age of 55 years; plaques having already been observed in brains by Blocq and Marinesco. In the 1960s, Martin Roth and colleagues at Newcastle were first to look at the pathological basis of dementia in AD and they identified neuritic plaques and tangles as the key dete...

Introduction Alzheimer’s disease (AD) is a progressive, irreversible neurodegenerative disease associated with β-amyloid (Aβ) neuritic plaques, neurofibrillary tangles and neuronal and synaptic degeneration (Selkoe 2001; Blennow et al. 2006). AD is the leading cause of dementia among the elderly. It is characterised by progressive cognitive decline and memory loss, eventually leading to death. ...