Amyloid beta
Amyloid beta peptide (beta-APP) | |||||||||
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Identifiers | |||||||||
Symbol | APP | ||||||||
Pfam | PF03494 | ||||||||
InterPro | IPR013803 | ||||||||
SCOP2 | 2lfm / SCOPe / SUPFAM | ||||||||
TCDB | 1.C.50 | ||||||||
OPM superfamily | 304 | ||||||||
OPM protein | 2y3k | ||||||||
Membranome | 45 | ||||||||
|
amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease) | |||||||
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Identifiers | |||||||
Symbol | APP | ||||||
Alt. symbols | AD1 | ||||||
NCBI gene | 351 | ||||||
HGNC | 620 | ||||||
OMIM | 104760 | ||||||
RefSeq | NM_000484 | ||||||
UniProt | P05067 | ||||||
Other data | |||||||
Locus | Chr. 21 q21.2 | ||||||
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Amyloid beta (A
A study has suggested that APP and its amyloid potential is of ancient origins, dating as far back as early deuterostomes.[10]
Normal function
[edit]The normal function of A
The glymphatic system clears metabolic waste from the mammalian brain, and in particular amyloid beta.[25] A number of proteases have been implicated by both genetic and biochemical studies as being responsible for the recognition and degradation of amyloid beta; these include insulin degrading enzyme[26] and presequence protease.[27] The rate of removal is significantly increased during sleep.[28] However, the significance of the glymphatic system in A
Disease associations
[edit]A
Alzheimer's disease
[edit]Research suggests that soluble oligomeric forms of the amyloid beta may be causative agents in the development of Alzheimer's disease.[33] It is generally believed that A
Brain A
Increases in either total A
The "amyloid hypothesis" — that the plaques are responsible for the pathology of Alzheimer's disease — is accepted by the majority of researchers, but is not conclusively established. An alternative hypothesis is that amyloid oligomers rather than plaques are responsible for the disease.[34][46]
Cancer
[edit]While A
Down syndrome
[edit]Adults with Down syndrome had accumulation of amyloid in association with evidence of Alzheimer's disease, including declines in cognitive functioning, memory, fine motor movements, executive functioning, and visuospatial skills.[49]
Formation
[edit]A
Genetics
[edit]Autosomal-dominant mutations in APP cause hereditary early-onset Alzheimer's disease (familial AD, fAD). This form of AD accounts for no more than 10% of all cases, and the vast majority of AD is not accompanied by such mutations.[52] However, familial Alzheimer's disease is likely to result from altered proteolytic processing. This is evidenced by the fact that many mutations that lead to fAD occur near
The gene for the amyloid precursor protein is located on chromosome 21, and accordingly people with Down syndrome have a very high incidence of Alzheimer's disease.[57]
Structure and toxicity
[edit]Amyloid beta is commonly thought to be intrinsically unstructured, meaning that in solution it does not acquire a unique tertiary fold but rather populates a set of structures. As such, it cannot be crystallized and most structural knowledge on amyloid beta comes from NMR and molecular dynamics. Early NMR-derived models of a 26-aminoacid polypeptide from amyloid beta (A
Low-temperature and low-salt conditions allowed to isolate pentameric disc-shaped oligomers devoid of beta structure.[62] In contrast, soluble oligomers prepared in the presence of detergents seem to feature substantial beta sheet content with mixed parallel and antiparallel character, different from fibrils;[63] computational studies suggest an antiparallel beta-turn-beta motif instead for membrane-embedded oligomers.[64]
Immunotherapy research
[edit]Immunotherapy may stimulate the host immune system to recognize and attack A
Measuring amyloid beta
[edit]Imaging compounds, notably Pittsburgh compound B, (6-OH-BTA-1, a thioflavin), can selectively bind to amyloid beta in vitro and in vivo. This technique, combined with PET imaging, is used to image areas of plaque deposits in those with Alzheimer's.[67]
Post mortem or in tissue biopsies
[edit]Amyloid beta can be measured semiquantitatively with immunostaining, which also allows one to determine location. Amyloid beta may be primarily vascular, as in cerebral amyloid angiopathy, or in amyloid plaques in white matter.[68]
One sensitive method is ELISA which is an immunosorbent assay which utilizes a pair of antibodies that recognize amyloid beta.[69][70]
Atomic force microscopy, which can visualize nanoscale molecular surfaces, can be used to determine the aggregation state of amyloid beta in vitro.[71]
Vibrational microspectroscopy is a label-free method that measures the vibration of molecules in tissue samples.[72] Amyloid proteins like A
Dual polarisation interferometry is an optical technique which can measure early stages of aggregation by measuring the molecular size and densities as the fibrils elongate.[74][75] These aggregate processes can also be studied on lipid bilayer constructs.[76]
See also
[edit]- TPM21
- Sylvain Lesné – A
β *56
References
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