elderly law
Understanding the Texas Medicaid Estate Recovery Program (MERP)
The Texas Medicaid program pays almost half the cost of all nursing home and other long term care expenses. So in March of 2005, Texas implemented the Medicaid Estate Recovery Program (MERP) to comply with federal laws. This program allows the state to file a claim against the estate of a deceased Medicaid recipient, age 55 or older, who received payments for certain long-term care services. Claims can include the cost of services, hospital care and prescription drugs paid for by Medicaid. However, the state will not file claims in the following situations:
a) where there are estates valued less than $10,000,
b) where the costs were less than $3,000,
c) where the cost of selling the property would be result in no value.
The state will not file a claim when there is a surviving spouse, there is a surviving child under 21 years of age, there is a child who is blind or totally disabled, or where there is a an unmarried child living in the Medicaid recipient’s homestead for at least one year prior to the death. The state also allows a hardship waiver to be filed in certain situations.
The State will not collect certain types of assets that fall outside a person’s estate. Therefore it may be necessary to do your estate planning with consideration given to Medicaid rules.
The personal representative of an estate (executor or administrator) is required by law to give the State of Texas notice of Medicaid recipient’s death thereby allowing the state to file a claim. Such a claim by the State of Texas is a Class 7 claim which is paid after funeral bills, administration expenses, secured claims, child support, taxes, and it is paid before all other creditors and before the beneficiaries are compensated.
The Department of Aging and Disability Services administers the MERP and they provide a wonderful guide for those with additional questions.
http://www.dads.state.tx.us/news_info/publications/brochures/DADS121_merp.html
The future of Alzheimer’s
One of the largest burdens on American’s health care system is caused by Alzheimer’s disease and other related dementia. Currently over 5.4 million people are living with the disease and more than 15 million Americans are caring for persons with Alzheimer’s and other dementias. Alzheimer’s disease is the sixth-leading cause of death in the US and the ONLY cause among the top 10 that has no cure, prevention treatment or can even be slowed. Is Alzheimer’s our new Cancer?
A strategic plan is being developed by the Journal of Alzheimer’s Association. States across the country are vamping up their APS departments, elderly abuse divisions of district attorneys offices are popping up, and drug companies are trying to find cures, ways to predict the disease and even ways to slow the disease down.
The pharmaceutical company Eli Lilly & Co. show promise with new experimental Alzheimer’s treatment due to decline of cognition in some patients. Read the Article. Researches find promise in attacking a key building block of the Alzheimer’s disease. Read the Article. TauRx Therapeutics is conducting a clinical trial on a new treatment for Pick’s Disease (a form of Dementia which is similar to Alzheimer’s. Read the Article.
A Cancer drug reverses Alzeheimer’s Disease in Mice
Researchers at Case Western Reserve University have discovered that a drug currently used to treat cancer patients can reverse the cognitive deficits related to Alzheimer’s disease in mice, and what’s more, it accomplishes this feat in a remarkably short period of time.
The drug, called bexarotene, has been approved for the treatment of a type of skin cancer since 1999. In the new experiments with genetically engineered mice, the drug quickly cleared away the beta-amyloid plaques in the brain that are believed to cause cognitive deficits in Alzheimer’s disease.
This is not the first time that scientists have essentially cured Alzheimer’s in rodents. A decade ago, scientists got excited when a potential Alzheimer’s vaccine appeared to chew up nerve-destroying amyloid protein deposits in animal brains, but were equally disappointed when it failed to do the same in human patients.