By the time that the symptoms of
dementia emerge in Alzheimer's disease, tissue damage is well underway in the
brain. Now, scientists propose that specific psychiatric symptoms – such as
depression, anxiety, sleep disruption, and loss of appetite – may serve as
markers of very early brain changes in Alzheimer's.
Depression and anxiety may be signs of
early-stage Alzheimer's.
Working with the Brazilian Biobank
for Aging Studies (BBAS) at the University of São Paulo, investigators at the
University of California in San Francisco (UCSF) studied results of postmortem
brain tissue tests and compared them with psychiatric symptoms obtained from
detailed interviews conducted with people who knew the deceased well, such as
relatives and carers.
They
suggest that their study — a paper on which now features in the Journal of Alzheimer's Disease —
reveals that psychiatric symptoms are not the cause of Alzheimer's, but more
likely early indicators of the disease.
Such markers could help doctors to
diagnose Alzheimer's disease much
earlier and thus increase opportunities for slowing its progress, they note.
Better
understanding of Alzheimer's
The authors also propose that the
findings could alter our understanding of how the biology of Alzheimer's leads
to psychiatric symptoms in people who develop the disease.
"The discovery," says
senior study author Dr. Lea T. Grinberg, who is a principal investigator and
associate professor in neurology at UCSF, "that the biological basis for
these symptoms is the early Alzheimer's pathology itself was quite
surprising."
"It
suggests these people with neuropsychiatric symptoms are not at risk of
developing Alzheimer's disease — they already have it," she explains.
There are around 5.7 million
people with Alzheimer's disease living in the United States.
This figure is likely to reach almost 14 million by 2050.
If doctors could diagnose the
disease more accurately, and earlier, it could save the nation trillions of
dollars in care and medical costs.
Alzheimer's is the leading cause
of dementia and has some
specific biological features. The main hallmarks are two types of abnormal
proteins found inside and around the brain cells in people who have died with
the disease.
The abnormal proteins found inside
the brain cells are known as tau tangles and the ones found between the cells
are called beta-amyloid plaques.
Brain
samples from a large cohort
For their study, Dr. Grinberg and
colleagues used brain tissue samples from the BBAS. The BBAS is a large and
unique bank that stores the brain tissue that scientists retrieve during
postmortems in São Paulo, where an autopsy follows every death.
This allowed them to study autopsied
brain tissue from 1,092 adults aged over 50 who died between 2004 and 2014 and
who were representative of São Paulo's general population.
In
addition, the BBAS records included data from "postmortem interviews with
reliable informants" on the psychiatric symptoms and mental capacity of
the deceased.
The team excluded 637 brain samples
that showed abnormalities that were not related to Alzheimer's disease. This
left 455 samples from people who either had signs of Alzheimer's disease, such
as beta-amyloid plaques and tau tangles, or no signs of neurodegeneration.
To assess the amount of
Alzheimer-related neurodegeneration, researchers evaluated each sample using a
method called "Braak staging" to measure tau tangle burden, and a
"CERAD neuropathology score," to measure beta-amyloid burden.
The investigators evaluated
psychiatric symptoms using a "12-item neuropsychiatric inventory" and
cognitive status using a tool called the "CDR-SOB score."
They then analyzed the psychiatric
and cognitive evaluations against the measures of Alzheimer-related
neurodegeneration for all of the 455 brains.
Improved
diagnosis of Alzheimer's
The results showed significant links
between psychiatric and cognitive measures and patterns of tau tangle burden,
but no links to beta-amyloid burden.
Symptoms of anxiety,
agitation, depression, sleep
disruption, and appetite changes, for example, had links to early-stage
Alzheimer's in which tau tangles appear in the brain stem. The link was present
even though the individuals concerned had shown no noticeable changes in memory
capacity before they died.
As Alzheimer's progresses, tau
tangles start to build up in the outer cortex of the brain. Samples from
individuals in which there were signs that this process had begun had links to
a higher risk of agitation.
Also, samples from individuals in
which tau tangles had already progressed to the outer cortex, were linked to
dementia symptoms that are typical of Alzheimer's disease, such as a decline in
memory and thinking ability and delusions.
The team suggests that the findings
could impact trials for drugs that target early Alzheimer's disease in which
there is a need for measurable outcomes in addition to cognitive decline.
The results could also be added to
screening — alongside brain scans and blood tests — for improving the diagnosis
of early-stage Alzheimer's.
"If we could use this new
knowledge to find a way to reduce the burden of these conditions in aging
adults, it would be absolutely huge."
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