RGD Reference Report - Lewy body variant of Alzheimer's disease: selective neocortical loss of t-SNARE proteins and loss of MAP2 and alpha-synuclein in medial temporal lobe. - Rat Genome Database

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Lewy body variant of Alzheimer's disease: selective neocortical loss of t-SNARE proteins and loss of MAP2 and alpha-synuclein in medial temporal lobe.

Authors: Mukaetova-Ladinska, EB  Xuereb, JH  Garcia-Sierra, F  Hurt, J  Gertz, HJ  Hills, R  Brayne, C  Huppert, FA  Paykel, ES  McGee, MA  Jakes, R  Honer, WG  Harrington, CR  Wischik, CM 
Citation: Mukaetova-Ladinska EB, etal., ScientificWorldJournal. 2009 Dec 16;9:1463-75.
RGD ID: 6483091
Pubmed: PMID:20024519   (View Abstract at PubMed)
PMCID: PMC5823105   (View Article at PubMed Central)
DOI: DOI:10.1100/tsw.2009.151   (Journal Full-text)

Lewy bodies (LBs) appear in the brains of nondemented individuals and also occur in a range of neurodegenerative disorders, such as dementia with Lewy bodies (DLB) and Parkinson's disease. A number of people with a definite diagnosis of Alzheimer's disease (AD) also exhibit these intraneuronal inclusions in allo- and/or neocortical areas. The latter, referred to as Lewy body variant of AD (LBV), bears a clinical resemblance to AD in terms of age at onset, duration of illness, cognitive impairment, and illness severity. Since the presence of LBs is accompanied by neuronal cytoskeleton changes, it is possible that the latter may influence neuronal connectivity via alterations to the synaptic network. To address this, we examined the expression of synaptic proteins (synaptophysin, syntaxin, SNAP-25, and alpha-synuclein) and two cytoskeletal proteins (tau and MAP2) in the brain tissue of subjects enrolled in a population-based autopsy study (n = 47). They were divided into groups with no memory problems (control group, n = 15), LBV (n = 5), AD devoid of LBs (n = 17), cerebrovascular dementia (n = 3), and mixed dementia (n = 7). The LBV and AD groups had a similar degree of cognitive impairment and neuropathological staging in terms of Braak staging and CERAD score. In comparison with the control group and the dementia groups without LBs, the LBV group had significantly lower levels of syntaxin and SNAP-25 (23%) in the neocortex, and depletion of MAP2 (64%), SNAP-25 (34%), and alpha-synuclein (44%) proteins in the medial temporal lobes. These findings suggest that the t-SNARE complex deficit present in LBV may be associated with the presence of LB-related pathology and may explain the more profound cholinergic loss seen in these patients.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Lewy body dementia  IEP 6483091 RGD 
Lewy body dementia  ISOMAP2 (Homo sapiens)6483091; 6483091 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Map2  (microtubule-associated protein 2)

Genes (Mus musculus)
Map2  (microtubule-associated protein 2)

Genes (Homo sapiens)
MAP2  (microtubule associated protein 2)


Additional Information