Familial Alzheimer's disease with the amyloid precursor protein position 717 mutation and sporadic Alzheimer's disease have the same cytoskeletal pathology
References (20)
- et al.
The purification of tau protein and the occurrence of two phosphorylation states of tau in brain
J. Biol. Chem.
(1984) - et al.
Antibodies raised against different portions of A4 protein identify a subset of plaques in Down's syndrome
Neurosci. Lett.
(1990) - et al.
Defined neurofilament, ι, and β-amyloid precursor protein epitopes distinguish Alzheimer from non-Alzheimer senile plaques
- et al.
The distribution of tau in the mammalian central nervous system
J. Cell. Biol.
(1985) - Brion, J.-P., Hanger, D.P., Couck, A.-M. and Anderton, B.H., A68 proteins in Alzheimer's disease are composed of...
- et al.
Characterization of a partial cDNA specific for the high molecular weight microtubule-associated protein MAP2 that encodes epitopes shared with paired helical filaments of Alzheimers Disease
Dementia
(1990) - et al.
A4 amyloid protein deposition and the diagnosis of Alzheimer's disease: prevalence in aged brains determined by immunocytochemistry compared with conventional neuropathologic techniques
Neurology
(1988) - et al.
Diffuse Lewy body disease: light and electron microscopic immunochemistry of senile plaques
Acta Neuropathol.
(1989) - et al.
Effects of injected Alzheimer β-amyloid cores in rat brain
- et al.
Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease
Nature
(1991)
Cited by (85)
Cerebral Small Vessel Disease in Sporadic and Familial Alzheimer Disease
2021, American Journal of PathologyCitation Excerpt :The most common type of CAA is Aβ angiopathy, which is reported to be as high as 90% in AD.105 The majority of pathologically verified familial AD subjects exhibit CAA.47,56,106–153 The first case in Argentina with marked vascular pathology including CAA carried the APP Ala171Thr mutation.154
Contribution of Alzheimer's disease neuropathologic change to the cognitive dysfunction in human brains with Lewy body–related pathology
2020, Neurobiology of AgingCitation Excerpt :Despite these findings, it is still unclear whether the cooccurrence of LRP and ADNC results from synergistic interaction or distinct independent processes. On the one hand, there is evidence that patients with amyloid precursor protein mutation (at codon 717) can also present cortical LB deposition (Lantos et al., 1992), and both amyloid plaque and LB can stain with antibody to N-terminus portion of amyloid precursor protein (Van Gool et al., 1995), which supports the hypothesis of synergistic interaction between LRP and ADNC; on the other hand, there is no significant correlation between the densities of LRP and ADNC in cortical and limbic regions (Armstrong et al., 2000; Kazee and Han, 1995), which makes them appear to be 2 distinct processes. A faster decline of cognitive function due to ADNC has been noticed in patients with LBD (Malek-Ahmadi et al., 2019).
A systematic review of familial Alzheimer's disease: Differences in presentation of clinical features among three mutated genes and potential ethnic differences
2016, Journal of the Formosan Medical AssociationCitation Excerpt :We have included an unreported pedigree with p.His163Arg missense mutation of PSEN1 diagnosed in Hong Kong, including two affected family members: a female patient with AOO at 42 years and a male patient with AOO at 41 years. The combined dataset contains 658 pedigrees, 1890 individuals, of whom 790 were affected by FAD with known AOO7–94 (please refer to supplementary materials online for a full list of references included). From each of the study, clinical features of the patients were extracted.
Early-onset Alzheimer's Disease: Nonamnestic Subtypes and Type 2 AD
2012, Archives of Medical ResearchCitation Excerpt :Patients with EOAD not only show more severe cortical atrophy, but also have more glucose hypometabolism than patients with LOAD (48,55,57,63,65–69). On 18fluoro-deoxyglucose positron emission tomography (FDG-PET) studies, comparably demented patients with EOAD (with embedded variants) showed greater regional hypometabolism, particularly in parietal areas, than normal controls and those with LOAD (67,68,70,71–74). In our study, EOAD patients, compared to LOAD patients, also had greater focal hypometabolism in the parietal regions (left worse than right), whereas LOAD patients, compared to the EOAD patients, had greater hypometabolism in the bilateral inferior temporal regions and inferior frontal regions (right worse than left) (Figure 2) (75).