11527 RESULTS
COMMENT The actions of TREM2 are extraordinarily complicated and not easily understood, at least so far. Some of the essential issues have been confounded by the complexity of the science, the use of a narrow range of disease endpoints, and the use of only a few
COMMENT We and others have consistently shown that the LOAD-associated TREM2 H157Y variant—which occurs right at TREM2’s ADAM10/17 cleavage site—increases shedding of sTREM2. It therefore decreases TREM2 signaling and function, because signaling-competent cell su
COMMENT This paper provides more evidence that interactions between APOE-HSPG may be involved in AD. Additionally, neurons secrete SPOCK1, which encodes testican1, which is a heparan sulfate and chondroitin sulfate proteoglycan. SPOCK1 is essential in forming and
COMMENT Variants of APOE have been known for years to influence disease risk and progression. However, teasing apart the cell types that are important to APOE’s effects has remained a challenge. Papers using iPSC-derived cell types in monoculture, co-culture, and
COMMENT The R136S Christchurch mutation is in the domain involved in the interaction between ApoE and heparan sulfate proteoglycans (HSPGs) which binds the low-density lipoprotein (LDL) and LDL receptor-related protein (LRP) receptors. The astrocyte-secreted HSPG
COMMENT The identification of rare variants in APOE that appear to protect against Alzheimer’s disease, such as V236E (Jacksonville) and R136S (Christchurch), present an exciting opportunity to better understand the mechanisms by which APOE may influence differen
COMMENT and-negative astrocytes within PSP by RNAscope. Sharma et al. do not comment on such a change in their
COMMENT In AD and in vascular dementia, microglia also mop up myelin debris. Since this debris is high in iron content, the microglia are killed via ferroptosis (Adeniyi et al., 2023). stromeyerc_235326 0 Ferroptosis of Microglia in Aging Human White Matter Injur
COMMENT The concept of using biomarkers to monitor disease is so appealing that it sometimes leads us to forget essential scientific critical thinking. This move follows a long process that increasingly equates dementia of the Alzheimer's type to the presenc
COMMENT It is strange to read this article and the two positive comments from Drs. Salloway and Knopman.
COMMENT Amyloid PET imaging offers advantages over CSF analysis for establishing the presence of elevated brain amyloid, and this has implications for routine diagnosis but especially for therapeutics. As we enter the new therapeutic era with lecanemab, the CMS d
COMMENT I welcome the CMS decision to end the CED for PET amyloid imaging and the removal of the limit on amyloid PET to a single lifetime scan. Assuming that local MACs follow suit, this should provide wider access for amyloid PET in clinical practice, opening t
COMMENT This manuscript is enormously important for understanding disease mechanisms in PSP and FTD. In Alzheimer’s, the identification of many genetic risk variants over the last decade had shown us the crucial involvement of lipid metabolism, immune dysfunction
COMMENT Tau pathology is a common feature of several neurodegenerative diseases, but there are intriguing disease-specific differences: Each tauopathy is associated with a different spectrum of genetic risk factors, distinct cell types are affected, and recent cr
COMMENT It is exciting to start seeing results of the worldwide push to understand and map the complexity of the brain in order to both better understand what makes us human and to pave the way for treatments for neurological and psychiatric diseases. As a neuros
