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Protein spesifik sebagai missing link  untuk perubahan awal dikenal hilang dalam patologi Alzheimer

Temuan dapat mempengaruhi strategi untuk pengobatan

Date:

July 21, 2015

Source:

Nathan Kline Institute for Psychiatric Research

Summary:

Sebuah studi baru-baru ini berimplikasi biang keladi baru dalam pengembangan penyakit Alzheimer . Penelitian mengungkapkan bahwa pendahulu dari peptida amiloid beta bertindak pada tahap awal Alzheimer untuk memulai berbagai kelainan yang menyebabkan hilangnya kelompok neuron penting untuk pembentukan memori .

........... Temuan penelitian terbaru yang melibatkan ßCTF memiliki implikasi signifikan bagi strategi pengobatan dan melanjutkan jalannya pengembangan obat Alzheimer . Saat ini, strategi yang paling umum untuk mengobati penyakit Alzheimer menargetkan amiloid peptida ß , yang telah sukses sederhana dalam uji klinis . Temuan dari penelitian ini menunjukkan bahwa obat yang dapat mengurangi tingkat βCTF serta beta - amyloid , seperti kelas inhibitor BACE1 saat ini sedang dikembangkan , dapat membantu memperlambat atau menghentikan perkembangan penyakit Alzheimer ....more

Specific protein
as missing link for earliest known change in Alzheimer's pathology

Findings may influence strategies for treatment

Date:

July 21, 2015

Source:

Nathan Kline Institute for Psychiatric Research

Summary:

A recent study implicates a new culprit in Alzheimer's disease development.
The research reveals that a precursor of an amyloid beta peptide acts at the
earliest stage of Alzheimer's to initiate a range of abnormalities leading to
the loss of groups of neurons critical for memory formation.

..........................

A recent study conducted at Nathan S. Kline Institute for Psychiatric
Research (NKI) and NYU Langone Medical Center implicates a new culprit in
Alzheimer's disease development. The research reveals that ßCTF -- the
precursor of the amyloid beta (Aß) peptide -- acts at the earliest stage of
Alzheimer's to initiate a range of abnormalities leading to the loss of groups
of neurons critical for memory formation. Results from the study are published
online July 21, 2015 in the journal, Molecular Psychiatry, and the article has been selected for an issue
cover.

The recent study findings involving ßCTF have significant implications for
treatment strategies and furthering the course of Alzheimer's drug development.
Presently, the most common strategy for treating Alzheimer's disease is
targeting the amyloid ß peptide, which has had modest success in clinical
trials. Findings from this research suggest that drugs that may reduce βCTF
levels as well as beta-amyloid, such as the class of BACE1 inhibitors currently
under development, may help slow or stop the progression of Alzheimer's
disease.

βCTF is formed during endocytosis, the process by which cells absorb
nutrients and sample various materials from the outside environment. It has
been known for some time that abnormalities of endocytosis develop very early
in Alzheimer's disease, well before clinical symptoms, and that variant forms
of genes controlling endocytosis are frequently implicated as risk factors
promoting Alzheimer's. Endosomes -- the membranous vesicles mediating
endocytosis -- start to swell abnormally in some neurons beginning even in
infancy in Down syndrome -- a developmental disability that almost invariably
leads to early-onset AD. Research indicates that more than 75 percent of those
with Down's, aged 65 and older, have Alzheimer's disease.

The NYU Langone -- NKI research team led by Ralph Nixon, MD, PhD, professor
in the departments of psychiatry and cell biology at NYU Langone School of
Medicine and director of the Center for Dementia Research at the Nathan S.
Kline Institute for Psychiatric Research found that, in Alzheimer's and Down
Syndrome, βCTF forms more rapidly on endosomes triggering a molecular pathway
leading to loss of neurons involved with memory. The researchers discovered
APPL1, a protein unrelated to amyloid precursor protein (APP) despite its
similar acronym, directly links βCTF to a second protein, rab5, known to
activate the molecular chain of events leading to neurodegeneration. Lowering
APPL1 levels in cells of individuals with Down syndrome abolished the abnormal
endocytosis, indicating the vital role of APPL1 in this molecular cascade. The
identification of APPL1 as the missing link in a well-described chain of events
associated with very early Alzheimer pathology implies a direct contribution of
ßCTF to Alzheimer's disease development. Notably, a recently discovered APP
mutation that uniquely lowers, rather than raising, risk for Alzheimer's is
believed to act by slowing the formation of ßCTF.

While the current findings do not place any more or less importance to Aß
as a culprit and a target for Alzheimer's therapy, they now underscore the
importance of ßCTF as a key contributor to disease development. "It will
be important to consider the role of βCTF in the design of future therapies for
Alzheimer's disease and in the interpretation of current clinical trials of
BACE1 inhibitors. BACE1 inhibitor trials have been considered a test of the
Aß/amyloid hypothesis but the primary action of these inhibitors is actually to
block formation of ßCTF, the precursor of Aß," said Ralph A. Nixon, MD,
PhD.







Story Source:

The above post is reprinted from materials provided by Nathan
Kline Institute for Psychiatric Research. Note: Materials may be edited
for content and length.







Journal Reference:

1.   
S Kim, Y Sato, P S Mohan, C Peterhoff, A Pensalfini, A Rigoglioso, Y Jiang,
R A Nixon. Evidence that the rab5 effector APPL1 mediates
APP-βCTF-induced dysfunction of endosomes in Down syndrome and Alzheimer’s
disease. Molecular Psychiatry, 2015; DOI:10.1038/MP.2015.97

http://www.sciencedaily.com/releases/2015/07/150721150221.htm

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