Correlations of synaptic and pathological markers with cognition of the elderly
References (47)
- et al.
Cholinergic fiber loss occurs in the absence of synaptophysin depletion in Alzheimer's disease primary visual cortex
Neurosci. Lett.
(1992) - et al.
Morphological adaptive response of the synaptic junctional zones in the human dentate gyrus during aging and Alzheimer's disease
Brain Res.
(1990) - et al.
Occurrence of neuropil threads in the senile human brain and in Alzheimer's disease: A third location of paired helical filaments outside of neurofibrillary tangles and neuritic plaques
Neurosci. Lett.
(1986) - et al.
Alteration in the pattern of nerve terminal protein immunoreactivity in the perforant pathway in Alzheimer's disease and in rats after entorhinal lesions
Neurobiol. Aging
(1992) - et al.
Reduced GAP-43 message levels are associated with increased neurofibrillary tangle density in the frontal association cortex (area 9) in Alzheimer's disease
Neurobiol. Aging
(1992) - et al.
A quantitative morphometric analysis of the neuronal and synaptic content of the frontal and temporal cortex in patients with Alzheimer's disease
J. Neurol. Sci.
(1987) - et al.
Large amounts of neocortical beta/A4 deposits without neuritic plaques nor tangles in a pyschometrically assessed, nondemented person
Neurosci. Lett.
(1990) - et al.
Beta-amyloid deposition and paired helical filament formation: Which histopathological feature is more significant in Alzheimer's disease?
Neurobiol. Aging
(1989) - et al.
Regional synaptic pathology in Alzheimer's disease
Neurobiol. Aging
(1992) - et al.
Monoclonal antibodies to study the brain in schizophrenia
Brain Res.
(1989)
Alzheimer's disease and aging: Effects on perforant pathway perikarya and synapses
Neurobiol. Aging
Immunohistochemical quantification of the synapse-related protein synaptophysin in Alzheimer disease
Neurosci. Lett.
Dendritic degeneration and regrowth in the cerebral cortex of patients with Alzheimer's disease
J. Neurol. Sci.
Quantitative assessment of cortical synaptic density in Alzheimer's disease
Neurobiol. Aging
Observations on the brains of nondemented old people
J. Neurol. Sci.
Plaques, tangles and dementia: A quantitative study
J. Neurol. Sci.
Structural plasticity of synapses in Alzheimer's disease
Mol. Neurobiol.
A simple dot-immunobinding assay for quantification of synaptophysin-like immunoreactivity in human brain
J. Histochem. Cytochem.
Women, myocardial infarction, and dementia in the very old
Neurology
The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects
Br. J. Psychiatry
Clinicopathologic studies in dementia: Nondemented subjects with pathologically confirmed Alzheimer's disease
Neurology
Pathological markers associated with normal aging and dementia in the elderly
Ann. Neurol.
TG3: A better antibody than Alz-50 for the visualization of Alzheimer-type neuronal pathology
Soc. Neurosci. Abstr.
Cited by (375)
Preventing amyloid-β oligomerization and aggregation with berberine: Investigating the mechanism of action through computational methods
2024, International Journal of Biological MacromoleculesPresubiculum principal cells are preserved from degeneration in knock-in APP/TAU mouse models of Alzheimer's disease
2023, Seminars in Cell and Developmental BiologyGenetic deletion of α7 nicotinic acetylcholine receptors induces an age-dependent Alzheimer's disease-like pathology
2021, Progress in NeurobiologyCitation Excerpt :The Cholinergic Hypothesis (Appel, 1981) has been supported by several evidences indicating that cholinergic transmission is affected in early AD. Indeed, loss of cholinergic neurons in the nucleus basalis of Meynert, decrease of choline acetyltransferase (ChAT) activity and reduction of nicotinic receptors (nAChRs) have been highly correlated with dementia and its progression (Burghaus et al., 2000; Dickson et al., 1995; Engidawork et al., 2001; Kuhn et al., 2015; Mufson et al., 2007; Strada et al., 1992; Whitehouse et al., 1981). On the other hand, the Aβ Hypothesis (Hardy and Allsop, 1991) posits that the increase and accumulation of Aβ represent the primum movens in AD pathophysiology, responsible of synaptic dysfunction triggering downstream events leading to dementia [reviewed in (Gulisano et al., 2018a)].
Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease
2021, Molecular and Cellular NeurosciencePresenilin 1 increases association with synaptotagmin 1 during normal aging
2020, Neurobiology of Aging