AD and Loss of Smell

[Guest guest]

This came from a newswire report we received at work. Interesting reading.

Just hope no quacks twist it around......I love the elderly and it would really

piss me off to have someone like YL get a hold of this.

 

Dale

 

 

 

3/15/2004 5:31:22 AM

Loss of Smell Linked to Key Protein in Alzheimer's Disease; Penn Study Shows

First Signal of Disease Could Provide Future Test for Early Stages of

[ASCRIBE]

ASCRIBE via NewsEdge Corporation : PHILADELPHIA -- Researchers at the University

of Pennsylvania School of Medicine have linked smell loss in mice with excessive

levels of a key protein associated with Alzheimer's and Parkinson's disease.

Smell loss is well documented as one of the early and first clinical signs of

such diseases. If smell function declines as the levels of this protein increase

in brain regions associated with smelling, the research could validate the use

of smell tests for diagnosing Alzheimer's disease. Their findings appear in the

March 12th issue of the journal Brain Research, the commemorative volume 1000.

 

The loss of smell - or olfactory dysfunction - has been known for more than a

decade as an early sign of several neurodegenerative diseases, but we have never

been able to link it to a pathological entity that is measurable over time, said

Richard Doty, PhD, Professor and Director of Penn's Smell and Taste Center, who

is also the team leader of the study. By tying decrements in the ability to

smell to the presence of key disease proteins, such as tau, we may well be able

to assess the degree of progression of selected elements of Alzheimer's disease

and related disorders by scores on quantitative smell tests.

 

A total of ten mice were evaluated in this experiment - five mice that were

genetically engineered to be a model for human Alzheimer's and Parkinson's

disease, and five normal control mice that do not overexpress tau proteins.

Olfactory dysfunction was evaluated by measuring the amount of time the mice

spent investigating unfamiliar odors, such as peppermint or vanillin. Unlike

normal mice, those with smell deficits do not spend much time investigating such

odors, and do not show a preference for novel odors over familiar odors.

 

The results of the Penn study showed that only the control mice, with no excess

of tau proteins, expressed an interest in new odors, indicating a normal sense

of smell. The mice that had excess in tau protein showed little or no interest

in such odors, implying olfactory dysfunction. Analysis of brain tissue from the

diseased mice confirmed a link between the olfactory loss and the presence of

excess tau proteins in brain structures important for smelling. Additionally,

the genetically engineered mice exhibited a significant amount of

neurofibrillary tangles, structures also linked to Alzheimer's disease.

 

No test currently exists for the detection of Alzheimer's disease. A definitive

diagnosis is only confirmed upon death when the brain tissue becomes available

for testing of the presence of such proteins and other physiological markers of

the disease.

 

The process for diagnosis before death is less certain and involves several

kinds of tests - for memory, problem solving, attention and counting - plus

review of a patient's complete medical history from a primary care physician,

and possibly brain scans and consultations from other specialists. With several

diagnostic tools and criteria, physicians can make a diagnosis of moderate to

severe stages of Alzheimer's disease with 90 percent accuracy. However,

diagnosis is less certain for the early stages of the illness.

 

No explanation exists for what causes the alterations in smell perception

associated with neurodegenerative disorders. What is known is that key

physiological markers for these illnesses - deposits of neurofibrillary tangles

or amyloid plaques, Lewy bodies or tau and alpha-synuclein proteins - are

commonly found in brain regions associated with the perception of odors in the

bodies of people who suffer from these illnesses.

 

The mice who overexpress tau, a protein associated with a family of neurological

disorders that includes Alzheimer's disease and Parkinson's disease, have

decreased ability to smell, said Doty. We next plan to study the progression of

the disease entities in the brain as it relates to smell dysfunction. These

experiments are part and parcel to better understanding the physical causes of

such neurodegenerative diseases.

 

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