Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive thalamus
John C. Dalrymple‐AlfordBruce HarlandElena A. LoukavenkoBrook A. L. PerryS.A. MercerDavid A. CollingsKatharina UlrichWickliffe C. AbrahamNeil McNaughtonMathieu Wolff
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Retrosplenial cortex
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Retrograde amnesia
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Under the auspices of the EURO-CNS Including course books and e-learning modules: - Basic neuropathology - Neurodegenerative diseases - Leukoencephalopathies - Tumors of the CNS and PNS - Developmental neuropathology - Muscle and nerve pathology - Forensic neuropathology
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OBJECTIVE: To investigate the genetics of Late-onset Alzheimer disease by reducing phenotypic heterogeneity and studying AD coincident phenotypes. BACKGROUND: To investigate the underlying genetic mechanisms of Late-onset Alzheimer Disease (LOAD), we have performed a genome-wide association study of AD neuropathology and coincident phenotypes, including a neuropathology-confirmed case-control analysis, analyses of coincident features, including neuritic plaques (NP), lewy bodies (LB), amyloid angiopathy (AA), medial temporal sclerosis (MTS), AD Braak stage, and vascular brain injury (VBI). We used this expanded neuropathology approach to limit the effects of phenotypic heterogeneity, and provide additional insights into AD subphenotypes. DESIGN/METHODS: We examined 4914 samples with neuropathology data from 11 datasets in the Alzheimer Disease Genetics Consortium genotyped with high-density chips. Statistical aassociation was performed using logistic regression for binary traits and polytomous logistic regression for ordinal traits, followed by meta-analysis. Subjects examined included 3,887 neuropathologically-confirmed LOAD cases and 1,027 neuropathologically-confirmed cognitive controls. RESULTS: Associations of APOE and BIN1 with LOAD were confirmed. Additionally, several novel LOAD associations were found, including PHF21B (P=2.0×10-8), and SMOX (P=9.0×10-7). Multiple loci were associated with the presence of neuritic plaques, including APOE (P=1.8x10-30), GALNT7 (P=6.0×10-9), ABCG1 (P=8.0×10-9), and a region near LMX1B (P=4.3×10-8). Additional loci were found to be associated with several ordinal neuropathology traits including LB, AA, MTS, VBI, and Braak. Twelve of the 21 genetic risk loci for clinically-defined AD dementia were confirmed in our clinico-pathologic sample, with nine of these showing larger ORs in the clinic-pathologic sample. At the known loci there was strong positive correlation between AD dementia effect sizes and NFT/NP effect sizes, while VBI effect sizes showed a moderate negative correlation; other coincident features showed only nominal association with known loci. CONCLUSIONS: These results confirm several known AD risk loci and implicate novel loci in the etiology of LOAD neuropathology features, particularly neuritic plaque. Additionally, they suggest a role of AD risk loci in the development of VBI, but not other coincident features.
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To test the hypothesis that use of antihypertensive medication is associated with lower Alzheimer disease (AD) neuropathology.This was a postmortem study of 291 brains limited to those with normal neuropathology or with uncomplicated AD neuropathology (i.e., without other dementia-associated neuropathology) in persons with or without hypertension (HTN) who were and were not treated with antihypertensive medications. Neuritic plaque (NP) and neurofibrillary tangle (NFT) densities, quantified in selected brain regions according to the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) neuropathologic criteria, with additional cortical NP counts, yielded 24 neuropathologic regional measures or summaries. Medicated hypertension (HTN-med; n = 77), nonmedicated HTN (HTN-nomed; n = 42), and non-HTN (no-HTN; n = 172) groups were compared by analyses of variance.The HTN-med group had significantly less neuropathology than the no-HTN group. The no-HTN group averaged over 50% higher mean NP and NFT ratings, and double the mean NP count, of the HTN-med group. The HTN-nomed group had significantly more neuropathology than the HTN-med group, but not significantly less than the no-HTN group.There was substantially less Alzheimer disease (AD) neuropathology in the medicated hypertension group than the nonhypertensive group, which may reflect a salutary effect of antihypertensive medication against AD-associated neuropathology.
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A case of retrosplenial amnesia was reported. The patient was an 81-year-old right-handed male. He developed amnesic syndrome following cerebral infarction situated left retrosplenial region. His immediate memory was preserved. Recent memory for both verbal and nonverbal modalities was disturbed. He also showed retrograde amnesia for 2 years. The is the first report of retrosplenial amnesia in Japan. We should take into account of the retrosplenial region as a causative site of amnesic syndrome.
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