The importance of neuritic plaques and tangles to the development and evolution of AD

  title={The importance of neuritic plaques and tangles to the development and evolution of AD},
  author={Pietro Tiraboschi and Lawrence A. Hansen and Leon Thal and Jody Corey-Bloom},
  pages={1984 - 1989}
Objective: To determine the relation of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) to the development and evolution of Alzheimer disease (AD). Methods: An autopsy series of 102 patients with dementia and pathologically confirmed AD and 29 normal control subjects (NCs) was studied. AD cases were stratified according to their last Mini-Mental State Examination (MMSE) before death as mild, moderate, severe, or very severe. NPs and NFTs were enumerated in the midfrontal (MF… 

Tables from this paper

Neuropathology and Cognitive Impairment in Alzheimer Disease: A Complex but Coherent Relationship

It is argued that existing data strongly support the hypothesis that both amyloid plaques and NFTs contribute to cognitive impairment, and whether individuals without antemortem cognitive impairment can harbor severe AD-type pathological findings at autopsy.

Characterization of Japanese-American men with a single neocortical AD lesion type

Neocortical variation of Abeta load in fully expressed, pure Alzheimer's disease.

A marked heterogeneity in the extent of Abeta deposition even in AD brains at final stages of disease that cannot be completely explained by a simple, regular build up of this pathologic protein in the cerebral cortex during the course of the disease is documented.

Neuritic and Diffuse Plaque Associations with Memory in Non-Cognitively Impaired Elderly.

Results suggest that decreases in cognition in elderly NCI individuals are associated with an increase in NPs and not DPs when age at death, education, gender, APOE ɛ4 status, and Braak stage are taken into consideration.

Coexisting Cholinergic and Parahippocampal Degeneration: A Key to Memory Loss in Dementia and a Challenge for Transgenic Models?

It is proposed that combining AD transgenic mouse models with additional experimental damage to both the CBF and entorhinal regions might provide a unique opportunity to further understand the evolution of the disease and improve treatments of severe cognitive dysfunction in neurodegenerative dementias.

Lesions without symptoms: understanding resilience to Alzheimer disease neuropathological changes

The heterogeneity of clinical manifestations associated with the presence of plaques and tangles is considered, and insights derived from the rare yet informative individuals who display high amounts of amyloid and tau deposition in their brains without manifesting dementia during life are focused on.

Certain new aspects of etiology and pathogenesis of Alzheimer’s disease

The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood, and that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development.

Clinicopathologic Correlations in a Large Alzheimer Disease Center Autopsy Cohort: Neuritic Plaques and Neurofibrillary Tangles "Do Count" When Staging Disease Severity

The data show that there are many important contributory causes to cognitive decline in older persons and NFTs and NPs should not be dismissed as irrelevant in AD based on clinicopathologic correlation.



Alzheimer disease without neocortical neurofibrillary tangles

Although lacking overt tangle formation, the POAD group displayed abnormal phosphorylated tau immunoreactivity in neocortical pyramidal neurons, which may contribute to cognitive decline in these subjects.

Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease

The severity of dementia was positively related to the number of NFTs in neocortex, but not to the degree of SP deposition, and N FTs accumulate in a consistent pattern reflecting hierarchic vulnerability of individual cytoarchitectural fields.

Regional distribution of neuritic plaques in the nondemented elderly and subjects with very mild Alzheimer disease.

Findings are consistent with the hypothesis that NPs are among the earliest neuropathological lesions in AD, and even very mild or questionable dementia is associated with increased density of neocortical NPs that do not distinguish between clinically questionable vs definite dementia.

Neurofibrillary tangles in nondemented elderly subjects and mild Alzheimer disease.

Neurofibrillary tangles are present in the entorhinal cortex and hippocampus of most elderly individuals irrespective of their cognitive status, but the density of NFTs increases as a function of dementia severity.

Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease

There was a substantial increase over other nondemented cases, both in the number of tangles and in the rate of increase in tangles with age, suggesting an interaction between amyloid and neurofibrillary change at this stage of Alzheimer's disease.

Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease

It is suggested that neuronal loss in association areas such as the superior temporal sulcus contributes directly to cognitive impairment in AD.

Neuritic pathology and dementia in alzheimer's disease

Quantitative analysis showed that dystrophic neurites were significantly increased in patients with AD compared with control subjects and the number of dystroph neurites and neurofibrillary tangles correlated with the clinical severity of dementia.

The decline in synapses and cholinergic activity is asynchronous in Alzheimer’s disease

The results imply an asynchronous pattern of decline of synapses and cholinergic activity, with Syn loss preceding ChAT decrements in AD, however, neither MF synapse reduction norCholinergic dysfunction appears to be an early event in AD.

Neocortical neurofibrillary tangles correlate with dementia severity in Alzheimer's disease.

Data support the notion that neocortical neuronal degeneration, as indicated by NFT formation, is a critical determinant of the clinical progression of Alzheimer's disease and suggest that medial temporal lobe structures may represent the initial site of NFT Formation.

Neocortical Lewy Body Counts Correlate with Dementia in the Lewy Body Variant of Alzheimer's Disease

It is suggested that neocortical LB combined with entorhinal NFT or subcortical Parkinson's disease- type pathology may equalize the degree of dementia seen in LBV with that encountered in classical AD.