Alzheimer’s Australia Discussion Paper: Dementia, Lesbians
and Gay Men
The impact of dementia on the gay, lesbian, bisexual, transgender and Intersex
(GLBTI) community is already beginning to present itself. Although lesbians and
gay men face many of the same challenges associated with dementia as
heterosexuals, such as advanced care planning, assessment, and community or
residential care, many also face additional challenges such as social isolation,
relationship recognition, and navigating a complicated legislative environment.
Alzheimer’s Australia’s discussion paper, Dementia, Lesbians and Gay Men,
addresses these challenges. It provides practical advice on the issues many
lesbians and gay men with dementia and their carers may face. In addition, it is
a valuable resource for practitioners working in health care and related fields.
The paper is attached but is also available on the Alzheimer’s Australia website:
The heritability and genetics of frontotemporal lobar
There are many forms of dementia and some of these forms fall into the category
of frontotemporal lobar degeneration. These disorders are genetically and
pathologically diverse but all cause degeneration of the brain.
A group of researchers from the Institute of Neurology, London, undertook
research examining whether different forms of frontotemporal lobar degeneration
are heritable, and if so, which ones are heritable and to what degree. Two
hundred and twenty-five people who had been diagnosed with frontotemporal
lobar degeneration spectrum were included in the study.
The researchers collected blood samples for genetic examination and took each
person’s family history to determine whether any first-degree relatives (e.g.
mother, father, sister, brother) had been diagnosed with frontotemporal lobar
degeneration. Each participant was given a score from 1 to 4, depending on his
or her family history. A score of 1 indicated a clear autosomal dominant history
of frontotemporal lobar degeneration. (A genetic trait is autosomal dominant
when only one copy of the gene from one parent is needed in order for an
individual to show the characteristic that is coded for by that gene. For example,
genes that code for brown eyes are dominant over genes that code for any other
eye colour). A score of 4 was given to individuals who had no family history of
dementia. Of the 225 study participants, 41.8% had some family history of
dementia, although only 10.2% had a clear score of 1.
The researchers also looked for mutations in each of the five known disease-
causing genes: MAPT, GRN, VCP, CHMP2B, and TARDP, and the FUS gene,
which is known to cause motor neuron disease. Mutations were found in the
MAPT gene in 8.9% of study participants, and in the GRN gene in 8.4% of study
participants. Both the MAPT and GRN genes are associated with frontotemporal
lobar degeneration. No mutations were found in any of the other genes.
Degrees of heritability were found to vary across the different types of
frontotemporal lobar degeneration. The “behavioral variant” was found to be the
most heritable form. The least heritable forms were found to be frontotemporal
dementia-motor neuron disease and the language syndromes, particularly
semantic dementia, which refers to a progressive loss of the ability to remember
the meaning of words, faces, and objects.
Reference: Rohrer JD, Guerreiro R, Vandrovcova J, Uphill J, et al. (2009). The
heritability and genetics of frontotemporal lobar degeneration. Neurology
Muscle strength, Alzheimer disease, and cognitive decline
As people age they commonly lose muscle strength, which is associated with a
number of adverse health issues. Yet little research to date has been conducted
into whether there is an association between muscle strength and the risk of
developing Alzheimer disease or mild cognitive impairment.
A group of researchers from Rush Alzheimer's Disease Center, Rush University
Medical Center, Illinois, tested the hypothesis that muscle strength is associated
with Alzheimer’s disease and mild cognitive impairment in a prospective
observational study involving more than 900 community-based older persons
who came from retirement communities across the Chicago, Illinois, metropolitan
region. None of the study participants had dementia at the beginning of the
As well as being evaluated for cognitive fitness, all participants had their strength
measured in nine muscle groups in the arms and legs, and in the core body
muscles. Data on several other variables were also gathered, including age, sex,
education status, body mass index, levels of physical activity, lung function,
vascular risk factors, vascular diseases, and genetic status for apolipoprotein E4
(the apolipoprotein E4 genetic variant is associated with Alzheimer’s disease).
Participants were followed for nearly four years, during which time 138 persons
developed Alzheimer’s disease and 275 developed mild cognitive impairment.
After analyzing the results, the researchers found that increased muscle strength
was associated with a slower rate of decline in all aspects of cognitive function.
Those who developed Alzheimer's disease were older, had lower cognitive
function, and decreased strength in several muscles compared to those
participants who remained dementia-free. In fact, the stronger participants’
muscles were, the lower was their risk of developing Alzheimer's disease.
Muscle strength was also associated with a decreased risk of developing mild
cognitive impairment, which appears to be a precursor to Alzheimer’s disease.
These findings suggest that there may be a link between muscle strength,
Alzheimer’s disease, and cognitive decline in older persons.
Reference: Boyle PA, Buchman AS, Wilson RW, Leurgans SE, Bennett DA (2009).
Association of muscle strength with the risk of Alzheimer disease and the rate of
cognitive decline in community-dwelling older persons. Arch Neurol.; 66(11):1339-1344.
Family history, genetic status for apolipoprotein E4, and
Two areas of interest in research into dementia are the influences on cognitive
decline of a family history of Alzheimer dementia and the possession of a variant
of a gene that codes for the production of a form of a protein called
apolipoprotein E. (The variant of apolipoprotein E that is associated with
Alzheimer’s disease is apolipoprotein E4.)
Researchers from a number of institutions, including Duke University Medical
Center, The Johns Hopkins Bloomberg School of Public Health, the University of
Colorado, the Utah State University, and the University of Washington, invited
residents of Cache County, Utah, who were aged 65 years or older, to participate
in a study to examine the relationships between family history, genetic status,
and Alzheimer disease. The 2957 participants who took part provided DNA for
examination of their apolipoprotein E status and gave detailed family histories of
Alzheimer dementia. They also had their cognitive status evaluated with the
Modified Mini-Mental State Examination. Cognitive status was reexamined after
three years and again after seven years.
At the beginning of the study, those participants with the apolipoprotein E4
genetic variant scored lower on the Modified Mini-Mental State Examination than
participants who did not have either apolipoprotein E4 or a family history of
Those participants who had a family history of Alzheimer disease and the
apolipoprotein E4 genetic variant showed faster cognitive faster over the seven-
year study than those who did not, but each factor alone did not appear to be
associated with cognitive decline. The researchers concluded that much of the
apparent association among family history of Alzheimer disease, genetic status
for apolipoprotein E4, and cognitive decline may be attributed to disease that had
been undetected at the beginning of the study.
Reference: Hayden KM; Zandi PP; West NA; Tschanz JT; Norton MC; Corcoran C;
Breitner JCS; Welsh-Bohmer KA (2009). Effects of Family History and Apolipoprotein
E4 Status on Cognitive Decline in the Absence of Alzheimer Dementia: The Cache
County Study. Arch Neurol.; 66(11):1378-1383.