Alzheimers / Parkinson's / Loss of Smell

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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 AD.

 

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.

 

The Public Interest Newswire / http://www.ascribe.org

 

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