Cited by 93Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAmyotrophic Lateral Sclerosis Research

Clinicopathological features of familial Alzheimer's disease associated with the M139V mutation in the presenilin 1 gene. Pedigree but not mutation specific age at onset provides evidence for a further genetic factor

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Fox, N.·1997·Brain

Abstract

Sixteen affected individuals are described from two families with early onset autosomal dominant familial Alzheimer's disease. A mutation at codon 139 in the presenilin 1 gene on chromosome 14 results in a methionine to valine substitution which cosegregates with the disease in these families. Onset of dementia was before the age of 50 years in all individuals. The ages at onset within each family were tightly clustered but were significantly different between the families; this difference could not be accounted for by apolipoprotein E status and suggests the existence of a further genetic factor that modifies age at disease onset. The pattern of cognitive decline was similar in both families: early memory loss (initially selective for verbal memory in some individuals) was followed soon after by loss of arithmetic skills while naming and object perception skills were relatively preserved. A speech production deficit was observed in three members of one family but not in the other. Seizures were common and usually predated by myoclonic jerks by a number of years. Serial MRIs showed progressive cortical atrophy with periventricular white matter change appearing 3-4 years into the disease. PET revealed parieto-temporal hypometabolism in all individuals scanned. The diagnosis of Alzheimer's disease was confirmed with typical histopathology in one individual from each family.

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Crossref · 10.1093/brain/120.3.491

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  • Cerebrovascular pathology with BBB breakdown was shown by neuropathological studies in patients with specific PSEN1 mutations including T113-114 insertion, P117L, M139V, M146V, L153V, H163R, E184D, G209V, A260V, C260T, E280A, L282V, C285T, L420R, and Δe9 deletion.

    “Particularly, cerebrovascular pathology with BBB breakdown was shown by neuropathological studies in patients with PSEN1 T113-114 insertion (544), P117L (573, 639), M139V (183, 389), M146V (389), L153V (289), H163R (280), E184D (668), G209V (389), A260V (389), C260T (274), E280A (354), L282V (143), C285T (274), and L420R (440) missense mutations, and 𝚫 e9 deletion (280).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [183]

  • Human PSEN1 mutation carriers have notable BBB breakdown and cerebrovascular dysfunction including cerebellar amyloid angiopathy and CAA, disrupted meningeal, subpial, and cortical arterioles, degeneration of pericytes and SMCs, cerebral perivascular amyloid deposits, and diminished FDG transport across the BBB in an early asymptomatic stage.

    “Human PSEN1 mutation carriers have notable BBB breakdown and cerebrovascular dysfunction including cerebellar amyloid angiopathy and CAA (143, 183, 274, 280, 354, 389, 440, 500, 544, 573, 639, 668); disrupted meningeal, subpial, and cortical arterioles (274, 389, 440); degeneration of pericytes and SMCs (573); cerebral perivascular amyloid deposits (25, 274, 289, 354, 573, 668); and diminished FDG”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [183]

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References 9 · Cited by 93

Authors
Fox, N.
Affiliations
National Hospital for Neurology and Neurosurgery (GB)
Corresponding author
Fox, N.
ORCID
Fox, N.
Venue
Brain
Published
1997-03-01
Volume
120
Issue
3
Pages
491-501
ISSN
  • 0006-8950 (ISSN-L)
  • 1460-2156
OpenAlex
W2139238476
Cited by
93
References
9
Citations by year
2026: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 2 · 2013: 6 · 2012: 4
FWCI
3.05
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Brain (publishedVersion)
  • PubMed (publishedVersion)
  • Own your potential (DEAKIN) (submittedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Figshare (submittedVersion, cc-by)
Funders
  • National Institutes of Health (1r01ag011871-01, 5r01ag012028-02)
  • National Institute on Aging (AG-11871, AG 12028)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
familial Alzheimer's disease, presenilin 1, age of onset, genetic modifiers, autosomal dominant inheritance, cognitive decline, speech production deficits, seizures, cortical atrophy, apolipoprotein E, clinicopathological features
MeSH terms
Adult, Alzheimer Disease, Apolipoproteins E, Brain, Female, Humans, Intelligence, Male, Memory, Middle Aged, Mutation, Neuropsychological Tests, Pedigree, Perception

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