Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment

@article{Terry1991PhysicalBO,
  title={Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment},
  author={Robert D. Terry and Eliezer Masliah and David P. Salmon and Nelson Butters and Richard M. DeTeresa and Robert Hill and Lawrence A. Hansen and Robert Katzman.},
  journal={Annals of Neurology},
  year={1991},
  volume={30}
}
We present here both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of 15 patients with Alzheimer's disease and 9 neuropathologically normal subjects. The statistical data show only weak correlations between psychometric indices and plaques and tangles, but the density of neocortical synapses measured by a new immunocytochemical/densitometric technique… Expand
Alzheimer’s Disease and the Aging Brain
  • R. Terry
  • Psychology, Medicine
  • Journal of geriatric psychiatry and neurology
  • 2006
TLDR
The frequencies of each of the several types of dementia are enumerated, showing that Alzheimer’s disease is present in about 80% of cases and the strongest structural correlate with cognitive tests is synapse loss, which is probably caused by Aβ oligopeptides in the terminal axons and dendrites. Expand
Synaptic pathology in the pathogenesis of Alzheimer dementia
TLDR
Data from a cohort of AD patients and other recent morphologic data do not support the hypothesis that amyloid deposition is a major pathogenic factor of both neuronal and synaptic loss in aging and AD. Expand
Alzheimer's disease-related alterations in synaptic density: neocortex and hippocampus.
TLDR
The ultrastructural studies assessing AD-related synaptic loss are reviewed and the possible compensatory changes in the synaptic complex that occur as a result of the loss in brain connectivity are reviewed. Expand
Pathological substrates of cognitive decline in Alzheimer's disease.
TLDR
The present review discusses the complex structure/function relationships in brain aging and AD within the theoretical framework of the functional neuropathology of brain aging. Expand
Neocortical neurofibrillary tangles correlate with dementia severity in Alzheimer's disease.
TLDR
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. Expand
Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment
TLDR
This study supports the concept that synapse loss is an early event in the disease process and suggests that MCI may be a transition stage between eAD and NCI with synaptic loss a structural correlate involved in cognitive decline. Expand
Correspondence amongst the PENO Test Battery Cognitive Results and Hippocampal Lesions in Alzheimer's Disease
Alzheimer’s disease (AD) is characterized by a decline of cognitive functions. Distinctive histopathological hallmarks are neuritic plaques, neurofibrillary tangles, and synaptic alterations.Expand
Synaptic Pathology in Dementia
TLDR
This chapter reviews and summarizes some of the morphological evidence for Alzheimer-related synaptic loss in the neocortex and hippocampus and suggests decline in synaptic plasticity may represent a loss of brain plasticity. Expand
Clinical correlates of cortical and nucleus basalis pathology in Alzheimer dementia.
TLDR
The specificity of pathology in cortical vs subcortical locations for predicting a particular quality of neuropsychological deficit probably reflects disruption of corticocortical connections vs derangement of the basal forebrain cholinergic system. Expand
Altered synaptic function in Alzheimer's disease.
TLDR
This review will discuss additional studies which also provide evidence of a neurotransmitter-specific pathology as well as comment on the potential explanations for the observed vulnerabilities, touching upon metabolic demand, trophic support and receptor mediated activation. Expand
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