ProHealth health Vitamin and Natural Supplement Store and Health
Home  |  Log In  |  My Account  |  View Cart  View Your ProHealth Vitamin and Supplement Shopping Cart
800-366-6056  |  Contact Us  |  Help
Facebook Google Plus
Fibromyalgia  Chronic Fatigue Syndrome & M.E.  Lyme Disease  Natural Wellness  Supplement News  Forums  Our Story
Store     Brands   |   A-Z Index   |   Best Sellers   |   New Products   |   Deals & Specials   |   Under $10   |   SmartSavings Club

Trending News

Meta-analysis adds evidence to association between omega-3 supplementation and lower heart rate

Friendly User's Guide for the Timing of Nutritional Supplements

The Health Benefits of Manuka Honey

Increase Your Magnesium Intake

Vitamin D supplementation could ease IBS symptoms

Top Tips to Boost Your Immunity

Essential Oils Lower Blood Pressure

11 Amazing Health Benefits of Using Baking Soda

Nicotinamide riboside shows promise for treatment of Alzheimer’s disease

Exercise, calcium, vitamin D, and other factors linked with fewer injurious falls

Print Page
Email Article

"Untangling" Tau: New Mouse Model Shows Key Feature of Alzheimer's Disease

  [ Not Yet Rated ]   [ Discuss This Article ]
By Press Release by the National Institute on Aging • • November 23, 1999

Scientists have succeeded in producing a hallmark of Alzheimer's disease in a laboratory animal model. The much-anticipated transgenic mouse model is genetically engineered with the human gene coding for a form of the brain protein tau. The new mouse strain will enable investigators to study tau-containing lesions in a number of brain disorders, including the insoluble tau-containing tangles that build up and form one of the key pathological features of Alzheimer's disease (AD). It joins several other partial models of Alzheimer's disease and may help to hasten the development of potential treatments for AD. The National Institute on Aging (NIA) funded the study, which appears in this month's issue of the journal Neuron. *

In the study, scientists inserted human tau genes into mice which later developed masses of abnormal tau filaments in nerve cells within the spinal cord, cortex and brainstem, three critical regions of the central nervous system. As the mice aged, insoluble masses of tau filaments grew in number. The animals also showed evidence of nerve cell degeneration and impaired movement, unlike their littermates lacking the inserted tau gene. The strain was created under the direction of Virginia M-Y. Lee, Ph.D., MBA, and John Q. Trojanowski, M.D., Ph.D. at the University of Pennsylvania's Center for Neurodegenerative Disease Research in Philadelphia.

The mice do not completely model AD, but they more closely resemble other human brain diseases that accumulate AD-like tau deposits in regions deep within the central nervous system, Dr. Lee is careful to point out. "We know that tau-containing tangles are an important feature of Alzheimer's disease, but we're not sure about how it fits into the development and progression of the disease, so the tau mouse model is very important," says Dr. D. Stephen Snyder, who directs studies of the Etiology of Alzheimer's Disease at NIA's Neuroscience and Neuropsychology of Aging Program. "It should help us look at normal and abnormal tau function, for example, to study and measure the accumulation of tau and to determine how the known mutations lead to the death of neurons. Less clear is whether tau will eventually prove to be a useful diagnostic marker for the tauopathies and, importantly, for AD."

The two neuropathlogical hallmarks of Alzheimer's disease are senile plaques, which are made of a protein fragment called beta amyloid, and neurofibrillary tangles, which are made of abnormal twisted strands of the protein, tau. Tau formation is related to the severity of disease; the more advanced the stage of disease, the more tau deposits in the brain. Animal models already exist for other features of Alzheimer's disease, including strains bred with mutated forms of the human amyloid precursor protein, which causes amyloid to form, and mice bred with the presenilin and apoE4 genes, also implicated in Alzheimer's disease.

Dementia refers to a loss of memory and reasoning and specifically to a progressive deterioration that is severe enough to prevent normal functioning. AD is the most common cause of dementia among people age 65 and older. AD affects as many as 4 million Americans in the United States. The prevalence of AD doubles every 5 years beyond age 65. Some studies indicate that nearly half of all people age 85 and older have symptoms of AD.

Researchers use the term "tauopathy" to describe a grouping of dementing diseases in which tau is implicated, such as a unique form of dementia which involves several mutations in the tau gene affecting over twenty distinct families. They also include Pick's disease and progressive supranuclear palsy (PSP), which are not caused by tau genetic mutations. Tauopathies differ from AD in a number of important ways. Clinical signs associated with tauopathies vary widely and range from schizophrenia and Parkinsonian-like tremors to language and behavioral disturbances. In addition, people with tauopathies may have abundant AD-like deposits of tau filaments, but they may not have deposits of beta amyloid. Masses of tau filaments accumulate in different brain regions from those affected by AD and the tau filaments themselves often have a slightly different structure from those in AD. And because memory loss in some tauopathies is similar to that experienced by patients with AD, the prevalence of tauopathies - distinct from AD - remains uncertain.

Scientists do not yet know how tau and amyloid deposits form, or how they cause cells to die in AD. The two may form independently of one another, or one before the other. Scientists are also working to understand how the two produce disease in the brain, and to understand why and how tau deposits accumulate. But they know that the protein is critical to cell survival and helps maintain the cell's internal support structure or cytoskeleton.

*Ishihara, Takeshi; Hong, Ming; Zhang, Bin; Nakagawa, Yasushi; Lee, Michael K.; Trojanowski, John Q.; and Lee, Virginia M.-Y. "Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpress the Shortest Human Tau Isoform," Neuron, Vol. 24, No. 1-20, November, 1999, pp. 751-762. (Accompanied by a mini-review, "Neurodegenerative Tauopathies: Human Disease and Transgenic Mouse Models," pp. 507-510.)
Other contacts: Univ. of Penn. Press Office 215-662-2560 Neuron: 617-661-7057

Source: National Institute on Aging Press Release: November 23, 1999

Contact: Stephanie E. Clipper,, (301)-496-1752

Post a Comment

Featured Products From the ProHealth Store
Mitochondria Ignite™ with NT Factor® Vitamin D3 Extreme™ Energy NADH™ 12.5mg

Article Comments

Be the first to comment on this article!

Post a Comment

Optimized Curcumin Longvida with Omega-3

Featured Products

FibroSleep™ FibroSleep™
The All-in-One Natural Sleep Aid
Mitochondria Ignite™ with NT Factor® Mitochondria Ignite™ with NT Factor®
Reduce Fatigue up to 45%
Vitamin D3 Extreme™ Vitamin D3 Extreme™
50,000 IU Vitamin D3 - Prescription Strength
Ultra EPA  - Fish Oil Ultra EPA - Fish Oil
Ultra concentrated source of essential fish oils

Natural Remedies

Could a B-12 Deficiency Be Causing Your Symptoms? Could a B-12 Deficiency Be Causing Your Symptoms?
Are You Obtaining the Proper Enzymes? Are You Obtaining the Proper Enzymes?
Soothe, Heal and Regulate Your Digestive System with Nutrient-Rich Aloe Vera Soothe, Heal and Regulate Your Digestive System with Nutrient-Rich Aloe Vera
Block Acid Reflux to Prevent Esophageal Problems! Block Acid Reflux to Prevent Esophageal Problems!
The Fast-Acting Solution for Healthy Digestive Function The Fast-Acting Solution for Healthy Digestive Function

ProHealth, Inc.
555 Maple Ave
Carpinteria, CA 93013
(800) 366-6056  |  Email

· Become a Wholesaler
· Vendor Inquiries
· Affiliate Program
Credit Card Processing
Get the latest news about Fibromyalgia, M.E/Chronic Fatigue Syndrome, Lyme Disease and Natural Wellness

CONNECT WITH US ProHealth on Facebook  ProHealth on Twitter  ProHealth on Pinterest  ProHealth on Google Plus

© 2018 ProHealth, Inc. All rights reserved. Pain Tracker App  |  Store  |  Customer Service  |  Guarantee  |  Privacy  |  Contact Us  |  Library  |  RSS  |  Site Map