Degenerative and vascular lesions of the brain have synergistic effects in dementia of the elderly.
The relative importance of vascular and Alzheimer's disease (AD) lesions, their interaction in the development of cognitive impairment and the very existence of mixed dementia induced by the potentiation of both mechanisms remain controversial. The aim of this study was to assess whether the patients with infarcts and lacunes have fewer plaques and tangles than those without vascular lesions, for similar severity of clinical dementia. We performed a prospective clinicopathological study in elderly patients of a long-stay care unit. The severity of clinical dementia was assessed by psychometry performed according to standardized methods less than 6 months before death. A volumetric study of cerebral vascular lesions was performed at post-mortem study of the brain. The density of neuritic plaques (SP), Amyloid beta focal deposits (A beta FD), and neurofibrillary tangles (NFT) in the temporal and frontal isocortex was quantified. According to DSM III criteria, 28 of the 33 patients for whom autopsies were performed had dementia. Twenty-four of the included patients had degenerative or vascular lesions, or both. The volume of infarcts and lacunes was significantly correlated with the severity of cognitive impairment. The density of SP, A beta FD and NFT in the temporal and frontal isocortex was significantly lower when vascular lesions were present. For similar clinical severity of dementia, there were fewer AD lesions in patients with vascular lesions than in those without vascular lesions.
Zekry
Dina
D
Laboratoire de Neuropathologie Raymond Escourolle, Hôpital de la Salpêtrière, INSERM U 106 and 360, Association Claude Bernard, Pierre et Marie Curie University, 47 Bd de l'Hôpital, 75013 Paris, France.
Duyckaerts
Charles
C
Moulias
Robert
R
Belmin
Joël
J
Geoffre
Caroline
C
Herrmann
François
F
Hauw
Jean-Jacques
JJ
D000368:Aged; D000544:Alzheimer Disease / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000032:analysis; D002536:Cerebral Arteries / Q000473:pathology* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000473:pathology* / Q000503:physiopathology; D002544:Cerebral Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D015140:Dementia, Vascular / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D018450:Disease Progression; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D002537:Intracranial Arteriosclerosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D008833:Microcirculation / Q000473:pathology / Q000503:physiopathology; D016874:Neurofibrillary Tangles / Q000473:pathology; D009474:Neurons / Q000473:pathology*; D058225:Plaque, Amyloid / Q000473:pathology; D011446:Prospective Studies; D017966:Pyramidal Cells / Q000473:pathology
D016229:Amyloid beta-Peptides