Discovery Sheds Lite On Why Alzheimer's Medications Rarely Help

Current medications create non process Alzheimer's or terminate it from progressing; they alone temporarily lessen symptoms, such equally retention loss in addition to confusion

Current medications create non process Alzheimer Discovery Sheds Light on Why Alzheimer's Medications Rarely Help

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UCLA uncovering sheds lite on why Alzheimer's meds rarely help

Target of today's drugs is molecularly dissimilar from suspected culprit

FINDINGS

In unraveling oligomers' molecular structure, UCLA scientists discovered that Aβ has a vastly dissimilar organization inwards oligomers than inwards amyloid plaques.
Their finding could shed lite on why Alzheimer's drugs designed to seek out amyloid plaques convey no lawsuit on oligomers.

JOURNAL

The report was published equally the "paper of the week" inwards the June 28 number of the peer-reviewed Journal of Biological Chemistry.

BACKGROUND

The nonprofit Alzheimer's Association projects that the number of people living alongside Alzheimer's illness volition soar from five 1 K 1000 to 13.8 1 K 1000 past times 2050 unless scientists educate novel ways to terminate the disease.
Current medications create non process Alzheimer's or terminate it from progressing; they alone temporarily lessen symptoms, such equally retention loss in addition to confusion.
Current Alzheimer's drugs aim to cut back the amyloid plaques — gummy deposits that construct upwards inwards the encephalon — that are a visual trademark of the disease.
These plaques are made of long fibers of a poly peptide called amyloid beta, or Aβ.
Recent studies, however, advise that the existent culprit behind Alzheimer's may endure pocket-sized Aβ clumps called oligomers that look inwards the encephalon years earlier plaques develop.

IMPACT

The UCLA report suggests that recent experimental Alzheimer's drugs failed inwards clinical trials because they nix inwards on plaques in addition to create non operate on oligomers. Future studies on oligomers volition assist speed the evolution of novel drugs specifically aiming at Aβ oligomers, the researchers say.

AUTHORS

Zhefeng Guo, an assistant professor of neurology at the David Geffen School of Medicine at UCLA in addition to a fellow member of UCLA's Brain Research Institute in addition to Molecular Biology Institute, is available for interviews.

FUNDING